Category: Flu Virus

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Will the Flu Arrive by October 2022? – Precision Vaccinations

September 3, 2022

(Precision Vaccinations)

According to the latest U.S. Center for Disease Control and Prevention (CDC) report, the 2022-2023 influenza viruses have yet to arrive in the USA.

While seasonal influenza (flu) viruses are detected year-round, the exact timing and duration of flu seasons vary. Influenza activity often increases in October, with peakactivitybetween December and February, says the CDC.

In the CDC's Weekly U.S. Influenza Surveillance Report, published on September 2, 2022, the results of 10,805 influenza tests performed by public health laboratories nationwide identified only 40positive specimens.

Nationwide during week #34, about 1.8% of patient visits were due to respiratory illness that included fever plus a cough or sore throat, also referred to as Influenza-like Illness (ILI).

The CDC says multiple respiratory viruses are co-circulating, and the relative contribution of influenza virus infection to ILI varies by location.

Moreover, theNational Center for Health StatisticsMortality Surveillance data available on September 1, 2022, about 9.2% of the deaths that occurred during week #34were due to pneumonia, influenza, and/or COVID-19 (PIC).

Among the 2,117 PIC deaths reported last week, 1,120 had COVID-19 listed as an underlying or contributing cause of death on the death certificate, 898 had pneumonia listed,and just eight listed influenza.

This data indicates that current PIC mortality is due primarily to COVID-19 and pneumonia, but not influenza.

Globally, the World Health Organization (WHO) publishedInfluenza Update N 426, which concluded, 'In the temperate zones of the southern hemisphere, overall influenza activity appeared to decrease during this reporting period.'

The WHO stated, 'Various measures implemented by the Member States to reduce SARS-CoV-2 coronavirus transmission have likely played a role in reducing influenza virus transmission.'

Given the apparent lull in influenza activity, a common question is 'when should people get their annual flu shot?

The good news is over 100 million vaccinesfor the 2022-2023 flu season have already arrived in the USA.

The CDC confirmed on August 23, 2022, 'The best way to reduce your risk from seasonal flu and its potentially serious complications is for most people sixmonths and older toget vaccinated yearly.'

September and October are generally good times to get vaccinated for most people who need only one dose for the season.

While ideally, it's recommended to get vaccinated by the end of October, it's essential to know that vaccination after October can still protect during the peak of flu season, says the CDC.

As with every vaccination, the best immunization decisions are made between a person and their doctors, nurse, or pharmacists.

Additional flu shot news is posted at PrecisionVaccinations.com/Flu.

Note: These CDC and WHO data are preliminary and may change as more data are received and processed.

PrecisionVaccinations publishes fact-checked, research-based vaccine news curated for mobile readership.

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Will the Flu Arrive by October 2022? - Precision Vaccinations

Synthetic DNA nasal spray could stop COVID, flu, and other viruses – Freethink

September 3, 2022

Researchers around the world have been racing to develop new vaccines, antivirals, and other therapies to blunt SARS-CoV-2s attack, even while the virus evolves to become an endemic problem.

While existing vaccines are capable of reducing severe cases of COVID-19, at least with a recent booster, continued mutations and the difficulty of maintaining high booster rates mean that better defenses will need to be developed.

Vaccines are making a huge difference, but vaccines are not universal, and there is still a tremendous need for other approaches, Anders Nr, a professor of metabolic biology at UC Berkeley, said.

While existing vaccines are capable of reducing severe cases of COVID-19, continued mutations and the difficulty of maintaining high booster rates mean that other defenses will need to be developed.

Nr and his Cal colleagues approach uses inhalable, DNA-like molecules to throw a wrench into the coronaviruss replication machine.

A nasal spray that is cheaply available everywhere and that could prevent someone from getting infected or prevent serious disease could be immensely helpful, Nr said.

Gumming up the works: The Berkeley teams nasal spray, published in Nature Communications, uses short snippets of synthetic DNA called antisense oligonucleotides or ASOs for short.

ASOs can be programmed to glom onto specific strings of RNA blocking them from being copied or turned into proteins.

Nr has been studying the use of ASOs for over a decade, trying to figure out how to use them to affect RNA involved in conditions like type 2 diabetes, Duchenne muscular dystrophy, and fatty liver disease.

But when the pandemic hit, they set their sights on a different type of RNA virus RNA.

The SARS-CoV-2 genome is single-stranded RNA, similar to messenger RNA or microRNA, Nr said. We thought perhaps we could use these ASOs to stick onto the viral RNA and prevent it from working.

The nasal spray uses DNA-like molecules to gum up SARS-CoV-2s replication.

The hairpin bend: Working with the Innovative Genomics Institute and Berkeley researcher Sarah Stanleys lab, the team sicced hundreds of different ASOs all designed to attack different parts of the genome on SARS-CoV-2.

One target in particular proved effective: a non-coding portion of the virus RNA that forms a hairpin and seems to play a key role in replication. With an ASO stuck to its hairpin, the virus was unable to replicate.

The ASOs stopped the coronavirus from replicating in human cells in the lab, and in animal experiments, it both prevented infection, when given early, and treated COVID-19 after infection.

We showed that if you bind an ASO to this hairpin, it dissolves the hairpin, and the RNA forms a straight line instead of a bubble structure, Nr said. We think that this prevents the virus from effectively translating and replicating, and we found that it was incredibly effective at preventing viral replication in human cells.

When sprayed in the noses of mice and hamsters, the ASO protected against and treated COVID-19, but just as importantly, it did not spark an immune response of its own suggesting it likely wont cause toxic side effects in people.

The hairpin is found in all known variants of SARS-CoV-2, and the teams ASOs were shown to be effective against variants of concern, including Delta and Omicron.

A nasal spray that is cheaply available everywhere and that could prevent someone from getting infected or prevent serious disease could be immensely helpful.

Next steps: ASOs are stable and relatively cheap to produce at scale, the researchers said, making them a potential boon for fighting the virus around the world.

Theyre also a promising way to attack other RNA viruses, like influenza, RSV, and other respiratory viruses, since they can be designed to stick to any RNA genome. The team has already found an ASO which sticks to a target in SARS-1, and they have begun preliminary work on influenza.

More research will be required before human clinical trials can begin, though.

Its very clear that this virus is not going away, Nr said. We need a lot of different avenues to tackle it, and therapeutics like ours that are agnostic to the variants could play a major role.

Wed love to hear from you! If you have a comment about this article or if you have a tip for a future Freethink story, please email us at [emailprotected]

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Synthetic DNA nasal spray could stop COVID, flu, and other viruses - Freethink

What to know about the tomato flu virus doctors are tracking in India – WATE 6 On Your Side

September 3, 2022

(NEXSTAR) In case we didnt have enough viruses to worry about, reports of a tomato flu outbreak in India started to surface this month. The virus, named for the bursting red blisters it causes, has infected at least 100 children.

The virus was first identified in Kerala in May, where it infected 82 children all under the age of 5 by the end of July, according to The Lancet medical journal. At least 26 more cases were also confirmed in neighboring states of India.

The most common symptoms appear to be fever, joint pain and the rash that gives the virus its new nickname. Tomato flu gained its name on the basis of the eruption of red and painful blisters throughout the body that gradually enlarge to the size of a tomato, The Lancet reported.

News outlets started to report on the disease as a new virus, but new testing out of the United Kingdom seems to indicate the tomato flu isnt new at all nor is it a type of flu.

Viral swabs were taken from two children who had recently returned from India showing the bright red rash, reports the British medical journal BMJ. The test came back positive for Coxsackie A16, a pathogen commonly associated with Hand, Foot, and Mouth Disease (or HFMD).

According to the Centers for Disease Control and Prevention, HFMD is very common among children, even here in the United States, because of how contagious it is. The symptoms including fever, mouth sores and skin rashes last seven to 10 days for most kids.

When there is a rash with HFMD, the rash usually is not itchy and looks like flat or slightly raised red spots, sometimes with blisters that have an area of redness at their base, says the CDC.

This common disease may have been initially mistaken as a new tomato flu virus because the blisters observed in India were larger.

Doctors in Kerala told BMJ that even in the cases they have seen over the past few months, they have yet to admit any children to the hospital. All of the patients have recovered on their own thus far.

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What to know about the tomato flu virus doctors are tracking in India - WATE 6 On Your Side

Omicron boosters targeting the BA.4, BA.5 subvariants are coming to Colorado. Here’s what you need to know. – Denver 7 Colorado News

September 3, 2022

DENVER New COVID-19 boosters that target the most prominent omicron strains of the novel coronavirus currently spreading throughout the country will soon be available in Colorado.

While the current vaccines still offer strong protection against hospitalization and death, immunity against infection has dropped significantly as more immune evasive variants have emerged over the course of the pandemic.

The arrival of the BA.4/5 COVID-19 boosters is good news for those looking for added protection, but how much of it they will create remains to be seen.

Denver7 spoke with Heather Roth, the Colorado Department of Public Health and Environment's immunization branch chief, to talk about their efficacy, how they were approved, what the new boosters mean for families looking to vaccinate their kids as we enter a new school year, and more.

Please note: This interview has been edited for time and clarity.

1. The CDC has approved the bivalent COVID-19 BA.4/5 boosters, meaning the vaccine has components from the wild type strain (the original Wuhan strain of the novel coronavirus) and the BA.4/5 sublineages of the omicron variant.

What do we know about the efficacy of these boosters against severe disease, and, more importantly, against transmission and infection, given that no human neutralization data was submitted and only mice data was used, as it is done with the flu vaccine each year?

I think the important thing to know is that the updated vaccines were developed and manufactured using the same process as the original vaccines, except that they now contain a second component, right? And that is a component targeting the omicron BA.4 and BA.5 subvariants.

In kind of reviewing the data in making this decision, both the FDA and CDC looked at the safety and effectiveness data from the original mRNA vaccines that have been administered to hundreds of millions of people in the U.S. alone. They also looked at safety and immune response from the bivalent booster studies of about 1,400 people that included the original strain and what had been the BA.1 variant. And then, as you mentioned, data from a study of the new omicron vaccines in mice. Based on all of that kind of taken together, the vaccines are expected to increase protection against the currently circulating omicron BA.4/BA.5 subvariants.

2. Many people skeptical of COVID-19 vaccines and the virus itself will say its just a cold or its just a flu. First of all, is COVID-19 the same as the flu?

No, they're obviously two different viruses and they cause different severe effects if you end up getting sick.

There's no such thing as long flu but there is such a thing as long COVID, right? There are two separate things and they're both quite real, and we're heading into the fall; they're both going to be circulating at the same time.

3. Knowing that COVID is not the same as the flu, should it concern people that the CDC is applying a flu-like approach to these boosters before humantrial data is complete? After all, flu shots typically arent very effectiveso wouldnt we want to know how effective these COVID boosters are going to be before rolling them out?

I think comparing development of flu vaccines to really any other vaccine is like comparing apples to oranges. The science the data that kind of the guessing game that goes behind flu vaccine development is very different than what we're talking about with COVID, where we know exactly which subvariants are circulating predominantly in the U.S. and in Colorado right now.

Back to the mice study, youre asking about how effective these are going to be. Those mice studies suggest that these new vaccines will be about 20 times more protective against Omicron than the original vaccines that we've been having for more than two years now, and about 5 times more protective than the manufacturers first attempt at Omicron-specific bivalent vaccines with that BA.1 component.

I will add that human clinical trials are going on right now with the BA.4/BA.5 components and so we'll have more data in another month or two on that particular piece (of the puzzle).

3. When are the updated booster shots arriving to Colorado and when will I be able to get one?

So actually, the first shipment started arriving yesterday and we're going to have about 294,000 doses available on our first two waves of shipments. I think the majority of the doses will be arriving after Labor Day next week.

You'll be able to find a vaccine appointment at many of the same providers that have been offering COVID vaccines, again, for two years now so your retail pharmacies, your primary care providers, local public health agencies, and then our state-run clinics too so our mobile buses and our community vaccine sites that will be coming online very soon.

4. Is the state going to host a news conference when these boosters are available or is there going to be some sort of statewide communication via text telling Coloradans that these updated boosters are here and its time to go and get yours?

We haven't quite gotten to the point where we'll be doing direct outreach. I can see that happening after the first couple of weeks of rollout as that initial demand might decrease where we do some performed outreach to people to make sure they're aware of this change and this new vaccine.

5. The updated boosters are only available for people 12 and older (Pfizer) and 18 and older (Moderna). When will kids under the age of 12 be able to get these updated boosters?

I think that the manufacturers have said that it's going to be another month or two before they have the data that they would need to submit an application to the FDA for omicron-containing booster doses for kids under the age of 12.

6. Should parents wait until theyre approved, or should parents get their kids a booster from the original COVID-19 vaccine instead, even though the variant currently circulating in the state right now is omicron?

The guidance that has been in place for a long time hasn't changed. If you are due for a booster dose now, you should get it now. There is still some protection offered, particularly against severe disease and severe outcomes that come through the original vaccine for those younger age groups.

So if youre due I would get it now, knowing that something's coming along the way and in a month or two that you would be eligible for as well.

7. Where do we stand as far as children and their overall vaccination requirements.We saw the vaccination rates fall at the start of the pandemic for children.Has that percentage increased?If not, is the state looking at any programs to increase overall vaccination rates?

So you're right that COVID has disrupted just kind of our routine wellness child visits, our routine regular vaccine visits, and we've seen some increases over the last couple of years where we've kind of climbed out of that valley and out of that decrease.

But we are seeing continued, sustained decreases in other vaccines, in other age groups. One of the things the Colorado Department of Public Health and Environment has done recently is actually doing direct text and email outreach to families whose children are overdue for you know, required school vaccines for example, making sure that they're aware that their kids are missing one or more vaccines, and then linking them up with resources to get them back on track.

8. Should there be any hesitation about combining shots (i.e.: COVID and flu shots or COVID and monkeypox)?

I would say overall, no. If we're talking about flu and a new omicron dose, now is a perfect time to actually roll up both sleeves and get the flu in one arm, your omicron dose in the other, and that really has to do with timing: September and October are the best months to get your seasonal flu vaccine, it gives your body enough time to build protection before that flu virus is circulating widely and it's completely safe and effective to get multiple vaccines on the same day.

There are some special considerations for monkeypox. I don't have the data at hand, but I know it has to do with monkeypox and COVID mRNA vaccines and the theoretical risk of increased myocarditis or pericarditis if those are given on the same day.

(Editor's note: Myocarditis is an inflammation of the heart, whereas pericariditis is an inflammation of the pericardium - a two-layered, sac-like membrane that surrounds the heart.)

9. What about whooping cough (also known as pertussis). Theres reports that cases are on the rise in certain parts of the country. Are we seeing a rise? What is the real concern? Should people get vaccinated against whooping cough?

I don't know what our pertussis case rates look like right now. I'm unaware of any concerning equal increases, but I can say that based on data that we collected from schools and childcare centers for last school year, that we have seen some decreases in vaccine uptake that prevent pertussis from spreading.

Pertussis is a really contagious communicable disease and we want to make sure that we keep our rates high, to keep that out of out of communities and out of schools.

Editors note: Pertussis is a highly contagious respiratory disease caused by the bacterium Bordetella pertussis. The illness is known for uncontrollable, violent coughing which often makes it hard to breathe. A CDC fact sheet states pertussis can affect people of all ages, but can be very serious, even deadly, for babies less than a year old.

10. The BA.5 variant is the predominant in Colorado, but infections, hospitalizations and the states positivity rate are all trending downward. The COVID-19 modeling team even estimates immunity from infection and hospitalization has increased over the past two months: Colorado has upwards of 60-65% immunity against infection and around 85-90% immunity against severe disease. Is it worth getting the BA.4/5 booster at this point for the fall if immunity from the BA.5 variant is this high?

I think it's a personal decision that someone can make and have conversations with their healthcare provider, but as the virus has evolved, so has the vaccine.

This is really exciting that we have science kind of closer to where variants are, that we're not chasing variants quite as much as we have been over the last couple of years. It's the latest and greatest vaccine that's available and getting this updated vaccine is really the safest and easiest way to be protected at maximum levels through the fall and winter.

Those wanting to get the bivalent omicron COVID-19 boosters should get them at least two months after their most recent dose of the COVID-19 vaccine. If you were recently infected, the CDPHE says you should wait at least three months after your SARS-CoV-2 infection before getting a BA.4/5 booster.

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Omicron boosters targeting the BA.4, BA.5 subvariants are coming to Colorado. Here's what you need to know. - Denver 7 Colorado News

Why is swine flu seeing a resurgence in India this year? – Scroll.in

September 3, 2022

Seventy-two people in Maharashtra have died from swine flu in the past three months. The viral infection, which is caused by the H1N1 virus, is seeing a resurgence in western India this year, with Maharashtra alone recording 1,870 cases till August 23.

The caseload across India is likely to have crossed at least 2,800 so far this year, a threefold jump from the previous year. In contrast, H1N1 deaths for the entire country in 2021 stood at 12.

Does the resurgence of the H1N1 virus have anything to do with Covid-19 on the verge of turning endemic or is the virus following a cyclic pattern? Scroll.in spoke to doctors and scientists to understand why H1N1 cases plunged during the past two years only to bounce back this year.

H1N1 is a viral infection with symptoms involving cold, fever, sore throat, body ache and headache. In severe cases, it leads to pneumonia and acute respiratory distress syndrome.

The H1N1 pandemic first broke out in April 2009 and, unlike Covid-19, subsided quickly by 2010. The World Health Organization had declared the end of the H1N1 influenza pandemic by August 2010.

Since then it has been endemic, occurring in the form of a seasonal flu. Epidemiologist Dr Jayaprakash Muliyil, chairperson of the Scientific Advisory Committee at the National Institute of Epidemiology, said that once 40% of the population had attained herd immunity in the 2009-10 outbreak, the virus transmission slowed down.

Note that H1N1 is not as transmissible as coronavirus, he said. Each virus has a different threshold. According to Muliyil, even though 60% of the population was unexposed, the number of H1N1 cases began rapidly declining.

Swine flu made a reappearance in 2012, with a high number of cases in Maharashtra, Karnataka, Kerala, Tamil Nadu, Andhra Pradesh and Rajasthan. Because the susceptibility to infection increased in the population over a period of time, he said.

Since then, H1N1 has maintained a cyclic pattern. Cases spike around monsoon and winter, with the monsoons recording a larger share of cases than winters in India. Its susceptibility builds up over a year or two and then cases rise in the following year, Muliyil said, explaining that herd immunity against the virus wanes.

Before vaccination was rolled out, the measles epidemic too occurred once in two to three years, and rubella once in six to seven years. While a vaccine against influenza to prevent H1N1 was introduced in late 2009, its uptake in India remains low.

In the last decade, H1N1 cases surged in 2015 then 2017 and then in 2019. Since the past two years, however, the number of H1N1 cases have been at an all-time low. Cases in India dropped from 28,798 in 2019 to 2,752 with 44 deaths in 2020. In 2021, there was a further decline to 778 cases and 12 deaths.

But this year, cases are rising again. Data provided by the National Centre for Disease Control for H1N1 till June 30 showed that India recorded 424 cases and 12 deaths in the first half of this year. By July-end, the figure rose to 1,455 cases. At least 17 deaths were recorded in July alone. Trends indicate these figures are expected to rise further in August.

Gujarat and Karnataka are also seeing a rising trend in cases. In 2021, Karnataka had recorded 13 cases but as of July-end, it had 283 cases of H1N1. Gujarat had recorded 33 cases in 2021 and by July-end this year it had 205 cases.

Some medical experts say the lull in H1N1 over the past two years may have been related to the outbreak of the Covid-19 pandemic in early 2020. For one, Covid-19 appears to have diverted testing resources, which may have led to an underdetection of swine flu cases.

But some medical experts believe Covid-19 may have contributed to low H1N1 circulation as well. Dr Rajesh Karyakarte, Professor and Head of Microbiology Department at BJ Government Medical College, said whenever Covid-19 waves rose, other viruses sort of disappeared.

We saw this with all the three waves, he said. Now that Covid-19 is ebbing, H1N1 rise is not surprising. According to Karyakarte, when a virus infects a person, the body releases interferons. These are signalling proteins released by the bodys immune system to fight infection and other diseases.

Karyakarte noted that Covid-19, due to its high transmissibility, infected almost the entire population. When an H1N1 virus tried to infect the same person, the interferons would respond making it difficult for H1N1 to cause infection, he said.

Dr Pradeep Awate, Maharashtra state epidemiologist, also said that coronavirus managed to wipe out other viruses during the peak of the pandemic.

But Muliyil and Dr Gagandeep Kang, professor at the Christian Medical College, Vellore, said there is no scientific evidence to suggest that a dominant virus drives away other viruses.

According to Muliyil, what may have happened is that when two viral infections occur simultaneously in a body, one virus may modify the clinical outcome, duration of infection and severity caused by the other virus. That may have been the fate of H1N1 infection these past two years, he said.

Kang said that in the same family of a virus, a dominant variant may replace a weaker one, as seen with the Omicron variant of Covid-19. But there is no evidence to suggest that the coronavirus replaced H1N1 in 2020 and 2021. Influenza is not as transmissible as Covid-19. Mask adherence may have deterred its transmission further, she said.

An analysis of the 72 deaths in Maharashtra showed that 85% of the deceased were 40 years of age or older while 65% had another illness or suffered from a comorbidity.

In 30 to 35% deaths, oseltamivir medicine was started for the patient within two days of symptoms, Awate said. Oseltamivir is an antiviral used to treat H1N1. Awate added that the high fatality cannot be attributed to only the delay in treatment.

In Maharashtra, the current case fatality rate, or number of people dying out of those diagnosed, stands at 3.8%. Awate said that not all symptomatic cases are being tested, hence the base pool to calculate fatality rate is small.

There are four categories of patients those under A and B have mild symptoms such as a cold and low-grade fever that can be managed at home. Doctors and hospitals may or may not recommend a test for them.

In category C, patients develop pneumonia or have lung involvement leading to breathlessness while in category D, the symptoms are severe. Category C and D require hospitalisation and they are being actively tested, Awate said.

There are also few government laboratories in India that are testing H1N1 as of now. Some laboratories have raised concerns about the lack of sufficient testing kits. At private facilities, the cost per test is between Rs 4,000-Rs 5,000. In Maharashtra, senior health officials have urged the state government to cap the rates of H1N1 testing. The state government is yet to announce a price cap.

Kang, from the Christian Medical College, said 72 deaths in just three months in one state is a high figure. This is just the apex of the pyramid, she said. Essentially, it is telling you there is a lot of virus circulating.

Globally, the death rate of H1N1 is less than 1%. A higher fatality rate in India indicates a lack of adequate diagnosis. Kang said that compared to the issue of not diagnosing all H1N1 cases, a bigger concern is the complete lack of diagnosis of other influenza-like illnesses. It is like looking under a lamppost where there is light, said Kang. There are other influenza [viruses] which are in the dark and not even getting detected.

This reporting was supported by a grant from the Thakur Family Foundation. Thakur Family Foundation has not exercised any editorial control over the contents of this article.

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Why is swine flu seeing a resurgence in India this year? - Scroll.in

Fauci warns of bad flu season brewing as he nears office exit – The Peninsula

September 3, 2022

National Institute of Allergy and Infectious Diseases Director Dr. Anthony Fauci attends the daily coronavirus task force briefing at the White House in Washington, on April 13, 2020. File Photo / Reuters

Washington: President Joe Bidens medical adviser Anthony Fauci warned that the US should be prepared for "pretty bad flu season coupled with continued Covid-19 cases this winter when hell be stepping down from his post as the nations top infectious disease official.

The Southern Hemisphere, which annually sees new strains of flu appear before the North, has already experienced a more severe season than usual, Fauci said on Wednesday in an interview, and Americans should get flu shots when they become available.

An early uptick in influenza cases has alarmed Australian public health officials, where the flu season runs from April to September. They expect the season could be similar that of 2019, which saw record-setting levels of infections. That set off warning signals for the US about a potentially severe seasonal influenza this fall and winter, Fauci said.

"We should be prepared for that superimposed upon what I hope is the residual and not another spike of Covid, said Fauci, whos also director of the National Institute of Allergy and Infectious Diseases. "We better pay attention.

Fauci spoke with Bloomberg about his expectations for the nations continued fight against Covid, flu and other threats with pandemic potential just over a week after he announced plans to step down in December. His departure will end a historic career in which he advised seven presidents over nearly four decades on outbreaks ranging from HIV to Ebola and now monkeypox.

Earlier on Wednesday, the US Food and Drug Administration cleared new Covid-19 boosters from Moderna Inc. and the partnership of Pfizer Inc. and BioNTech SE that are tailored to the latest omicron variants, a move toward additional protection as concern grows about potential new waves in the fall and winter. The clearance, which was based on animal data rather than human studies, is similar to the process in which flu shots are approved, Fauci said.

"Im comfortable with that decision, he said.

He added that the new boosters could help stymie a double-whammy of Covid and flu this winter, while acknowledging concern about low vaccination rates in the US. Looking ahead, Fauci hopes that the US continues to innovate and improve existing vaccines and therapeutics as the virus evolves.

"One of the mistakes weve made is that we concentrate on the problem thats right in front of you, and put of focusing on what might be a problem in the future, he said.

Fauci helped launch the Antiviral Program for Pandemics last year with the aim of developing and discovering next-generation treatments for Covid and other infectious diseases. He said he sees promise in a Covid therapeutic candidate from Japanese drugmaker Shionogi & Co. and believes that combination therapies will soon be necessary to counter resistance that can occur as the virus learns to evade more drugs.

Fauci said hes been in touch with drugmaker Pfizer Inc. and its Chief Executive Officer Albert Bourla about the need to test combinations of drugs including Paxlovid, the companys Covid antiviral. These studies could include collaborations with the National Institutes of Health, he said.

"Sooner or later, youre going to get resistance to Paxlovid, he said.

Faucis upcoming exit will cover all his government posts, wrapping up an NIH career spanning more than a half century, including 38 years leading NIAID. As infectious diseases chief, he leads the second-largest of the NIHs 27 institutes and centers, with a $6.3 billion budget.

Even if the pandemic takes a turn for the worse, hell go ahead with his plans to step down, he said. Biden has been "extraordinarily supportive of his decision, Fauci said.

While long one of the most visible US scientists, Covid-19 propelled him into the spotlight, where he became a household name. Hes been both lionized and vilified amid increasingly political divisions over public health measures such as masking.

Despite the divisions and vitriol, "I believe his enduring legacy as a physician-scientist and humanitarian is assured, Francis Collins, the former longtime NIH director and acting White House science adviser, said in an email. He called Fauci "the most dedicated public servant I have ever known.

Fauci said hell continue his work advancing public health and science outside of the government while mentoring the next generation of scientists, particularly those focused on HIV.

"Im not going to re-establish my laboratory, but I will be advising from a scientific standpoint because I do have a lot of experience in vaccinology and in HIV, he said. "I will be making input probably in advisory panels and on boards of scientific councils and things like that to go for a vaccine.

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Fauci warns of bad flu season brewing as he nears office exit - The Peninsula

Influenza – Wikipedia

August 30, 2022

Infectious disease, "the flu"

Medical condition

Influenza, commonly known as "the flu", is an infectious disease caused by influenza viruses. Symptoms range from mild to severe and often include fever, runny nose, sore throat, muscle pain, headache, coughing, and fatigue. These symptoms begin from one to four days after exposure to the virus (typically two days) and last for about 28 days. Diarrhea and vomiting can occur, particularly in children. Influenza may progress to pneumonia, which can be caused by the virus or by a subsequent bacterial infection. Other complications of infection include acute respiratory distress syndrome, meningitis, encephalitis, and worsening of pre-existing health problems such as asthma and cardiovascular disease.

There are four types of influenza virus, termed influenza viruses A, B, C, and D. Aquatic birds are the primary source of Influenza A virus (IAV), which is also widespread in various mammals, including humans and pigs. Influenza B virus (IBV) and Influenza C virus (ICV) primarily infect humans, and Influenza D virus (IDV) is found in cattle and pigs. IAV and IBV circulate in humans and cause seasonal epidemics, and ICV causes a mild infection, primarily in children. IDV can infect humans but is not known to cause illness. In humans, influenza viruses are primarily transmitted through respiratory droplets produced from coughing and sneezing. Transmission through aerosols and intermediate objects and surfaces contaminated by the virus also occur.

Frequent hand washing and covering one's mouth and nose when coughing and sneezing reduce transmission. Annual vaccination can help to provide protection against influenza. Influenza viruses, particularly IAV, evolve quickly, so flu vaccines are updated regularly to match which influenza strains are in circulation. Vaccines currently in use provide protection against IAV subtypes H1N1 and H3N2 and one or two IBV subtypes. Influenza infection is diagnosed with laboratory methods such as antibody or antigen tests and a polymerase chain reaction (PCR) to identify viral nucleic acid. The disease can be treated with supportive measures and, in severe cases, with antiviral drugs such as oseltamivir. In healthy individuals, influenza is typically self-limiting and rarely fatal, but it can be deadly in high-risk groups.

In a typical year, 515% of the population contracts influenza. There are 35 million severe cases annually, with up to 650,000 respiratory-related deaths globally each year. Deaths most commonly occur in high-risk groups, including young children, the elderly, and people with chronic health conditions. In temperate regions of the world, the number of influenza cases peaks during winter, whereas in the tropics influenza can occur year-round. Since the late 1800s, large outbreaks of novel influenza strains that spread globally, called pandemics, have occurred every 1050 years. Five flu pandemics have occurred since 1900: the Spanish flu in 19181920, which was the most severe flu pandemic, the Asian flu in 1957, the Hong Kong flu in 1968, the Russian flu in 1977, and the swine flu pandemic in 2009.

The time between exposure to the virus and development of symptoms, called the incubation period, is 14 days, most commonly 12 days. Many infections, however, are asymptomatic.[8] The onset of symptoms is sudden, and initial symptoms are predominately non-specific, including fever, chills, headaches, muscle pain or aching, a feeling of discomfort, loss of appetite, lack of energy/fatigue, and confusion. These symptoms are usually accompanied by respiratory symptoms such as a dry cough, sore or dry throat, hoarse voice, and a stuffy or runny nose. Coughing is the most common symptom.[1] Gastrointestinal symptoms may also occur, including nausea, vomiting, diarrhea,[9] and gastroenteritis,[10] especially in children. The standard influenza symptoms typically last for 28 days.[11] A 2021 study suggests influenza can cause long lasting symptoms in a similar way to long COVID.[12]

Symptomatic infections are usually mild and limited to the upper respiratory tract, but progression to pneumonia is relatively common. Pneumonia may be caused by the primary viral infection or by a secondary bacterial infection. Primary pneumonia is characterized by rapid progression of fever, cough, labored breathing, and low oxygen levels that cause bluish skin. It is especially common among those who have an underlying cardiovascular disease such as rheumatic heart disease. Secondary pneumonia typically has a period of improvement in symptoms for 13 weeks[13] followed by recurrent fever, sputum production, and fluid buildup in the lungs,[1] but can also occur just a few days after influenza symptoms appear.[13] About a third of primary pneumonia cases are followed by secondary pneumonia, which is most frequently caused by the bacteria Streptococcus pneumoniae and Staphylococcus aureus.[8][1]

Influenza viruses comprise four species. Each of the four species is the sole member of its own genus, and the four influenza genera comprise four of the seven genera in the family Orthomyxoviridae. They are:[1][14]

IAV is responsible for most cases of severe illness as well as seasonal epidemics and occasional pandemics. It infects people of all ages but tends to disproportionately cause severe illness in the elderly, the very young, and those who have chronic health issues. Birds are the primary reservoir of IAV, especially aquatic birds such as ducks, geese, shorebirds, and gulls,[15][16] but the virus also circulates among mammals, including pigs, horses, and marine mammals. IAV is classified into subtypes based on the viral proteins haemagglutinin (H) and neuraminidase (N).[17] As of 2019, 18 H subtypes and 11 N subtypes have been identified. Most potential combinations have been reported in birds, but H17-18 and N10-11 have only been found in bats. Only H subtypes H1-3 and N subtypes N1-2 are known to have circulated in humans,[17] the current IAV subtypes in circulation being H1N1 and H3N2.[2] IAVs can be classified more specifically to also include natural host species, geographical origin, year of isolation, and strain number, such as H1N1/A/duck/Alberta/35/76.[1][9]

IBV mainly infects humans but has been identified in seals, horses, dogs, and pigs.[17] IBV does not have subtypes like IAV but has two antigenically distinct lineages, termed the B/Victoria/2/1987-like and B/Yamagata/16/1988-like lineages,[1] or simply (B/)Victoria(-like) and (B/)Yamagata(-like).[17][2] Both lineages are in circulation in humans,[1] disproportionately affecting children.[9] IBVs contribute to seasonal epidemics alongside IAVs but have never been associated with a pandemic.[17]

ICV, like IBV, is primarily found in humans, though it also has been detected in pigs, feral dogs, dromedary camels, cattle, and dogs.[10][17] ICV infection primarily affects children and is usually asymptomatic[1][9] or has mild cold-like symptoms, though more severe symptoms such as gastroenteritis and pneumonia can occur.[10] Unlike IAV and IBV, ICV has not been a major focus of research pertaining to antiviral drugs, vaccines, and other measures against influenza.[17] ICV is subclassified into six genetic/antigenic lineages.[10][18]

IDV has been isolated from pigs and cattle, the latter being the natural reservoir. Infection has also been observed in humans, horses, dromedary camels, and small ruminants such as goats and sheep.[17][18] IDV is distantly related to ICV. While cattle workers have occasionally tested positive to prior IDV infection, it is not known to cause disease in humans.[1][9][10] ICV and IDV experience a slower rate of antigenic evolution than IAV and IBV. Because of this antigenic stability, relatively few novel lineages emerge.[18]

Influenza viruses have a negative-sense, single-stranded RNA genome that is segmented. The negative sense of the genome means it can be used as a template to synthesize messenger RNA (mRNA).[8] IAV and IBV have eight genome segments that encode 10 major proteins. ICV and IDV have seven genome segments that encode nine major proteins.[10] Three segments encode three subunits of an RNA-dependent RNA polymerase (RdRp) complex: PB1, a transcriptase, PB2, which recognizes 5' caps, and PA (P3 for ICV and IDV), an endonuclease.[19] The matrix protein (M1) and membrane protein (M2) share a segment, as do the non-structural protein (NS1) and the nuclear export protein (NEP).[1] For IAV and IBV, hemagglutinin (HA) and neuraminidase (NA) are encoded on one segment each, whereas ICV and IDV encode a hemagglutinin-esterase fusion (HEF) protein on one segment that merges the functions of HA and NA. The final genome segment encodes the viral nucleoprotein (NP).[19] Influenza viruses also encode various accessory proteins, such as PB1-F2 and PA-X, that are expressed through alternative open reading frames[1][20] and which are important in host defense suppression, virulence, and pathogenicity.[21]

The virus particle, called a virion, is pleomorphic and varies between being filamentous, bacilliform, or spherical in shape. Clinical isolates tend to be pleomorphic, whereas strains adapted to laboratory growth typically produce spherical virions. Filamentous virions are about 250 nanometers (nm) by 80nm, bacilliform 120250 by 95nm, and spherical 120nm in diameter.[22] The virion consists of each segment of the genome bound to nucleoproteins in separate ribonucleoprotein (RNP) complexes for each segment, all of which are surrounded by a lipid bilayer membrane called the viral envelope. There is a copy of the RdRp, all subunits included, bound to each RNP. The envelope is reinforced structurally by matrix proteins on the interior that enclose the RNPs,[3] and the envelope contains HA and NA (or HEF[18]) proteins extending outward from the exterior surface of the envelope. HA and HEF[18] proteins have a distinct "head" and "stalk" structure. M2 proteins form proton ion channels through the viral envelope that are required for viral entry and exit. IBVs contain a surface protein named NB that is anchored in the envelope, but its function is unknown.[1]

The viral life cycle begins by binding to a target cell. Binding is mediated by the viral HA proteins on the surface of the evelope, which bind to cells that contain sialic acid receptors on the surface of the cell membrane.[1][15][3] For N1 subtypes with the "G147R" mutation and N2 subtypes, the NA protein can initiate entry. Prior to binding, NA proteins promote access to target cells by degrading mucous, which helps to remove extracellular decoy receptors that would impede access to target cells.[3] After binding, the virus is internalized into the cell by an endosome that contains the virion inside it. The endosome is acidified by cellular vATPase[20] to have lower pH, which triggers a conformational change in HA that allows fusion of the viral envelope with the endosomal membrane.[21] At the same time, hydrogen ions diffuse into the virion through M2 ion channels, disrupting internal protein-protein interactions to release RNPs into the host cell's cytosol. The M1 protein shell surrounding RNPs is degraded, fully uncoating RNPs in the cytosol.[20][3]

RNPs are then imported into the nucleus with the help of viral localization signals. There, the viral RNA polymerase transcribes mRNA using the genomic negative-sense strand as a template. The polymerase snatches 5' caps for viral mRNA from cellular RNA to prime mRNA synthesis and the 3'-end of mRNA is polyadenylated at the end of transcription.[19] Once viral mRNA is transcribed, it is exported out of the nucleus and translated by host ribosomes in a cap-dependent manner to synthesize viral proteins.[20] RdRp also synthesizes complementary positive-sense strands of the viral genome in a complementary RNP complex which are then used as templates by viral polymerases to synthesize copies of the negative-sense genome.[1][3] During these processes, RdRps of avian influenza viruses (AIVs) function optimally at a higher temperature than mammalian influenza viruses.[11]

Newly synthesized viral polymerase subunits and NP proteins are imported to the nucleus to further increase the rate of viral replication and form RNPs.[19] HA, NA, and M2 proteins are trafficked with the aid of M1 and NEP proteins[21] to the cell membrane through the Golgi apparatus[19] and inserted into the cell's membrane. Viral non-structural proteins including NS1, PB1-F2, and PA-X regulate host cellular processes to disable antiviral responses.[1][21][3] PB1-F2 aso interacts with PB1 to keep polymerases in the nucleus longer.[16] M1 and NEP proteins localize to the nucleus during the later stages of infection, bind to viral RNPs and mediate their export to the cytoplasm where they migrate to the cell membrane with the aid of recycled endosomes and are bundled into the segments of the genome.[1][3]

Progenic viruses leave the cell by budding from the cell membrane, which is initiated by the accumulation of M1 proteins at the cytoplasmic side of the membrane. The viral genome is incorporated inside a viral envelope derived from portions of the cell membrane that have HA, NA, and M2 proteins. At the end of budding, HA proteins remain attached to cellular sialic acid until they are cleaved by the sialidase activity of NA proteins. The virion is then released from the cell. The sialidase activity of NA also cleaves any sialic acid residues from the viral surface, which helps prevent newly assembled viruses from aggregating near the cell surface and improving infectivity.[1][3] Similar to other aspects of influenza replication, optimal NA activity is temperature- and pH-dependent.[11] Ultimately, presence of large quantities of viral RNA in the cell triggers apoptosis, i.e. programmed cell death, which is initiated by cellular factors to restrict viral replication.[20]

Two key processes that influenza viruses evolve through are antigenic drift and antigenic shift. Antigenic drift is when an influenza virus's antigens change due to the gradual accumulation of mutations in the antigen's (HA or NA) gene.[15] This can occur in response to evolutionary pressure exerted by the host immune response. Antigenic drift is especially common for the HA protein, in which just a few amino acid changes in the head region can constitute antigenic drift.[2][18] The result is the production of novel strains that can evade pre-existing antibody-mediated immunity.[1][9] Antigenic drift occurs in all influenza species but is slower in B than A and slowest in C and D.[18] Antigenic drift is a major cause of seasonal influenza,[23] and requires that flu vaccines be updated annually. HA is the main component of inactivated vaccines, so surveillance monitors antigenic drift of this antigen among circulating strains. Antigenic evolution of influenza viruses of humans appears to be faster than influenza viruses in swine and equines. In wild birds, within-subtype antigenic variation appears to be limited but has been observed in poultry.[1][9]

Antigenic shift is a sudden, drastic change in an influenza virus's antigen, usually HA. During antigenic shift, antigenically different strains that infect the same cell can reassort genome segments with each other, producing hybrid progeny. Since all influenza viruses have segmented genomes, all are capable of reassortment.[10][18] Antigenic shift, however, only occurs among influenza viruses of the same genus[19] and most commonly occurs among IAVs. In particular, reassortment is very common in AIVs, creating a large diversity of influenza viruses in birds, but is uncommon in human, equine, and canine lineages.[24] Pigs, bats, and quails have receptors for both mammalian and avian IAVs, so they are potential "mixing vessels" for reassortment.[17] If an animal strain reassorts with a human strain,[2] then a novel strain can emerge that is capable of human-to-human transmission. This has caused pandemics, but only a limited number have occurred, so it is difficult to predict when the next will happen.[1][9]

People who are infected can transmit influenza viruses through breathing, talking, coughing, and sneezing, which spread respiratory droplets and aerosols that contain virus particles into the air. A person susceptible to infection can then contract influenza by coming into contact with these particles.[13][25] Respiratory droplets are relatively large and travel less than two meters before falling onto nearby surfaces. Aerosols are smaller and remain suspended in the air longer, so they take longer to settle and can travel further than respiratory droplets.[25][4] Inhalation of aerosols can lead to infection,[26] but most transmission is in the area about two meters around an infected person via respiratory droplets[8] that come into contact with mucosa of the upper respiratory tract.[26] Transmission through contact with a person, bodily fluids, or intermediate objects (fomites) can also occur, such as through contaminated hands and surfaces[8][25] since influenza viruses can survive for hours on non-porous surfaces.[4] If one's hands are contaminated, then touching one's face can cause infection.[27]

Influenza is usually transmissible from one day before the onset of symptoms to 57 days after.[9] In healthy adults, the virus is shed for up to 35 days. In children and the immunocompromised, the virus may be transmissible for several weeks.[8] Children ages 217 are considered to be the primary and most efficient spreaders of influenza.[1][9] Children who have not had multiple prior exposures to influenza viruses shed the virus at greater quantities and for a longer duration than other children.[1] People who are at risk of exposure to influenza include health care workers, social care workers, and those who live with or care for people vulnerable to influenza. In long-term care facilities, the flu can spread rapidly after it is introduced.[9] A variety of factors likely encourage influenza transmission, including lower temperature, lower absolute and relative humidity, less ultraviolet radiation from the Sun,[26][28] and crowding.[25] Influenza viruses that infect the upper respiratory tract like H1N1 tend to be more mild but more transmissible, whereas those that infect the lower respiratory tract like H5N1 tend to cause more severe illness but are less contagious.[8]

In humans, influenza viruses first cause infection by infecting epithelial cells in the respiratory tract. Illness during infection is primarily the result of lung inflammation and compromise caused by epithelial cell infection and death, combined with inflammation caused by the immune system's response to infection. Non-respiratory organs can become involved, but the mechanisms by which influenza is involved in these cases are unknown. Severe respiratory illness can be caused by multiple, non-exclusive mechanisms, including obstruction of the airways, loss of alveolar structure, loss of lung epithelial integrity due to epithelial cell infection and death, and degradation of the extracellular matrix that maintains lung structure. In particular, alveolar cell infection appears to drive severe symptoms since this results in impaired gas exchange and enables viruses to infect endothelial cells, which produce large quantities of pro-inflammatory cytokines.[13]

Pneumonia caused by influenza viruses is characterized by high levels of viral replication in the lower respiratory tract, accompanied by a strong pro-inflammatory response called a cytokine storm.[1] Infection with H5N1 or H7N9 especially produces high levels of pro-inflammatory cytokines.[15] In bacterial infections, early depletion of macrophages during influenza creates a favorable environment in the lungs for bacterial growth since these white blood cells are important in responding to bacterial infection. Host mechanisms to encourage tissue repair may inadvertently allow bacterial infection. Infection also induces production of systemic glucocorticoids that can reduce inflammation to preserve tissue integrity but allow increased bacterial growth.[13]

The pathophysiology of influenza is significantly influenced by which receptors influenza viruses bind to during entry into cells. Mammalian influenza viruses preferentially bind to sialic acids connected to the rest of the oligosaccharide by an -2,6 link, most commonly found in various respiratory cells,[1][15][3] such as respiratory and retinal epithelial cells.[20] AIVs prefer sialic acids with an -2,3 linkage, which are most common in birds in gastrointestinal epithelial cells[1][15][3] and in humans in the lower respiratory tract.[29] Furthermore, cleavage of the HA protein into HA1, the binding subunit, and HA2, the fusion subunit, is performed by different proteases, affecting which cells can be infected. For mammalian influenza viruses and low pathogenic AIVs, cleavage is extracellular, which limits infection to cells that have the appropriate proteases, whereas for highly pathogenic AIVs, cleavage is intracellular and performed by ubiquitous proteases, which allows for infection of a greater variety of cells, thereby contributing to more severe disease.[1][24][30]

Cells possess sensors to detect viral RNA, which can then induce interferon production. Interferons mediate expression of antiviral proteins and proteins that recruit immune cells to the infection site, and they also notify nearby uninfected cells of infection. Some infected cells release pro-inflammatory cytokines that recruit immune cells to the site of infection. Immune cells control viral infection by killing infected cells and phagocytizing viral particles and apoptotic cells. An exacerbated immune response, however, can harm the host organism through a cytokine storm.[1][11][20] To counter the immune response, influenza viruses encode various non-structural proteins, including NS1, NEP, PB1-F2, and PA-X, that are involved in curtailing the host immune response by suppressing interferon production and host gene expression.[1][21]

B cells, a type of white blood cell, produce antibodies that bind to influenza antigens HA and NA (or HEF[18]) and other proteins to a lesser degree. Once bound to these proteins, antibodies block virions from binding to cellular receptors, neutralizing the virus. In humans, a sizeable antibody response occurs ~1 week after viral exposure.[31] This antibody response is typically robust and long-lasting, especially for ICV and IDV.[1][18] In other words, people exposed to a certain strain in childhood still possess antibodies to that strain at a reasonable level later in life, which can provide some protection to related strains.[1] There is, however, an "original antigenic sin", in which the first HA subtype a person is exposed to influences the antibody-based immune response to future infections and vaccines.[2]

Annual vaccination is the primary and most effective way to prevent influenza and influenza-associated complications, especially for high-risk groups.[8][1][32] Vaccines against the flu are trivalent or quadrivalent, providing protection against an H1N1 strain, an H3N2 strain, and one or two IBV strains corresponding to the two IBV lineages.[8][2] Two types of vaccines are in use: inactivated vaccines that contain "killed" (i.e. inactivated) viruses and live attenuated influenza vaccines (LAIVs) that contain weakened viruses.[1] There are three types of inactivated vaccines: whole virus, split virus, in which the virus is disrupted by a detergent, and subunit, which only contains the viral antigens HA and NA.[33] Most flu vaccines are inactivated and administered via intramuscular injection. LAIVs are sprayed into the nasal cavity.[1]

Vaccination recommendations vary by country. Some recommend vaccination for all people above a certain age, such as 6 months,[32] whereas other countries recommendation is limited for high at risk groups, such as pregnant women, young children (excluding newborns), the elderly, people with chronic medical conditions, health care workers,[1] people who come into contact with high-risk people, and people who transmit the virus easily.[9] Young infants cannot receive flu vaccines for safety reasons, but they can inherit passive immunity from their mother if inactivated vaccines are administered to the mother during pregnancy.[34] Influenza vaccination also helps to reduce the probability of reassortment.[11]

In general, influenza vaccines are only effective if there is an antigenic match between vaccine strains and circulating strains.[8][2] Additionally, most commercially available flu vaccines are manufactured by propagation of influenza viruses in embryonated chicken eggs, taking 68 months.[2] Flu seasons are different in the northern and southern hemisphere, so the WHO meets twice a year, one for each hemisphere, to discuss which strains should be included in flu vaccines based on observation from HA inhibition assays.[8][3] Other manufacturing methods include an MDCK cell culture-based inactivated vaccine and a recombinant subunit vaccine manufactured from baculovirus overexpression in insect cells.[2][35]

Influenza can be prevented or reduced in severity by post-exposure prophylaxis with the antiviral drugs oseltamivir, which can be taken orally by those at least three months old, and zanamivir, which can be inhaled by those above seven years of age. Chemoprophylaxis is most useful for individuals at high-risk of developing complications and those who cannot receive the flu vaccine due to contraindications or lack of effectiveness.[8] Post-exposure chemoprophylaxis is only recommended if oseltamivir is taken within 48 hours of contact with a confirmed or suspected influenza case and zanamivir within 36 hours.[8][9] It is recommended that it be offered to people who have yet to receive a vaccine for the current flu season, who have been vaccinated less than two week since contact, if there is a significant mismatch between vaccine and circulating strains, or during an outbreak in a closed setting regardless of vaccination history.[9]

Hand hygiene is important in reducing the spread of influenza. This includes frequent hand washing with soap and water, using alcohol-based hand sanitizers, and not touching one's eyes, nose, and mouth with one's hands. Covering one's nose and mouth when coughing or sneezing is important.[36] Other methods to limit influenza transmission include staying home when sick,[1] avoiding contact with others until one day after symptoms end,[9] and disinfecting surfaces likely to be contaminated by the virus, such as doorknobs.[1] Health education through media and posters is often used to remind people of the aforementioned etiquette and hygiene.[8]

There is uncertainty about the use of masks since research thus far has not shown a significant reduction in seasonal influenza with mask usage. Likewise, the effectiveness of screening at points of entry into countries is not well researched.[36] Social distancing measures such as school closures, avoiding contact with infected people via isolation or quarantine, and limiting mass gatherings may reduce transmission,[1][36] but these measures are often expensive, unpopular, and difficult to implement. Consequently, the commonly recommended methods of infection control are respiratory etiquette, hand hygiene, and mask wearing, which are inexpensive and easy to perform. Pharmaceutical measures are effective but may not be available in the early stages of an outbreak.[37]

In health care settings, infected individuals may be cohorted or assigned to individual rooms. Protective clothing such as masks, gloves, and gowns is recommended when coming into contact with infected individuals if there is a risk of exposure to infected bodily fluids. Keeping patients in negative pressure rooms and avoiding aerosol-producing activities may help,[8] but special air handling and ventilation systems are not considered necessary to prevent the spread of influenza in the air.[4] In residential homes, new admissions may need to be closed until the spread of influenza is controlled. When discharging patients to care homes, it is important to take care if there is a known influenza outbreak.[9]

Since influenza viruses circulate in animals such as birds and pigs, prevention of transmission from these animals is important. Water treatment, indoor raising of animals, quarantining sick animals, vaccination, and biosecurity are the primary measures used. Placing poultry houses and piggeries on high ground away from high-density farms, backyard farms, live poultry markets, and bodies of water helps to minimize contact with wild birds.[1] Closure of live poultry markets appears to the most effective measure[15] and has shown to be effective at controlling the spread of H5N1, H7N9, and H9N2.[16] Other biosecurity measures include cleaning and disinfecting facilities and vehicles, banning visits to poultry farms, not bringing birds intended for slaughter back to farms,[38] changing clothes, disinfecting foot baths, and treating food and water.[1]

If live poultry markets are not closed, then "clean days" when unsold poultry is removed and facilities are disinfected and "no carry-over" policies to eliminate infectious material before new poultry arrive can be used to reduce the spread of influenza viruses. If a novel influenza viruses has breached the aforementioned biosecurity measures, then rapid detection to stamp it out via quarantining, decontamination, and culling may be necessary to prevent the virus from becoming endemic.[1] Vaccines exist for avian H5, H7, and H9 subtypes that are used in some countries.[15] In China, for example, vaccination of domestic birds against H7N9 successfully limited its spread, indicating that vaccination may be an effective strategy[24] if used in combination with other measures to limit transmission.[1] In pigs and horses, management of influenza is dependent on vaccination with biosecurity.[1]

Diagnosis based on symptoms is fairly accurate in otherwise healthy people during seasonal epidemics and should be suspected in cases of pneumonia, acute respiratory distress syndrome (ARDS), sepsis, or if encephalitis, myocarditis, or breaking down of muscle tissue occur.[13] Because influenza is similar to other viral respiratory tract illnesses, laboratory diagnosis is necessary for confirmation. Common ways of collecting samples for testing include nasal and throat swabs.[1] Samples may be taken from the lower respiratory tract if infection has cleared the upper but not lower respiratory tract. Influenza testing is recommended for anyone hospitalized with symptoms resembling influenza during flu season or who is connected to an influenza case. For severe cases, earlier diagnosis improves patient outcome.[32] Diagnostic methods that can identify influenza include viral cultures, antibody- and antigen-detecting tests, and nucleic acid-based tests.[39]

Viruses can be grown in a culture of mammalian cells or embryonated eggs for 310 days to monitor cytopathic effect. Final confirmation can then be done via antibody staining, hemadsorption using red blood cells, or immunofluorescence microscopy. Shell vial cultures, which can identify infection via immunostaining before a cytopathic effect appears, are more sensitive than traditional cultures with results in 13 days.[1][32][39] Cultures can be used to characterize novel viruses, observe sensitivity to antiviral drugs, and monitor antigenic drift, but they are relatively slow and require specialized skills and equipment.[1]

Serological assays can be used to detect an antibody response to influenza after natural infection or vaccination. Common serological assays include hemagglutination inhibition assays that detect HA-specific antibodies, virus neutralization assays that check whether antibodies have neutralized the virus, and enzyme-linked immunoabsorbant assays. These methods tend to be relatively inexpensive and fast but are less reliable than nucleic-acid based tests.[1][39]

Direct fluorescent or immunofluorescent antibody (DFA/IFA) tests involve staining respiratory epithelial cells in samples with fluorescently-labeled influenza-specific antibodies, followed by examination under a fluorescent microscope. They can differentiate between IAV and IBV but can't subtype IAV.[39] Rapid influenza diagnostic tests (RIDTs) are a simple way of obtaining assay results, are low cost, and produce results quickly, at less than 30 minutes, so they are commonly used, but they can't distinguish between IAV and IBV or between IAV subtypes and are not as sensitive as nucleic-acid based tests.[1][39]

Nucleic acid-based tests (NATs) amplify and detect viral nucleic acid. Most of these tests take a few hours,[39] but rapid molecular assays are as fast as RIDTs.[32] Among NATs, reverse transcription polymerase chain reaction (RT-PCR) is the most traditional and considered the gold standard for diagnosing influenza[39] because it is fast and can subtype IAV, but it is relatively expensive and more prone to false-positives than cultures.[1] Other NATs that have been used include loop-mediated isothermal amplification-based assays, simple amplification-based assays, and nucleic acid sequence-based amplification. Nucleic acid sequencing methods can identify infection by obtaining the nucleic acid sequence of viral samples to identify the virus and antiviral drug resistance. The traditional method is Sanger sequencing, but it has been largely replaced by next-generation methods that have greater sequencing speed and throughput.[39]

Treatment of influenza in cases of mild or moderate illness is supportive and includes anti-fever medications such as acetaminophen and ibuprofen,[40] adequate fluid intake to avoid dehydration, and resting at home.[9] Cough drops and throat sprays may be beneficial for sore throat. It is recommended to avoid alcohol and tobacco use while sick with the flu.[40] Aspirin is not recommended to treat influenza in children due to an elevated risk of developing Reye syndrome.[41] Corticosteroids likewise are not recommended except when treating septic shock or an underlying medical condition, such as chronic obstructive pulmonary disease or asthma exacerbation, since they are associated with increased mortality.[32] If a secondary bacterial infection occurs, then treatment with antibiotics may be necessary.[9]

Antiviral drugs are primarily used to treat severely ill patients, especially those with compromised immune systems. Antivirals are most effective when started in the first 48 hours after symptoms appear. Later administration may still be beneficial for those who have underlying immune defects, those with more severe symptoms, or those who have a higher risk of developing complications if these individuals are still shedding the virus. Antiviral treatment is also recommended if a person is hospitalized with suspected influenza instead of waiting for test results to return and if symptoms are worsening.[1][32] Most antiviral drugs against influenza fall into two categories: neuraminidase (NA) inhibitors and M2 inhibitors.[11] Baloxavir marboxil is a notable exception, which targets the endonuclease activity of the viral RNA polymerase and can be used as an alternative to NA and M2 inhibitors for IAV and IBV.[8][15][4]

NA inhibitors target the enzymatic activity of NA receptors, mimicking the binding of sialic acid in the active site of NA on IAV and IBV virions[1] so that viral release from infected cells and the rate of viral replication are impaired.[9] NA inhibitors include oseltamivir, which is consumed orally in a prodrug form and converted to its active form in the liver, and zanamivir, which is a powder that is inhaled nasally. Oseltamivir and zanamivir are effective for prophylaxis and post-exposure prophylaxis, and research overall indicates that NA inhibitors are effective at reducing rates of complications, hospitalization, and mortality[1] and the duration of illness.[11][32][4] Additionally, the earlier NA inhibitors are provided, the better the outcome,[4] though late administration can still be beneficial in severe cases.[1][32] Other NA inhibitors include laninamivir[1] and peramivir, the latter of which can be used as an alternative to oseltamivir for people who cannot tolerate or absorb it.[32]

The adamantanes amantadine and rimantadine are orally administered drugs that block the influenza virus's M2 ion channel,[1] preventing viral uncoating.[4] These drugs are only functional against IAV[32] but are no longer recommended for use because of widespread resistance to them among IAVs.[4] Adamantane resistance first emerged in H3N2 in 2003, becoming worldwide by 2008. Oseltamivir resistance is no longer widespread because the 2009 pandemic H1N1 strain (H1N1 pdm09), which is resistant to adamantanes, seemingly replaced resistant strains in circulation. Since the 2009 pandemic, oseltamivir resistance has mainly been observed in patients undergoing therapy,[1] especially the immunocompromised and young children.[4] Oseltamivir resistance is usually reported in H1N1, but has been reported in H3N2 and IBVs less commonly.[1] Because of this, oseltamivir is recommended as the first drug of choice for immunocompetent people, whereas for the immunocompromised, oseltamivir is recommended against H3N2 and IBV and zanamivir against H1N1 pdm09. Zanamivir resistance is observed less frequently, and resistance to peramivir and baloxavir marboxil is possible.[4]

In healthy individuals, influenza infection is usually self-limiting and rarely fatal.[8][9] Symptoms usually last for 28 days.[11] Influenza can cause people to miss work or school, and it is associated with decreased job performance and, in older adults, reduced independence. Fatigue and malaise may last for several weeks after recovery, and healthy adults may experience pulmonary abnormalities that can take several weeks to resolve. Complications and mortality primarily occur in high-risk populations and those who are hospitalized. Severe disease and mortality are usually attributable to pneumonia from the primary viral infection or a secondary bacterial infection,[1][9] which can progress to ARDS.[11]

Other respiratory complications that may occur include sinusitis, bronchitis, bronchiolitis, excess fluid buildup in the lungs, and exacerbation of chronic bronchitis and asthma. Middle ear infection and croup may occur, most commonly in children.[8][1] Secondary S. aureus infection has been observed, primarily in children, to cause toxic shock syndrome after influenza, with hypotension, fever, and reddening and peeling of the skin.[1] Complications affecting the cardiovascular system are rare and include pericarditis, fulminant myocarditis with a fast, slow, or irregular heartbeat, and exacerbation of pre-existing cardiovascular disease.[8][9] Inflammation or swelling of muscles accompanied by muscle tissue breaking down occurs rarely, usually in children, which presents as extreme tenderness and muscle pain in the legs and a reluctance to walk for 23 days.[1][9][13]

Influenza can affect pregnancy, including causing smaller neonatal size, increased risk of premature birth, and an increased risk of child death shortly before or after birth.[9] Neurological complications have been associated with influenza on rare occasions, including aseptic meningitis, encephalitis, disseminated encephalomyelitis, transverse myelitis, and GuillainBarr syndrome.[13] Additionally, febrile seizures and Reye syndrome can occur, most commonly in children.[1][9] Influenza-associated encephalopathy can occur directly from central nervous system infection from the presence of the virus in blood and presents as suddent onset of fever with convulsions, followed by rapid progression to coma.[8] An atypical form of encephalitis called encephalitis lethargica, characterized by headache, drowsiness, and coma, may rarely occur sometime after infection.[1] In survivors of influenza-associated encephalopathy, neurological defects may occur.[8] Primarily in children, in severe cases the immune system may rarely dramatically overproduce white blood cells that release cytokines, causing severe inflammation.[8]

People who are at least 65 years of age,[9] due to a weakened immune system from aging or a chronic illness, are a high-risk group for developing complications, as are children less than one year of age and children who have not been previously exposed to influenza viruses multiple times. Pregnant women are at an elevated risk, which increases by trimester[1] and lasts up to two weeks after childbirth.[9][32] Obesity, in particular a body mass index greater than 3540, is associated with greater amounts of viral replication, increased severity of secondary bacterial infection, and reduced vaccination efficacy. People who have underlying health conditions are also considered at-risk, including those who have congenital or chronic heart problems or lung (e.g. asthma), kidney, liver, blood, neurological, or metabolic (e.g. diabetes) disorders,[8][1][9] as are people who are immunocompromised from chemotherapy, asplenia, prolonged steroid treatment, splenic dysfunction, or HIV infection.[9] Current or past tobacco use also places a person at risk.[32] The role of genetics in influenza is not well researched,[1] but it may be a factor in influenza mortality.[11]

Influenza is typically characterized by seasonal epidemics and sporadic pandemics. Most of the burden of influenza is a result of flu seasons caused by IAV and IBV. Among IAV subtypes, H1N1 and H3N2 currently circulate in humans and are responsible for seasonal influenza. Cases disproportionately occur in children, but most severe causes are among the elderly, the very young,[1] and the immunocompromised.[4] In a typical year, influenza viruses infect 515% of the global population,[3][39] causing 35 million cases of severe illness annually[1][2] and accounting for 290,000650,000 deaths each year due to respiratory illness.[3][4][44] 510% of adults and 2030% of children contract influenza each year.[17] The reported number of influenza cases is usually much lower than the actual number of cases.[1][34]

During seasonal epidemics, it is estimated that about 80% of otherwise healthy people who have a cough or sore throat have the flu.[1] Approximately 3040% of people hospitalized for influenza develop pneumonia, and about 5% of all severe pneumonia cases in hospitals are due to influenza, which is also the most common cause of ARDS in adults. In children, influenza is one of the two most common causes of ARDS, the other being the respiratory syncytial virus.[13] About 35% of children each year develop otitis media due to influenza.[8] Adults who develop organ failure from influenza and children who have PIM scores and acute renal failure have higher rates of mortality.[13] During seasonal influenza, mortality is concentrated in the very young and the elderly, whereas during flu pandemics, young adults are often affected at a high rate.[11]

In temperate regions, the number of influenza cases varies from season to season. Lower vitamin D levels, presumably due to less sunlight,[28] lower humidity, lower temperature, and minor changes in virus proteins caused by antigenic drift contribute to annual epidemics that peak during the winter season. In the northern hemisphere, this is from October to May (more narrowly December to April[11]), and in the southern hemisphere, this is from May to October (more narrowly June to September[11]). There are therefore two distinct influenza seasons every year in temperate regions, one in the northern hemisphere and one in the southern hemisphere.[1][9][2] In tropical and subtropical regions, seasonality is more complex and appears to be affected by various climatic factors such as minimum temperature, hours of sunshine, maximum rainfall, and high humidity.[1][45] Influenza may therefore occur year-round in these regions.[11] Influenza epidemics in modern times have the tendency to start in the eastern or southern hemisphere,[45] with Asia being a key reservoir of influenza viruses.[11]

IAV and IBV co-circulate, so the two have the same patterns of transmission.[1] The seasonality of ICV, however, is poorly understood. ICV infection is most common in children under the age of 2, and by adulthood most people have been exposed to it. ICV-associated hospitalization most commonly occurs in children under the age of 3 and is frequently accompanied by co-infection with another virus or a bacterium, which may increase the severity of disease. When considering all hospitalizations for respiratory illness among young children, ICV appears to account for only a small percentage of such cases. Large outbreaks of ICV infection can occur, so incidence varies significantly.[10]

Outbreaks of influenza caused by novel influenza viruses are common.[19] Depending on the level of pre-existing immunity in the population, novel influenza viruses can spread rapidly and cause pandemics with millions of deaths. These pandemics, in contrast to seasonal influenza, are caused by antigenic shifts involving animal influenza viruses. To date, all known flu pandemics have been caused by IAVs, and they follow the same pattern of spreading from an origin point to the rest of the world over the course of multiple waves in a year.[1][9][32] Pandemic strains tend to be associated with higher rates of pneumonia in otherwise healthy individuals.[13] Generally after each influenza pandemic, the pandemic strain continues to circulate as the cause of seasonal influenza, replacing prior strains.[1] From 1700 to 1889, influenza pandemics occurred about once every 5060 years. Since then, pandemics have occurred about once every 1050 years, so they may be getting more frequent over time.[45]

It is impossible to know when an influenza virus first infected humans or when the first influenza pandemic occurred.[47] Possibly the first influenza epidemic occurred around 6,000 BC in China,[48] and possible descriptions of influenza exist in Greek writings from the 5th century BC.[45][49] In both 11731174 AD and 1387 AD, epidemics occurred across Europe that were named "influenza". Whether these epidemics and others were caused by influenza is unclear since there was no consistent naming pattern for epidemic respiratory diseases at that time, and "influenza" didn't become completely attached to respiratory disease until centuries later.[50] Influenza may have been brought to the Americas as early as 1493, when an epidemic disease resembling influenza killed most of the population of the Antilles.[51][52]

The first convincing record of an influenza pandemic was chronicled in 1510; it began in East Asia before spreading to North Africa and then Europe.[47] Following the pandemic, seasonal influenza occurred, with subsequent pandemics in 1557 and 1580.[50] The flu pandemic in 1557 was potentially the first time influenza was connected to miscarriage and death of pregnant women.[53] The 1580 flu pandemic originated in Asia during summer, spread to Africa, then Europe, and finally America.[45] By the end of the 16th century, influenza was likely beginning to become understood as a specific, recognizable disease with epidemic and endemic forms.[50] In 1648, it was discovered that horses also experience influenza.[47]

Influenza data after 1700 is more informative, so it is easier to identify flu pandemics after this point, each of which incrementally increased understanding of influenza.[54] The first flu pandemic of the 18th century started in 1729 in Russia in spring, spreading worldwide over the course of three years with distinct waves, the later ones being more lethal. The second flu pandemic of the 18th century was in 17811782, starting in China in autumn.[45] From this pandemic, influenza became associated with sudden outbreaks of febrile illness.[54] The next flu pandemic was from 1830 to 1833, beginning in China in winter. This pandemic had a high attack rate, but the mortality rate was low.[23][45]

A minor influenza pandemic occurred from 1847 to 1851 at the same time as the third cholera pandemic and was the first flu pandemic to occur with vital statistics being recorded, so influenza mortality was clearly recorded for the first time.[54] Highly pathogenic avian influenza was recognized in 1878[54] and was soon linked to transmission to humans.[47] By the time of the 1889 pandemic, which may have been caused by an H2N2 strain,[55] the flu had become an easily recognizable disease.[47]

Initially, the microbial agent responsible for influenza was incorrently identified in 1892 by R. F. J. Pfeiffer as the bacteria species Haemophilus influenzae, which retains "influenza" in its name.[47][54] In the following years, the field of virology began to form as viruses were identified as the cause of many diseases. From 1901 to 1903, Italian and Austrian researchers were able to show that avian influenza, then called "fowl plague",[24] was caused by a microscopic agent smaller than bacteria by using filters with pores too small for bacteria to pass through. The fundamental differences between viruses and bacteria, however, were not yet fully understood.[54]

From 1918 to 1920, the Spanish flu pandemic became the most devastating influenza pandemic and one of the deadliest pandemics in history. The pandemic, probably caused by H1N1, likely began in the USA before spreading worldwide by soldiers during and after the First World War. The initial wave in the first half of 1918 was relatively minor and resembled past flu pandemics, but the second wave later that year had a much higher mortality rate,[45] accounting for most deaths. A third wave with lower mortality occurred in many places a few months after the second.[23] By the end of 1920, it is estimated that about a third[11] to half of all people in the world had been infected, with tens of millions of deaths, disproportionately young adults.[45] During the 1918 pandemic, the respiratory route of transmission was clearly identified[23] and influenza was shown to be caused by a "filter passer", not a bacterium, but there remained a lack of agreement about influenza's cause for another decade and research on influenza declined.[54] After the pandemic, H1N1 circulated in humans in seasonal form[1] up until the next pandemic.[54]

In 1931, Richard Shope published three papers identifying a virus as the cause of swine influenza, a then newly recognized disease among pigs that was first characterized during the second wave of the 1918 pandemic.[53][54] Shope's research reinvigorated research on human influenza, and many advances in virology, serology, immunology, experimental animal models, vaccinology, and immunotherapy have since arisen from influenza research.[54] Just two years after influenza viruses were discovered, in 1933, IAV was identified as the agent responsible for human influenza.[53][57] Subtypes of IAV were discovered throughout the 1930s,[54] and IBV was discovered in 1940.[17]

During the Second World War, the US government worked on developing inactivated vaccines for influenza, resulting in the first influenza vaccine being licensed in 1945 in the United States.[1] ICV was discovered two years later in 1947.[17] In 1955, avian influenza was confirmed to be caused by IAV.[24] Four influenza pandemics have occurred since WWII, each less severe than the 1918 pandemic. The first of these was the Asian flu from 1957 to 1958, caused by an H2N2 strain[1][37] and beginning in China's Yunnan province. The number of deaths probably exceeded one million, mostly among the very young and very old.[45] Notably, the 1957 pandemic was the first flu pandemic to occur in the presence of a global surveillance system and laboratories able to study the novel influenza virus.[23] After the pandemic, H2N2 was the IAV subtype responsible for seasonal influenza.[1] The first antiviral drug against influenza, amantadine, was approved for use in 1966, with additional antiviral drugs being used since the 1990s.[4]

In 1968, H3N2 was introduced into humans as a result of a reassortment between an avian H3N2 strain and an H2N2 strain that was circulating in humans. The novel H3N2 strain first emerged in Hong Kong and spread worldwide, causing the Hong Kong flu pandemic, which resulted in 500,0002,000,000 deaths. This was the first pandemic to spread significantly by air travel.[3][23] H2N2 and H3N2 co-circulated after the pandemic until 1971 when H2N2 waned in prevalence and was completely replaced by H3N2.[3] In 1977, H1N1 reemerged in humans, possibly after it was released from a freezer in a laboratory accident, and caused a pseudo-pandemic.[23][54] Whether the 1977 "pandemic" deserves to be included in the natural history of flu pandemics is debatable.[45] This H1N1 strain was antigenically similar to the H1N1 strains that circulated prior to 1957. Since 1977, both H1N1 and H3N2 have circulated in humans as part of seasonal influenza.[1] In 1980, the current classification system used to subtype influenza viruses was introduced.[58]

At some point, IBV diverged into two lineages, named the B/Victoria-like and B/Yamagata-like lineages, both of which have been circulating in humans since 1983.[17] In 1996, HPAI H5N1 was detected in Guangdong, China[24] and a year later emerged in poultry in Hong Kong, gradually spreading worldwide from there. A small H5N1 outbreak in humans in Hong Kong occurred then,[30] and sporadic human cases have occurred since 1997, carrying a high case fatality rate.[15][39] The most recent flu pandemic was the 2009 swine flu pandemic, which originated in Mexico and resulted in hundreds of thousands of deaths.[23] It was caused by a novel H1N1 strain that was a reassortment of human, swine, and avian influenza viruses.[16][4] The 2009 pandemic had the effect of replacing prior H1N1 strains in circulation with the novel strain but not any other influenza viruses. Consequently, H1N1, H3N2, and both IBV lineages have been in circulation in seasonal form since the 2009 pandemic.[1][23][24]

In 2011, IDV was discovered in pigs in Oklahoma, USA, and cattle were later identified as the primary reservoir of IDV.[10][17] In the same year,[39] avian H7N9 was detected in China and began to cause human infections in 2013, starting in Shanghai and Anhui and remaining mostly in China. HPAI H7N9 emerged sometime in 2016 and has occasionally infected humans incidentally. Other AIVs have less commonly infected humans since the 1990s, including H5N6, H6N1, H7N2-4, H7N7, and H10N7-8,[15] and HPAI H subtypes such as H5N1-3, H5N5-6, and H5N8 have begun to spread throughout much of the world since the 2010s. Future flu pandemics, which may be caused by an influenza virus of avian origin,[24] are viewed as almost inevitable, and increased globalization has made it easier for novel viruses to spread,[23] so there are continual efforts to prepare for future pandemics[53] and improve the prevention and treatment of influenza.[1]

The word influenza comes from the Italian word influenza, from medieval Latin influentia, originally meaning "visitation" or "influence". Terms such as influenza di freddo, meaning "influence of the cold", and influenza di stelle, meaning "influence of the stars" are attested from the 14th century. The latter referred to the disease's cause, which at the time was ascribed by some to unfavorable astrological conditions. As early as 1504, influenza began to mean a "visitation" or "outbreak" of any disease affecting many people in a single place at once. During an outbreak of influenza in 1743 that started in Italy and spread throughout Europe, the word reached the English language and was anglicized in pronunciation. Since the mid-1800s, influenza has also been used to refer to severe colds.[59][60][61] The shortened form of the word, "(the) flu", is first attested in 1839 as flue with the spelling flu first attested in 1893.[62] Other names that have been used for influenza include epidemic catarrh, la grippe from French, sweating sickness, and, especially when referring to the 1918 pandemic strain, Spanish fever.[63]

Influenza research is wide-ranging and includes efforts to understand how influenza viruses enter hosts, the relationship between influenza viruses and bacteria, how influenza symptoms progress, and what make some influenza viruses deadlier than others.[64] Non-structural proteins encoded by influenza viruses are periodically discovered and their functions are continually under research.[21] Past pandemics, and especially the 1918 pandemic, are the subject of much research to understand flu pandemics.[45] As part of pandemic preparedness, the Global Influenza Surveillance and Response System is a global network of laboratories that monitors influenza transmission and epidemiology.[65] Additional areas of research include ways to improve the diagnosis, treatment, and prevention of influenza.

Existing diagnostic methods have a variety of limitations coupled with their advantages. For example, NATs have high sensitivity and specificity but are impractical in under-resourced regions due to their high cost, complexity, maintenance, and training required. Low-cost, portable RIDTs can rapidly diagnose influenza but have highly variable sensitivity and are unable to subtype IAV. As a result of these limitations and others, research into new diagnostic methods revolves around producing new methods that are cost-effective, less labor-intensive, and less complex than existing methods while also being able to differentiate influenza species and IAV subtypes. One approach in development are lab-on-a-chips, which are diagnostic devices that make use of a variety of diagnostic tests, such as RT-PCR and serological assays, in microchip form. These chips have many potential advantages, including high reaction efficiency, low energy consumption, and low waste generation.[39]

New antiviral drugs are also in development due to the elimination of adamantines as viable drugs and concerns over oseltamivir resistance. These include: NA inhibitors that can be injected intravenously, such as intravenous formulations of zanamivir; favipiravir, which is a polymerase inhibitor used against several RNA viruses; pimodivir, which prevents cap-binding required during viral transcription; and nitazoxanide, which inhibits HA maturation.[1][11] Reducing excess inflammation in the respiratory tract is also subject to much research since this is one of the primary mechanisms of influenza pathology.[11][13] Other forms of therapy in development include monoclonal and polyclonal antibodies that target viral proteins, convalescent plasma, different approaches to modify the host antiviral response,[32][66] and stem cell-based therapies to repair lung damage.[11]

Much research on LAIVs focuses on identifying genome sequences that can be deleted to create harmless influenza viruses in vaccines that still confer immunity.[21] The high variability and rapid evolution of influenza virus antigens, however, is a major obstacle in developing effective vaccines. Furthermore, it is hard to predict which strains will be in circulation during the next flu season, manufacturing a sufficient quantity of flu vaccines for the next season is difficult,[2] LAIVs have limited efficacy, and repeated annual vaccination potentially has diminished efficacy.[1] For these reasons, "broadly-reactive" or "universal" flu vaccines are being researched that can provide protection against many or all influenza viruses. Approaches to develop such a vaccine include HA stalk-based methods such as chimeras that have the same stalk but different heads, HA head-based methods such as computationally optimized broadly neutralizing antigens, anti-idiotypic antibodies, and vaccines to elicit immune responses to highly conserved viral proteins.[2][66] mRNA vaccines to provide protection against influenza are also under research.[67]

Aquatic birds such as ducks, geese, shorebirds, and gulls are the primary reservoir of IAVs.[15][16] In birds, AIVs may be either low pathogenic avian influenza (LPAI) viruses that produce little to no symptoms or highly pathogenic avian influenza (HPAI) viruses that cause severe illness. Symptoms of HPAI infection include lack of energy and appetite, decreased egg production, soft-shelled or misshapen eggs, swelling of the head, comb, wattles, and hocks, purple discoloration of wattles, combs, and legs, nasal discharge, coughing, sneezing, incoordination, and diarrhea. Birds infected with an HPAI virus may also die suddenly without any signs of infection.[38]

The distinction between LPAI and HPAI can generally be made based on how lethal an AIV is to chickens. At the genetic level, an AIV can be usually be identified as an HPAI virus if it has a multibasic cleavage site in the HA protein, which contains additional residues in the HA gene.[16][24] Most AIVs are LPAI. Notable HPAI viruses include HPAI H5N1 and HPAI H7N9. HPAI viruses have been a major disease burden in the 21st century, resulting in the death of large numbers of birds. In H7N9's case, some circulating strains were originally LPAI but became HPAI by acquiring the HA multibasic cleavage site. Avian H9N2 is also of concern because although it is LPAI, it is a common donor of genes to H5N1 and H7N9 during reassortment.[1]

Migratory birds can spread influenza across long distances. An example of this was when an H5N1 strain in 2005 infected birds at Qinghai Lake, China, which is a stopover and breeding site for many migratory birds, subsequently spreading the virus to more than 20 countries across Asia, Europe, and the Middle East.[15][24] AIVs can be transmitted from wild birds to domestic free-range ducks and in turn to poultry through contaminated water, aerosols, and fomites.[1] Ducks therefore act as key intermediates between wild and domestic birds.[24] Transmission to poultry typically occurs in backyard farming and live animal markets where multiple species interact with each other. From there, AIVs can spread to poultry farms in the absence of adequate biosecurity. Among poultry, HPAI transmission occurs through aerosols and contaminated feces,[1] cages, feed, and dead animals.[15] Back-transmission of HPAI viruses from poultry to wild birds has occurred and is implicated in mass die-offs and intercontinental spread.[16]

AIVs have occasionally infected humans through aerosols, fomites, and contaminated water.[1] Direction transmission from wild birds is rare.[24] Instead, most transmission involves domestic poultry, mainly chickens, ducks, and geese but also a variety of other birds such as guinea fowl, partridge, pheasants, and quails.[16] The primary risk factor for infection with AIVs is exposure to birds in farms and live poultry markets.[15] Typically, infection with an AIV has an incubation period of 35 days but can be up to 9 days. H5N1 and H7N9 cause severe lower respiratory tract illness, whereas other AIVs such as H9N2 cause a more mild upper respiratory tract illness, commonly with conjunctivitis.[1] Limited transmission of avian H2, H5-7, H9, and H10 subtypes from one person to another through respiratory droplets, aerosols, and fomites has occurred,[1][2] but sustained human-to-human transmission of AIVs has not occurred. Before 2013, H5N1 was the most common AIV to infect humans. Since then, H7N9 has been responsible for most human cases.[15]

Influenza in pigs is a respiratory disease similar to influenza in humans and is found worldwide. Asymptomatic infections are common. Symptoms typically appear 13 days after infection and include fever, lethargy, anorexia, weight loss, labored breathing, coughing, sneezing, and nasal discharge. In sows, pregnancy may be aborted. Complications include secondary infections and potentially fatal bronchopneumonia. Pigs become contagious within a day of infection and typically spread the virus for 710 days, which can spread rapidly within a herd. Pigs usually recover from infection within 37 days after symptoms appear. Prevention and control measures include inactivated vaccines and culling infected herds. The influenza viruses usually responsible for swine flu are IAV subtypes H1N1, H1N2, and H3N2.[68]

Some IAVs can be transmitted via aerosols from pigs to humans and vice versa.[1] Furthermore, pigs, along with bats and quails,[17] are recognized as a mixing vessel of influenza viruses because they have both -2,3 and -2,6 sialic acid receptors in their respiratory tract. Because of that, both avian and mammalian influenza viruses can infect pigs. If co-infection occurs, then reassortment is possible.[16] A notable example of this was the reassortment of a swine, avian, and human influenza virus in 2009, resulting in a novel H1N1 strain that caused the 2009 flu pandemic.[16][4] Spillover events from humans to pigs, however, appear to be more common than from pigs to humans.[16]

Influenza viruses have been found in many other animals, including cattle, horses, dogs, cats, and marine mammals. Nearly all IAVs are apparently descended from ancestral viruses in birds. The exception are bat influenza-like viruses, which have an uncertain origin. These bat viruses have HA and NA subtypes H17, H18, N10, and N11. H17N10 and H18N11 are unable to reassort with other IAVs, but they are still able to replicate in other mammals.[1] AIVs sometimes crossover into mammals. For example, in late 2016 to early 2017, an avian H7N2 strain was found to be infecting cats in New York.[1]

Equine IAVs include H7N7 and two lineages[1] of H3N8. H7N7, however, has not been detected in horses since the late 1970s,[19] so it may have become extinct in horses.[16] H3N8 in equines spreads via aerosols and causes respiratory illness.[1] Equine H3N8 perferentially binds to -2,3 sialic acids, so horses are usually considered dead-end hosts, but transmission to dogs and camels has occurred, raising concerns that horses may be mixing vessels for reassortment. In canines, the only IAVs in circulation are equine-derived H3N8 and avian-derived H3N2. Canine H3N8 has not been observed to reassort with other subtypes. H3N2 has a much broader host range and can reassort with H1N1 and H5N1. An isolated case of H6N1 likely from a chicken was found infecting a dog, so other AIVs may emerge in canines.[16]

Other mammals to be infected by IAVs include H7N7 and H4N5 in seals, H1N3 in whales, and H10N4 and H3N2 in minks.[19] Various mutations have been identified that are associated with AIVs adapting to mammals. Since HA proteins vary in which sialic acids they bind to, mutations in the HA receptor binding site can allow AIVs to infect mammals. Other mutations include mutations affecting which sialic acids NA proteins cleave and a mutation in the PB2 polymerase subunit that improves tolerance of lower temperatures in mammalian respiratory tracts and enhances RNP assembly by stabilizing NP and PB2 binding.[16]

IBV is mainly found in humans but has also been detected in pigs, dogs, horses, and seals.[17] Likewise, ICV primarily infects humans but has been observed in pigs, dogs, cattle, and dromedary camels.[10][17] IDV causes an influenza-like illness in pigs but its impact in its natural reservoir, cattle, is relatively unknown. It may cause respiratory disease resembling human influenza on its own, or it may be part of a bovine respiratory disease (BRD) complex with other pathogens during co-infection. BRD is a concern for the cattle industry, so IDV's possible involvement in BRD has led to research on vaccines for cattle that can provide protection against IDV.[17][18] Two antigenic lineages are in circulation: D/swine/Oklahoma/1334/2011 (D/OK) and D/bovine/Oklahoma/660/2013 (D/660).[17]

Original post:

Influenza - Wikipedia

‘Tomato Flu’: Everything you need to know about the virus

August 30, 2022

Recently, 'Tomato Flu' has been reported in some parts of Kerala among children under the age of five. After the reports of these cases surfaced, the neighboring state, Tamil Nadu, also increased surveillance at its borders. Total 'Tomato flu' cases in India mount to 100.

What causes 'Tomato Flu'?This rare contagious disease, Tomato fever, is caused by Coxsackie A 16 virus. In this infection, red and painful blisters come up on the patient's body, which gradually expand into the size of a tomato, and that's why, it has been named 'tomato flu'.

All you need to know about Tomato fever

is a rare virus that attacks only children especially those who are under the age of five.

it is not yet confirmed whether this (unknown fever) is viral or dengue, chikungunya.

Most of the children have had problems with rashes, skin irritation and dehydration. Blisters have also been seen in some parts of the body.

Tomato flu is named after the red-colored blisters visible on the body.

TreatmentThere is no specific drug to treat 'Tomato Flu', a self-limiting infection. And the treatment given to children is the same as those given in the case of dengue, chikungunya, and hand, foot, and mouth disease.

Moreover, this infectious disease which is triggered by intestinal viruses is rare to occur in adults. It's because the immune system in adults is strong enough to defend them against 'Tomato Flu' virus.

Those infected with the disease are advised to isolate and take plenty of fluid. Also, you can use a hot water sponge to relieve irritation and rashes.

As a precautionary measure, the Union Health Ministry has asked the states to conduct proper screening by the health authorities and to increase surveillance.

Disclaimer Statement: This content is authored by an external agency. The views expressed here are that of the respective authors/ entities and do not represent the views of Economic Times (ET). ET does not guarantee, vouch for or endorse any of its contents nor is responsible for them in any manner whatsoever. Please take all steps necessary to ascertain that any information and content provided is correct, updated, and verified. ET hereby disclaims any and all warranties, express or implied, relating to the report and any content therein.

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'Tomato Flu': Everything you need to know about the virus

What to know about the tomato flu virus doctors are tracking in India – KRQE News 13

August 30, 2022

(NEXSTAR) In case we didnt have enough viruses to worry about, reports of a tomato flu outbreak in India started to surface this month. The virus, named for the bursting red blisters it causes, has infected at least 100 children.

The virus was first identified in Kerala in May, where it infected 82 children all under the age of 5 by the end of July, according to The Lancet medical journal. At least 26 more cases were also confirmed in neighboring states of India.

The most common symptoms appear to be fever, joint pain and the rash that gives the virus its new nickname. Tomato flu gained its name on the basis of the eruption of red and painful blisters throughout the body that gradually enlarge to the size of a tomato, The Lancet reported.

News outlets started to report on the disease as a new virus, but new testing out of the United Kingdom seems to indicate the tomato flu isnt new at all nor is it a type of flu.

Viral swabs were taken from two children who had recently returned from India showing the bright red rash, reports the British medical journal BMJ. The test came back positive for Coxsackie A16, a pathogen commonly associated with Hand, Foot, and Mouth Disease (or HFMD).

According to the Centers for Disease Control and Prevention, HFMD is very common among children, even here in the United States, because of how contagious it is. The symptoms including fever, mouth sores and skin rashes last seven to 10 days for most kids.

When there is a rash with HFMD, the rash usually is not itchy and looks like flat or slightly raised red spots, sometimes with blisters that have an area of redness at their base, says the CDC.

This common disease may have been initially mistaken as a new tomato flu virus because the blisters observed in India were larger.

Doctors in Kerala told BMJ that even in the cases they have seen over the past few months, they have yet to admit any children to the hospital. All of the patients have recovered on their own thus far.

More here:

What to know about the tomato flu virus doctors are tracking in India - KRQE News 13

Flu and COVID-19 do not belong to the same virus family – Rappler

August 30, 2022

Influenza is caused by influenza viruses that belong to the Orthomyxoviridae virus family, while COVID-19 is caused by the SARS-COV-2 virus that belongs to the Coronaviridae virus family

Claim: The virus that causes influenza (flu) and the virus that causes COVID-19 belong to the same virus family.

Why we fact-checked this: The post containing the claim has over 4,629 views on YouTube, as of writing.

Different families: According to the United States Centers for Disease Control and Prevention (US CDC), flu and COVID-19 are caused by viruses from different virus families. Studies published by the National Library of Medicine (NLM) said that flu is caused by an influenza virus under the virus family of Orthomyxoviridae, while COVID-19 is caused by the SARS-COV-2 virus from the virus family of Coronaviridae.

What this means: The difference in where flu and COVID-19 originate means:

Vaccine schedule: According to the US CDC, flu and COVID-19 vaccines could be given at the same time, and possible side effects are generally similar whether vaccines are given alone or with other vaccines.

However, the US CDC says that, although there is no harm in taking both flu and COVID-19 vaccines at the same time, the public should follow the recommended schedule for either vaccine. The US CDC also recommends the public to get the COVID-19 vaccine as soon as possible and get the flu vaccine during the flu season.

According to the Philippine Department of Health, it is preferable to give flu vaccinations to Filipinos from February to June. Lorenz Pasion/Rappler.com

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The rest is here:

Flu and COVID-19 do not belong to the same virus family - Rappler

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