Category: Corona Virus

Two new studies provide more evidence that the coronavirus pandemic originated in a Wuhan, China market where live animals were sold further bolstering the theory that the virus emerged in the wild rather than escaping from a Chinese lab.

The research, published online Tuesday by the journal Science, shows that the Huanan Seafood Wholesale Market was likely the early epicenter of the scourge that has now killed nearly 6.4 million people around the world. Scientists conclude that the virus that causes COVID-19, SARS-CoV-2, likely spilled from animals into people two separate times.

"All this evidence tells us the same thing: It points right to this particular market in the middle of Wuhan," said Kristian Andersen a professor in the Department of Immunology and Microbiology at Scripps Research and coauthor of one of the studies. "I was quite convinced of the lab leak myself until we dove into this very carefully and looked at it much closer."

In one study, which incorporated data collected by Chinese scientists, University of Arizona evolutionary biologist Michael Worobey and his colleagues used mapping tools to estimate the locations of more than 150 of the earliest reported COVID-19 cases from December 2019. They also mapped cases from January and February 2020 using data from a social media app that had created a channel for people with COVID-19 to get help.

They asked, "Of all the locations that the early cases could have lived, where did they live? And it turned out when we were able to look at this, there was this extraordinary pattern where the highest density of cases was both extremely near to and very centered on this market," Worobey said at a press briefing. "Crucially, this applies both to all cases in December and also to cases with no known link to the market And this is an indication that the virus started spreading in people who worked at the market but then started to spread into the local community."

Andersen said they found case clusters inside the market, too, "and that clustering is very, very specifically in the parts of the market" where they now know people were selling wildlife, such as raccoon dogs, that are susceptible to infection with the coronavirus.

In the other study, scientists analyzed the genomic diversity of the virus inside and outside of China starting with the earliest sample genomes in December 2019 and extending through mid-February 2020. They found that two lineages A and B marked the pandemic's beginning in Wuhan. Study coauthor Joel Wertheim, a viral evolution expert at the University of California, San Diego, pointed out that lineage A is more genetically similar to bat coronaviruses, but lineage B appears to have begun spreading earlier in humans, particularly at the market.

"Now I realize it sounds like I just said that a once-in-a-generation event happened twice in short succession," Wertheim said. But certain conditions were in place such as people and animals in close proximity and a virus that can spread from animals to people and from person to person. So "barriers to spillover have been lowered such that multiple introductions, we believe, should actually be expected," he said.

Many scientists believe the virus jumped from bats to humans, either directly or through another animal. But in June, the World Health Organization recommended a deeper probe into whether a lab accident may be to blame. Critics had said the WHO was too quick to dismiss the lab leak theory.

"Have we disproven the lab leak theory? No, we have not," Andersen said. "But I think what's really important here is there are possible scenarios and there are plausible scenarios and it's really important to understand that possible does not mean equally likely."

The pandemic's origins remain controversial. Some scientists believe a lab leak is more likely and others remain open to both possibilities. But Matthew Aliota, a researcher in the college of veterinary medicine at the University of Minnesota, said in his mind the pair of studies "kind of puts to rest, hopefully, the lab leak hypothesis."

"Both of these two studies really provide compelling evidence for the natural origin hypothesis," said Aliota, who wasn't involved in either study. Since sampling an animal that was at the market is impossible, "this is maybe as close to a smoking gun as you could get."

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New studies bolster theory coronavirus emerged from the wild - CBS News

Cough, sore throat, fever, and chills: Not again! When a positive COVID-19 test comes back, you may feel like you just had it.

As time passes, immunity wanes, and new virus variants emerge. So, reinfections are certainly possible. But can you get COVID-19 twice in just 1 month?

While that specific scenario is pretty unlikely, the risk of reinfection is increasing. In this article, we discuss what we know so far about COVID-19 reinfections.

Generally, a number of factors contribute to COVID-19 reinfections. These include the:

According to the Centers for Disease Control and Prevention (CDC), were still learning many things about COVID-19 reinfections. This includes how soon reinfection can happen.

Before the arrival of the Omicron variant, reinfections werent that common. Researchers in a May 2022 study looked at reinfections from the start of the pandemic until Omicron. Overall, they found that reinfection risk was 6.7% in the 18 to 22 months after a first infection.

However, now Omicron and its subvariants have changed the landscape of reinfections. Heres what the research has found.

Reinfections werent that common before Omicron. Research found that protection from reinfection typically lasted for at least several months.

A 2021 study looking at PCR testing data from 2020 found that a prior infection still gave about 80% protection 6 months after a first infection.

A February 2022 study brought vaccination into the mix. Researchers looked at the effect of vaccination on reinfection from December 2020 to September 2021.

Immunity from a prior infection waned after 1 year in unvaccinated people. However, in people vaccinated after having COVID-19, immunity stayed high, even if a prior infection was over 18 months ago.

Viruses can change over time, and thats certainly been true with this coronavirus. As changes accumulate, they can make it easier for a virus to escape immunity generated by vaccination, a previous infection, or both.

A July 2022 study, still in preprint, looked into the qualities of protection that a pre-Omicron infection provided:

A June 2022 study looked at the protection previous infection and vaccination provided on symptomatic infections with the original Omicron variant (BA.1) or its first subvariant, BA.2. Overall, there was no difference in protection between people who were vaccinated, who had had a previous infection, or both.

The new BA.4 and BA.5 Omicron subvariants are now the main drivers of COVID-19 in the United States. Theyre also very good at escaping the immune system.

A July 2022 study looked into the neutralization of BA.4 and BA.5 by antibodies from vaccination or a previous COVID-19 infection. Neutralizing antibodies prevent the virus from binding to a host cell.

Antibodies from vaccinated people had a harder time neutralizing these subvariants. Neutralization was also lower with antibodies from people with a prior infection, including BA.1, the original Omicron variant that was dominant in late 2021 and early 2022.

Another July 2022 study supports this. Researchers found that neutralization of BA.4 and BA.5 was lower than that of BA.1 or BA.2 in both vaccinated people and those with a prior infection.

What this means is that if you had COVID-19 during the first or most recent (BA.2) Omicron wave, reinfection with BA.4 or BA.5 is possible now. However, its still pretty likely youre well protected at this point in time.

Researchers in a July 2022 study, still in preprint, found that while the effectiveness of a pre-Omicron infection against symptomatic BA.4 or BA.5 infections was only 15.1%, it was still rather high (76.1%) if you had a previous Omicron infection.

COVID-19 reinfections appear to be less severe than first infections. A 2021 study looked at the risk of serious illness or death from reinfections. Compared with first infections, reinfections had a 90% lower risk of serious illness or death.

An April 2022 study also found that COVID-19 reinfections carried a lower risk of death than first infections. Similar to first infections, age, sex, and underlying health conditions were risk factors for severe illness from reinfection.

However, theres some evidence that reinfections may increase the risk of lasting health effects. A June 2022 study, still in preprint, found that, compared with first infections, reinfections boosted the risk of:

These effects were seen regardless of vaccination status. The level of risk was also found to increase in line with the number of infections study participants reported.

One limitation of this study is that it may not reflect risk in the general population. Researchers focused on people using Veterans Affairs (VA) healthcare resources. As such, the study population is more likely to be older and male, and have poorer health.

Paxlovid is an antiviral drug doctors prescribe to treat mild to moderate COVID-19 in people at high risk of severe illness. To be effective, Paxlovid needs to be started within 5 days of symptom onset.

Rebounds of COVID-19 have been reported after Paxlovid treatment. While its still unclear why this happens, its possible that the coronavirus isnt completely cleared from the body while taking Paxlovid, allowing it to replicate again after treatment ends.

Increasing reports of these rebounds prompted the CDC to release a health advisory. In this advisory, the CDC noted that Paxlovid rebounds:

Rebounds after Paxlovid are rare. A June 2022 study found that, of 483 people treated with Paxlovid, only 4 (0.8%) had a rebound. Another June 2022 study, still in preprint, found a higher rebound rate: about 3.5% in the 7 days after treatment.

People experiencing COVID-19 rebound after Paxlovid may also be able to transmit the infection to others. A small May 2022 study, still in preprint, involving 10 people documented transmission to family members during rebounds.

The amount of virus during a rebound was also similar to where it was before Paxlovid treatment. Researchers stated that these findings support that people who are having a rebound should isolate until their symptoms go away.

COVID-19 rebounds may also happen without taking Paxlovid. A June 2022 research article mentions anecdotal reports of rebounds in people who never took Paxlovid. Authors note that perhaps Omicron takes longer to clear in some people than earlier virus variants.

Yes. A study published in March 2022 signaled an increased risk of reinfections due to Omicron. Within the study population, researchers noted that an increase in third infections was seen beginning in November 2021.

Researchers stated that people who had third infections had their first infection early in the pandemic and a second infection during the Delta variant wave. Their third infection was from Omicron.

The best way to prevent getting COVID-19 reinfections is to continue to take steps to protect yourself, including:

According to the CDC, we know little about the risk of transmission during COVID-19 reinfections. Overall, its best to err on the side of caution and assume you can transmit the virus to others.

A July 2022 study found that viral shedding (aka the contagious period) among people with Omicron infections can last up to 10 days.

So, its a good idea to isolate and quarantine for at least 10 days or until you are symptom-free and test negative from a rapid COVID-19 test.

According to the Food and Drug Administration (FDA), boosters targeting Omicron are slated to be available starting in fall 2022. The FDA has also recommended a BA.4 and BA.5 component be included in this booster.

Moderna has announced that its Omicron booster yields a significantly higher neutralizing antibody response to BA.4 and BA.5 than its current booster.

Pfizer-BioNTech stated that, compared with their current booster, their Omicron booster gave higher levels of neutralizing antibodies against BA.1. Neutralizing antibodies for BA.4 and BA.5 were present but to a lesser extent.

The risk of COVID-19 reinfections is increasing. Because of this, you may hear of more and more people in your life getting COVID-19 for a second time, sometimes not too long after their first infection.

The latest reinfections are largely driven by the Omicron BA.4 and BA.5 subvariants, which can escape immunity from vaccines and prior infections. Things like naturally waning immunity and reduced COVID-19 precautions also contribute.

Reinfections of COVID-19 are typically less severe than first infections. However, some research says that repeat infections increase the risk of health issues later. As such, its important to continue to take steps to prevent COVID-19.

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Can You Get COVID-19 Twice in a Month? Reinfections and Rebounds - Healthline

CLEVELANDFive Northeast Ohio counties have high COVID-19 transmission spread, according to information the Centers of Disease Control and Prevention released on Thursday.

The following counties are under high transmission rates:

There are a total of 2,817 cases in Cuyahoga County, which is a 19.92% increase over the last seven days. Out of those total cases, 228 of them are new.

Over 65% of the population in the county are fully vaccinated, with 75% with at least one dose.

The CDCs community-level classifications are now based on a mixture of new case numbers, new hospital admissions and the percentage of hospital beds devoted to COVID-19 patients.

Download the News 5 app for free to easily access local coronavirus coverage, and to receive timely and limited news alerts on major COVID-19 developments. Download now on your Apple device here, and your Android device here.

See complete coverage on our Coronavirus Continuing Coverage page.

Vaccinating Ohio - Find the latest news on the COVID-19 vaccines, Ohio's phased vaccination process, a map of vaccination clinics around the state, and links to sign up for a vaccination appointment through Ohio's online portal.

See data visualizations showing the impact of coronavirus in Ohio, including county-by-county maps, charts showing the spread of the disease, and more.

View a map of COVID-19 testing locations here.

Visit Ohio's Coronavirus website for the latest updates from the Ohio Department of Health.

View a global coronavirus tracker with data from Johns Hopkins University.

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COVID-19 levels 'high' in 5 Northeast Ohio counties - News 5 Cleveland WEWS

In a recent study published in Jama Network Open, researchers estimated the probability of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) reinfection following coronavirus disease 2019 (COVID-19) recovery. Additionally, they determined the effectiveness of the primary vaccination series in reducing the reinfection risk.

There is growing evidence that susceptibility to SARS-CoV-2 reinfection is much lower in individuals who have experienced a SARS-CoV-2 infection. Moreover, such individuals are at a lower risk of hospitalization and death even upon reinfection. However, SARS-CoV-2 infection-induced natural immunity wanes over time, thus necessitating vaccination to boost the immunity again. Therefore, it is crucial that studies comprehensively investigate the benefits of vaccination in preventing reinfection among these individuals and the overall dynamics of SARS-CoV-2 reinfection.

In the present population-based cohort study, researchers analyzed data from the adult population (12 years and older) of Rhode Islandbetween March 1, 2020, and December 9, 2021. The study cohort was unvaccinated when they first contracted reverse transcriptase-polymerase chain reaction (RT-PCR)-confirmed COVID-19. Also, these individuals remained unvaccinated for 90 days after their first positive RT-PCR test.

Further, the team categorized the study population into those living in long-term congregate care (LTCC), which included nursing homes and similar living facilities, LTCC employees, and the general population. LTCC settings typically have higher SARS-CoV-2 transmission rates, so residents and employees are at a higher risk of COVID-19-related morbidity and mortality.

The team conducted a survival analysis for all three sub-populations to characterize the risk of reinfection. All individuals who remained unvaccinated after the 90-day recovery period entered the risk cohort for SARS-CoV-2 reinfection. The researchers followed up with them from entry time to the risk cohort to the time of actual reinfection. They used the Kaplan-Meier method to calculate the three-, six-, and nine-month probability of reinfection for each study sub-population by vaccination status. The team recorded and categorized vaccination status as follows:

(1) CPVS, who received a two-dose regimen of the messenger ribonucleic acid (mRNA)-1273/BNT162b2 vaccine or one dose of the JNJ-78436735 vaccine,

(2) partly CPVS received one dose of the mRNA-1273/BNT162b2 vaccine, and

(3) unvaccinated

For all three subpopulations, the team also estimated vaccine effectiveness (VE) associated with preventing reinfection as a 1 adjusted hazard ratio (AHR), which they estimated using the Cox proportional hazards model.

The study data encompassed 3124 LTCC residents, 2877 LTCC employees, and 94,516 individuals belonging to the general population. During the follow-up period, 56,888 individuals received at least one vaccine dose. In the general population, the risk of reinfection was lower among men than women (AHR 0.74), higher among white individuals, and lower among individuals who were confirmed symptomatic (AHR 0.58). The researchers could not find proof of comparable associations among LTCC employees and residents.

Using prospective analysis and time as a covariate, residents, and employees of LTCC facilities had VE associated with CPVS of 49% after recovery from the first infection vs. 62% for the general population. These estimates adjusted for age, gender, ethnicity, community-level COVID-19 risk, hospitalization status, and symptoms during the first infection, as well as the calendar time of entry into the SARS-CoV-2 reinfection risk cohort. The researchers could not deduce formal statistical inference about VE associated with preventing more severe reinfections. However, they observed that reinfection-induced hospitalization and mortality were lower among vaccinated individuals compared to unvaccinated ones.

Furthermore, the study findings were in agreement with other similar studies. A study by Cavenaugh et al. conducted in Kentucky showed that the unvaccinated population had two-fold higher odds of reinfection than fully vaccinated individuals. Similarly, another study conducted among health care workers from the UK showed that individuals who were subsequently vaccinated after SARS-CoV-2 infection maintained over 90% immunity consistently.

The current study evidenced that the primary vaccination reduced the risk of reinfection by approximately half in individuals who had recovered from COVID-19. The study results showed that during the nine months of recovery from primary infection, LTCC employees and residents were at a 10% and 13% higher risk of SARS-CoV-2 reinfection, respectively; thus, they needed vaccination on priority compared to the general population at only 2% reinfection risk. Employees and residents of similar settings with greater SARS-CoV-2 exposure (e.g., health care workers, workers at correctional facilities) should also be encouraged to complete vaccinations to reduce their risk of reinfection.

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Vaccination after COVID-19 recovery reduces reinfection risk by almost 50% - News-Medical.Net

Hospitals have reported the largest sustained decline in coronavirus hospitalizations since March, with 64 fewer patients occupying hospital beds Wednesday than when the current surge peaked 10 days ago at 464 hospitalizations.

Hospital space remains in short supply, however, with only 8% of intensive care units available for patients statewide and 7% of regular hospital beds available.

Health officials warned Oregonians last week that the hospital system is again facing a crisis, even though COVID-19 hospitalizations amount to less than half of what they were during the delta and omicron surge peaks. The strain on hospitals is driven at least in part by delays in getting people out of hospitals, staff burnout and patients coming in for issues they had left untreated during the worst of the pandemic.

COVID-19 community levels are high in 19 Oregon counties, according to federal benchmarks that incorporate hospitalizations, hospital admissions and new case counts. They include Multnomah County, though not Washington and Clackamas counties, which were previously listed, too. At high levels, health officials recommend that everyone wear masks when in indoor public places.

New reported coronavirus cases fell for the second consecutive as of Wednesday, though the 5% decline this week coincided with a 10% decline in testing. The 8,751 cases reported over the last seven days are considered a profound undercount, as have all cases reported since at-home tests became widely available.

The share of positive tests, reported at nearly 13% Wednesday, has remained above 10% since May.

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Since it began: Oregon has reported 848,046 confirmed or presumed infections and 8,061 deaths.

Hospitalizations: 400 people with confirmed coronavirus infections are hospitalized, down 24 since Wednesday, July 20. That includes 43 people in intensive care, down two since July 20.

Vaccinations: As of July 25, the state has reported fully vaccinating 2,937,559 people (68.8% of the population), partially vaccinating 302,252 people (7.1%) and boosting 1,714,863 (40.2%).

New deaths: Since July 20, the Oregon Health Authority has reported 80 additional deaths connected to COVID-19.

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Coronavirus in Oregon: Hospitalizations fall in welcome sign of receding surge - OregonLive

A transmission-electron micrograph of SARS-CoV-2 Omicron virus particles (pink) replicating within the cytoplasm of an infected CCL-81 cell (teal). Photo: NIAID Integrated Research Facility/NIAD

Were still in the midst of one of the largest COVID waves of the pandemic, and its fueled by the Omicron BA.5 subvariant, the most contagious and most immune-evasive coronavirus strain yet. Scrippss Dr. Eric Topol, who has been one of the loudest voices sounding the alarm over BA.5, has repeatedly described the strain as the worst COVID variant on account of it having more fitness, growth advantage, and immune evasion than any of its predecessors. According to the latest CDC estimate, BA.5 now accounts for nearly 82 percent of all new infections in the U.S., where it has prompted a surge in reported cases, test-positivity rates, COVID wastewater levels, and, thanks to its immune evasion, reinfections. Last week, it even infected President Biden with his first-ever COVID case; this week, an outbreak hit the Senate.

The BA.5 wave has also been driving up the number of U.S. hospitalizations, along with a slight rise in the number of COVID deaths, but it hasnt produced severe outcomes anywhere near the scale seen in previous major waves. Indeed, the rapid onset of BA.5 and its subvariant brethren (BA.4, BA.2, and BA.2.12.1) without a corresponding surge in severe COVID has prompted a sense that were finally in a new phase of the pandemic where new strains come and go, COVID continues to spread and surge and unsettle, but our bolstered immune systems hold the line and we avoid the recurring nightmare of mass illness and death.

Scientists are still studying the new variant, and the BA.5 wave has been playing out differently in various countries, likely due to a complicated combination of factors. But while the far less severe impact of the BA.5 wave in the U.S. has, thus far, been a welcome departure from what weve encountered before, some COVID experts, like Topol, remain concerned. Though its been more than two and a half years since COVID arrived, were still not staying ahead of the virus.

Topol and immunologist Akiko Iwasaki just co-wrote a paper calling for an accelerated Operation Warp Speedlike initiative to pursue nasal COVID vaccines, which could provide mucosal immunity that stops the virus in the part of the body where it starts. Topol has also pushed for the development of other potentially variantproof vaccines, like pan-sarbecovirus and pan-coronavirus vaccines. This week, the White House hosted a summit on future COVID vaccines attended by many of the top minds in the field, including Iwasaki, but its far from clear that any of the promising ideas and goals discussed there will get the government funding theyd need to have an impact on the pandemic anytime soon.

I recently had a long conversation with Topol about BA.5, why hes troubled by it, and what the variant and its arrival portend for the future.

On one hand, here in the U.S. weve seen a significant drop in hospitalizations and deaths amid the wave of cases of BA.5 and the other earlier Omicron subvariants. But youve been calling attention to the fact that in some other countries, BA.5 has fueled some alarming spikes in cases, hospitalizations, and even deaths. So, is the U.S. through the worst of this?I agree that, overall, if you look at it globally, hospitalizations and deaths from BA.5 are not going to reach levels anywhere close to Omicron or previous waves, but theyre not trivial elevations. Deaths are going up over the whole world from BA.5. Our wave is still playing out right now. Were poorly vaccinated here in the U.S. poorly boosted, especially in high-risk people like seniors. So I wouldnt want to conclude that were out of the woods. We could be in for more trouble before the BA.5 wave is finished.

Im actually a very optimistic person. When we were coming down from Delta and had not seen Omicron, I thought, Wow, the worst is over. Then Omicron proved to be an onslaught in terms of spread by any metric as well as the toll it took in more serious outcomes. So with that background, the recent CDC report that came out about the vaccines really has me worried.

Whys that?Its not like all of a sudden theres going to be a variant with total immune escape from vaccines. But in the CDC morbidity and mortality report, it said that two-dose vaccine effectiveness against hospitalization for the original BA.1 Omicron strain were not talking about infections because were well past having good vaccine coverage for that but for hospitalization, it dropped to 61 percent for two doses. And for BA.2 and BA.2.12.1, the latter of which is more like BA.5 but not as bad, two doses against hospitalization dropped to 24 percent. That should set off alarms because we dont have a lot of people with a third shot. For three shots the efficacy jumped back up, but only to 52 to 69 percent with BA.2/2.12.1.

Kaiser Southern California has also had two reports on vaccine effectiveness in their big network of patients, and they show the same attrition against hospitalizations as was seen in this much larger new comparison from the CDC.

So how can you feel good about these data? I dont see how. This narrowing benefit of the vaccines, which I think is due to more immune escape, not due to more infections in the unvaccinated, its still a very big gap. To drop down almost 40 points in effectiveness against hospitalizations with only two shots this should be a signal that something is going on with our vaccine protection. But you dont see anybody raising concerns about this. All you hear is happy talk that we have great protection from hospitalizations and deaths. I dont know about that. These data dont support that.

So that suggests that hospitalizations will likely keep going up in the BA.5 wave? Yeah, theyre going to go up. The number of current U.S. hospitalizations is already over 40,000. I wouldnt be surprised if it gets to 50,000 or 60,000. It isnt going to get near 160,000, like it did with BA.1, only because so many people got infected with BA.1 and theres some cross-immunity. But the number of hospitalizations has been going up substantially. It had gotten down to 12,000 and now back up past 40,000. If you look at the curve, it has a new increased slope since BA.5 started to take effect, and its still on the way up. The question is does it get to 50,000? Does it get to 60,000? Thats a lot of sick people in the hospital.

And the other thing I would just say, parenthetically, is with BA.5, Ive never seen so many infections in my personal network, including family, friends, colleagues. Ive never seen infections last as long. After 10 days, still testing positive, after day 12, 13, 14. The behavior of BA.5 is different and the fact that our CDC still adheres to this five-day isolation recommendation, its incredulous. Theyre actually promoting spread by doing that.

Theres no question that this is a different effect from BA.5 in terms of the length of infectiousness, how much its spread, and maybe not more hospitalizations. But remember, thats with Paxlovid, which now has 90 percent efficacy in preventing hospitalizations for high-risk people.

Right, if a variant emerges that Paxlovid isnt as effective against, that could suddenly leave us much more vulnerable to severe COVID again.Yes. And I think most of us whove really zoomed into the mutations on MPro, the main protease of the virus that Paxlovid works on Id say its just a matter of time. Its inevitable. Already these mutations have appeared naturally because of the pressure that the virus is getting from Paxlovid. Its inevitable. Were going to see resistance to this drug, which, after the vaccines, is the second-most-important advance that we have had to take on the virus. But it may be short-lived, it could be that by years end or the beginning of next year, we wont have Paxlovid as a remedy or rescue anymore. Theres no question Paxlovid is helping keep the hospitalization number down.

Updated booster shots that better target the Omicron lineage are on the way. Will those help us stay ahead of the virus?We need variantproof boosters. No more chasing variants because we are not very good at that. Just get the vaccines that would take on all sarbecovirus and betacoronavirus so we can put an end to the whole idea of trying to anticipate the variant that well need a booster for. We know how to do that. We have over 25 incredibly potent broad neutralizing antibodies. We can make vaccines that induce several of those antibodies to never have to worry about a variant in terms of having protection.

But those arent the boosters arriving this fall.No. The booster plan is for BA.5. And saying that will be here for the fall is highly optimistic. It took seven months to get a BA.1 booster. Then the government sent the pharmaceutical companies back to go get us a BA.5 booster. Thinking that could be available in October or November thats highly optimistic. And we certainly dont know what variant is going to be with us at that time. It wont be BA.5 anymore. Therell be something else that will outcompete BA.5. Once that BA.5 booster is available, it may not work against the then circulating virus because it knows how to evolve.

Why arent these better boosters in the pipeline instead?Well, its pretty clear that Congress is unwilling to fund a dollar more for COVID. And thats, of course, the Republicans blocking any COVID bill. But there are even people in the Biden administration who arent sure how much these next-generation vaccines including variantproof, universal, and nasal are going to help us. Thats just, I think, being out of touch with the science. And any COVID bill dedicated to getting ahead of the virus would need to include better drugs, more drugs. Because we have to plan for Paxlovids obsolescence, and we dont have anything to replace it yet but there are many good candidates in the pipeline.

There seems to be at least anecdotal evidence that a small number of people are now getting reinfected within a matter of weeks. What do you make of that?Those added mutations that we first saw with BA.2.12.1 and now in BA.4 and BA.5 that immune evasion is whats responsible for all these early reinfections. Thats where this virus is going. Its got a flashing light: I have found ways to evade your immune system, and I can keep building on that. Reinfection is perhaps the best real-time signature of immune evasion.

Whats your sense of where long COVID is going? Is there any other way to avoid it than just not catching regular COVID in the first place, which is clearly getting harder to do at this point in the pandemic? Is there some other way to handle it?Well, youre right. Avoid the infection, first. Then, if you had a vaccine, that seems to avoid the chance of long COVID to some extent, but we also have to have treatments for it we dont have any yet that are validated. We have a billion dollars from the NIH toward long COVID, but youre not seeing any real contributions that funding has advanced yet. And we know that long COVID is not a homogeneous disorder. There are different components. Some are much more immune-mediated, some are much more autonomic nervous system-mediated. So theres a lot to unpack with that.

So what are you most worried about with regard to the future evolution of SARS-CoV-2?The known unknown, which is that this virus still has many more ways to become more resistant to our immune response and we should plan on that. We keep thinking weve reached some kind of limit. But the most important lesson from BA.5, to me, is that its worse. If it had come without BA.1 as a predecessor the only reason BA.5 doesnt look horrific right now is because BA.1 had built up the immunity wall. More than half of Americans have had BA.1 or BA.2. And were now seeing in BA.5 the most innovation, the most growth advantage, the most fitness of the virus yet and were just not dealing with it.

If some people think, Oh, it cant get worse, its going to get better. We dont know that. You have to plan for the worst-case scenario. And the worst-case scenario is that the virus further increases its immune evasion. Its already picking up things that worked in prior versions of the virus: For instance, BA.2.12.1 and BA.5 have the same key L452R mutation that the Delta variant had. Anyone who thinks the virus doesnt have room to evolve further is just not paying attention.

Is that a near-term threat? Can we predict a timetable for any of this evolution? No, but its accelerating. We know that much. The time its taken to get from BA.1 to BA.5 is not a good tempo for a whole new lineage to outcompete the prior one and achieve dominance worldwide.

So it doesnt look good. These new strains are clearly happening more frequently than they used to. In the first 12 months of the pandemic, there was no evolution of the virus. We basically had the original Wuhan strain, and then D614G, which arguably only had minor functional consequences. Alpha was mild compared to anything weve seen subsequently, then there was Delta, which obviously had more infectiousness and virulence. But now, with this whole Omicron family, its moving at a very rapid pace.

We cant predict the new mutations. We cant predict the timing. We can try to extrapolate, but even extrapolating, we had no good semblance of what Omicron would look like with its 57 spike mutations in BA.1. No one accurately predicted we would be looking at that.

And its too fast.Its the known unknown. Yeah.

UCL Genetics Institute director Francois Balloux recently explained that he wasnt as concerned about the emergence of further Omicron subvariants as he was about the reemergence of COVID lineages, like Delta, that have undergone a kind of underground evolution. So a strain circulating in some isolated part of the world; or one within an animal reservoir, i.e. an animal population the virus has spilled into from humans; or one that has evolved via a long-term chronic infection in someone who is immunocompromised which is how many scientists believe Omicron itself evolved. How worried are you about these paths?When an immunocompromised person gets infected, they really cant mount a good immune response. So the virus, instead of what its been doing globally for two and a half years, goes through this accelerated evolution in that person, picking up mutations left and right. It basically has unchecked potential to evolve in that person, and then that evolved virus infects other people. Thats pretty certainly what happened with Omicron.

I agree that the animal reservoirs are also a concern because weve already seen spillover to many different species, including hamsters, mink, cats, and deer. So thats another way that the virus can evolve, in an animal reservoir, and come back to spillover in humans.

We also havent contained the virus around the world, so it can continue to evolve through the millions of infections each day. And there are tens of millions of immunocompromised people in the world. It just takes one person, really, to trigger things. And then you have all these hybrid versions of the virus that were seeing, all these recombinants, which could bring about the worst elements of different parts of the virus. Most of the public focus on the evolution of SARS-CoV-2 has been spike-centric, but there are lots of other parts of the virus that can be troubling, that can make the virus more difficult to deal with. So again, theres lots of room for this virus to go.

There are too many paths. If youre just taking odds, and you have all these different routes and tens of millions of people that are immunocompromised around the world, are you going to bet against the virus evolving into something thats more challenging than what we have today? I dont think so.

Is there anything we can do to defend against COVID strains spilling back over from animal populations?No. No defense at all, unfortunately.

You and some other scientists have suggested that Omicron and particularly BA.5 are so different from any previously dominant COVID strains that in many ways we are now effectively dealing with a new virus. Youve also pointed out that if the original Omicron strain had the characteristics of BA.5,the Omicron wave would have been far worse. I understand thats a way to highlight why people should be concerned about BA.5 and what it means for COVIDs evolution, but is that actually possible? Can a BA.5 evolve on its own without there first having been a BA.1?Its a good question because we dont really know how BA.5 evolved. We just know it did. And could BA.5 have come in from an immunosuppressed person de novo without BA.1? Possibly. We just dont know. Basically new mutations showed up. Four key mutations showed up beyond BA.2 that have caused a lot of trouble, but we dont really know precisely how that occurred.

But we know why it occurred.Yeah. The virus is under pressure from vaccines and prior infections and now Paxlovid. So its finding ways to stand up to find new hosts. All viruses want is to find a new host. So they just keep mutating, and some of them dont work. Most of them fortunately dont work, but a lot of them do, and those are what were seeing.

Meanwhile, globally, were still giving COVID as many opportunities to evolve as we were a year ago if not more because now there are reinfections.Yeah, if not more. Were putting pressure on the virus to find new ways to circumvent our immune response and thats what it continues to do.

And at the same time, weve collectively done virtually nothing to prepare for whatever evolves next.Right. From day one of this pandemic, we have never tried to get ahead of the virus. Labs have come up with all sorts of broad neutralizing antibodies that would be variantproof. Nasal vaccines, to block transmission, to achieve mucosal immunity there are 12 in clinical trials. There are all these drugs in the hopper. Pan-coronavirus vaccines. These are all academic pursuits or largely from small companies. There hasnt been a national or a much larger international initiative to get ahead of the virus.

By initiative, you mean money.Money and an Operation Warp Speed 2, with collaborations and private-public industry partnerships. And not necessarily just the U.S., it should be global. But you dont see that, and its so stupid because look how successful we were. Operation Warp Speed showed how good we could be at this. But we havent done anything. We keep reacting and chasing instead of doing the things we know would get ahead of it.

I look at the data, and it says we can do better than this. I know we can; the science is there. Its just waiting in the hopper to be activated, but were just not taking it seriously enough. And I want to get out of this thing. I thought we were out of it as we came down with Delta in June 2021. Who wouldve thought we would get to now, a year-plus later, and theres still no light ahead of us? Thats why I want to take the aggressive get-ahead stance.

It seems like political will for that stance is nonexistent in the U.S. right now.Its also internationally. You dont see the U.K. which has been a model for science in the pandemic or many places around the world that are capable of it talking about going after pan-coronavirus vaccines. Why arent we making this a global priority?

Im optimistic that we can seize and achieve containment of the virus once and for all. Ive been optimistic like that for many months, but I feel like Im a Lone Ranger not a single voice, but one of a minority.

To be clear, you mean a pharmacological way to contain the virus. Because were never going back to nonpharmaceutical interventions like we saw in the first few years of the pandemic, or at least unless theres an enormous rise in hospitalizations and deaths.Yeah. In January 2021, my colleague Dennis Burton and I wrote in Nature that we need a variantproof vaccine. This virus is ideally suited, as compared to flu or HIV, for a variantproof vaccine. The initial success of Pfizers vaccine was 95 percent against symptomatic COVID. Theres never been a flu vaccine like that. Look at the success of Paxlovid: a 90 percent reduction in hospitalizations and deaths. This virus is vulnerable. Weve proven that. Were just not building on our successes. Its incredible. This is a less challenging, less hypermutating virus than the flu. Our COVID vaccines make flu vaccines look like a joke, or at least they did.

So we already have COVID on the ropes and can finish it off if we try.Thats why Im so optimistic. We can do this. But were not doing it.

This interview has been edited for length and clarity.

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BA.5 Shows COVID Is Evolving Fast. Why Aren't We Fighting Back? - New York Magazine

COVID-19 can have many impacts, both physical and psychological. One question that keeps coming up in the media and recent literature is whether there is a link between COVID-19 and erectile dysfunction.

In this article, we look at numerous studies on the associations between COVID-19 and erectile dysfunction (ED).

We also explore whether ED can increase the risk of COVID-19, potential complications of COVID-19, treatments for ED, and when to contact a doctor.

Several studies explore COVID-19s effects on ED.

Researchers involved in a 2021 pilot study examined the penile tissues of four people, two with a history of COVID-19 infection and two without. Results suggests the two that had COVID-19 showed a presence of the virus function in their biopsies. The scientists conclude that the bodys cell dysfunction from COVID-19 infection can contribute to ED.

A 2022 statistical study involving global data of over 66 million people excluding those that already had ED before January 2020 indicates there is a higher chance of getting ED after COVID-19 infection. However, this study relies on statistical data from a global database instead of a blind clinical study, which is an important limitation.

Another 2022 study among 348 participants attempts to determine if COVID-19 can cause testicular damage. Comparing testosterone levels before and after COVID-19 in a 1-year span, this study suggests those positive for COVID-19 had a greater decrease in testosterone levels than those who did not get the infection.

A 2022 report looking at 693 publications in the realm of COVID-19 and ED points to compelling evidence that the virus may harm males health and sexual function. This includes a nearly 6-fold higher risk of getting ED.

One 2022 study among 156 males at the beginning of COVID-19 infection and in the month after getting COVID-19 found they had more depression and anxiety and a lower erectile function score. This could indicate that COVID-19 may result in more anxiety, which in turn increases the chance of ED.

A 2020 report explores how experiencing an infection with severe acute respiratory syndrome in 2002 affected peoples mental health. It suggests that the infection was capable of having a long-term negative impact on mental health and that COVID-19 may be similar.

According to a 2022 report by the National Institutes of Health (NIH), people with chronic long-term depression or persistent feelings of loneliness were 81% more likely to experience hospitalization after a COVID-19 diagnosis. This suggests that COVID-19 may be a psychological risk factor for mental health.

A 2020 report states that sexual performance anxiety contributes to premature ejaculation and ED. Therefore, it seems reasonable that general anxiety may also have an effect. In fact, a 2021 study involving adult males suggests that those with anxiety disorders have a high risk of developing ED.

The above studies show an association between COVID-19, anxiety or depression, overall health, and ED.

However, people can have underlying health conditions that affect the results. Most of the studies state that more research is necessary to truly explore the link between COVID-19 and ED.

Very few studies have explored the risk of getting COVID-19 in people with ED.

One 2021 study looked at 100 participants, 25 of which were positive for a COVID-19 infection. It found that people with ED were more likely to have COVID-19 than those without ED.

This study points out that its results are preliminary and more research is necessary. It is also important to note that correlation does not equal causation.

However, there is also another viewpoint.

An older 2013 study found that males with ED have a higher chance of developing cardiovascular disease (CVD). According to a 2022 study, while scientists need to do larger studies, evidence suggests that CVD increases COVID-19 severity. This means there is an indirect association that ED may increase the risk of COVID-19.

The CDC recommend a number of ways to decrease the chance of getting COVID-19.

These include:

The CDC also states that people with a weakened immune system should take extra precautions.

According to the National Institue of Diabetes and Digestive and Kidney Diseases, treatments for ED include:

According to a 2020 article, other emerging treatments include low intensity shockwave therapy, stem cells, and nitrate oxide donors. However, scientists need to do long-term studies to determine their efficacy, safety, downsides, and overall results.

People with COVID-19 who have concerns about its long-term effects on their particular health condition should consult a doctor to see if there are any precautions or tests they can take. Many online health services can help people access a doctor, even if they cannot leave their house.

Similarly, those with CVD or any underlying medical condition that increases their chance of getting COVID-19 should also talk with a doctor to increase preventive measures. The CDC lists a number of conditions that pose a high risk of getting severe illness with COVID-19.

Some people may feel anxious or uncomfortable at the prospect of speaking with a doctor about ED. However, the condition is nothing to be embarrassed about, and a doctor or urologist can most likely help resolve or treat the symptoms.

Both COVID-19 and ED affect many people. Numerous studies suggest links between the two, including direct and indirect associations.

In particular, it seems that people with COVID-19 may have a higher chance of getting ED or worsening their current ED. The opposite could also be true. However, more research is necessary to determine the long-term impact.

One way to prevent ED may be to increase protection against COVID-19. There are numerous ways to do this, including wearing masks. People with a weakened immune system or ED and those experiencing complications from COVID-19 may find it helpful to speak with a doctor about their concerns.

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COVID-19 and erectile dysfunction: Link, risks, and more - Medical News Today

In a recent study posted to the medRxiv* preprint server, researchers estimated the impact of different coronavirus disease 2019 (COVID-19) messenger ribonucleic acid (mRNA) booster vaccinations in the United States (US) during fall 2022.

The continual emergence of severe acute respiratory syndrome coronavirus 2 (SARS-COV-2) variants of concern (VOCs) warrants the development of adapted SARS-CoV-2 vaccines as health authorities and policy-makers plan for COVID-19 vaccinations in fall 2022. Studies have reported that COVID-19 patients elicit lower neutralizing antibody (nAb) titers against the SARS-CoV-2 Omicron BA.4/5 VOC than against Omicron BA.1 VOC.

In the present study, researchers estimated the prevention of SARS-CoV-2 infections and associated hospitalizations by administering three different mRNA vaccine boosters against SARS-CoV-2 over six months (between September 2022 and February 2023) among adults residing in the US.

The participants were boosted with the mRNA-1273 monovalent vaccine (ancestral strain) from September 2022, the mRNA-1273.214 bivalent vaccine (ancestral strain + Omicron BA.1) from September 2022 onwards, or the mRNA-1273.222 bivalent vaccine (ancestral strain + Omicron BA.4/5) from November 2022. In addition, sensitivity analyses were performed based on SARS-CoV-2 transmissibility, mRNA vaccination coverage, masking, Paxlovid (nirmatrelvir/ritonavir) treatment, and antibody waning against SARS-CoV-2 over time.

Susceptible-exposed-infection-recovered (SEIR) compartmental modeling was used for the analysis stratified by age and SARS-CoV-2 transmission dynamics. The SIER model was calibrated between 31 January 31, 2020, and 31 May 2022 for matching all SARS-CoV-2 infections to IHME (institute for health metrics evaluation) estimates.

Sensitivity analyses around transmissibility, vaccine coverage, masking, and waning of natural and vaccine-induced immunity changed the magnitude of cases prevented but boosting with mRNA-1273.214 in September consistently prevented more cases of infection and hospitalization than the other two strategies.

It was assumed that the prime vaccinations for the study participants were combinations of the BNT162b2 and AD26.COV2.S and mRNA-1273 vaccines and that all participants received prime vaccinations and initial booster vaccinations before 31 May 2022, and the second booster vaccinations before 15 June 2022.

The model simulation period was divided into three timeframes: pre-Omicron (between 31 January 2020 and 30 November 2021); Omicron BA.1/2 (between 1 December 2021 and 14 August 2022); and Omicron BA.4/5 (between 15 August 2022 and 28 February 2023). Vaccine effectiveness (VE) was estimated for prime vaccinations, the first booster, and the second booster based on relative nAb titers [geometric mean titers (GMT)] for estimating the impact of vaccinations and newly emerging SARS-CoV-2 variants.

Compared to no boosters, the estimated decreases in SARS-CoV-2 infections by mRNA-1273, mRNA-1273.214, and mRNA-1273.222 vaccines were 34%, 40%, and 18%, respectively, over six months. Likewise, initiating booster vaccinations in September viz. mRNA-1273 and mRNA-1273.214, significantly prevented hospitalizations by 42% and 48%, respectively, than booster vaccination initiation in November by mRNA-1273.222 (25%) over six months in comparison to no boosters.

The model predicted that by September 2022, individuals who received only prime vaccinations or the first booster would elicit no vaccine-induced immunity, while VE for the second booster was <30%, and VE against COVID-19 severity was <50% for recipients of only prime vaccinations. The mRNA-1273.214 booster increased protection against SARS-CoV-2 by 70% and against infection severity by 90%.

If it is assumed that Omicron BA.4/5 would persist for >1 year, the mRNA-1273, mRNA-1273.214, and mRNA-1273.222 boosters were estimated to decrease SARS-CoV-2 infections by 36%, 47%, and 45%, respectively, in comparison to booster vaccinations in the fall period. The projected COVID-19 case counts were estimated to decrease with stronger natural immunity; however, the mRNA-1273.214 booster remained effective even after assuming that natural immunity waned at a rate of 50% with a 36% decrease in COVID-19 case counts in comparison to no boosters in the fall period.

The percent reduction in six months of COVID-19 cases when boosting with mRNA-1273.214 was 33%, and no fall booster was 36%. On delaying the enhancement in SARS-CoV-2 transmissibility from 15 August to 15 September 2022 and administering boosters from September onwards, the reduction in infection severity with mRNA-1273.214 in comparison to no fall booster was 42%.

If fall booster uptake was 25% of the estimated base case scenario, the estimated reductions in COVID-case counts were 27%, 14%, and 32% for the mRNA-1273, mRNA-1273.222, and mRNA-1273.214 boosters, respectively. Reducing the rate of antibody waning of the mRNA-1273.214 booster by 25% prevented 41% of infections, 50% prevented 42% of infections, and 75% prevented 43% of SARS-CoV-2 infections, respectively, in comparison to no fall booster.

Overall, the study findings showed that vaccinating with the bivalent mRNA-1273.214 booster was more effective over six months in preventing Omicron BA.4/5 infections and associated hospitalizations compared to the next-generation mRNA-1273.222 vaccine only because mRNA-1273.214 booster could be administered two months earlier than the mRNA-1273.222 booster. Booster vaccinations must not be delayed until an Omicron BA.4/5-specific vaccine is available.

medRxiv publishes preliminary scientific reports that are not peer-reviewed and, therefore, should not be regarded as conclusive, guide clinical practice/health-related behavior, or treated as established information.

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To what extent did the COVID-19 booster strategy prevent infections and hospitalizations in US adults? - News-Medical.Net

CRAIG T. KOJIMA / JAN. 17

A COVID-19 testing swab during testing at the Neal Blaisdell Center.

The Hawaii Department of Health today reported 4,075 new COVID-19 infections over the past week, bringing the total since the start of the pandemic to 325,944.

The states seven-day average of new cases was reported at 573, one fewer than 574 reported on July 20. DOHs daily average reflects new cases per day from July 16 to 22, which is an earlier set of days than the new infections count.

DOH also reported 23 more deaths, bringing the states coronavirus-related death toll to 1,571.

By island, there were 2,719 new infections reported on Oahu, 542 on Hawaii island, 527 on Maui, 176 on Kauai, 11 on Molokai, and five on Lanai. Another 95 infections were reported for out-of-state Hawaii residents.

Actual numbers are estimated to be at least five to six times higher since these figures do not include home test kit results, DOH Director Dr. Elizabeth Char has said previously.

The states average positivity rate, meanwhile, ticked up to 15.7% compared to 15.1% reported the previous week, representing tests performed between July 19 to 25.

The average positivity rates for Kauai County increased this week to 19.9% compared to 18.5% reported the previous week. The average positivity rate for Maui County jumped to 17.8%, up from 14.7% reported the previous week.

There were 163 patients with COVID in Hawaii hospitals today, according to the state dashboard, slightly higher than 159 reported the previous week. Of the 163, 11 are in intensive care and seven on ventilators.

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Hawaii Department of Health reports 4,075 new infections, 23 coronavirus-related deaths - Honolulu Star-Advertiser

The world has experienced a slew of surges caused by an alphabet of variants since the onset of the COVID-19 pandemic in March 2020. Thankfully, none of the variants has led to a significant increase in disease severity.

Becker's spoke to Jonathan Abraham, MD, PhD, an infectious diseases physician at Boston-based Brigham & Women's Hospital, to learn more about why the SARS-CoV-2 virus's evolution hasn't led to significant changes in disease severity from the ancestral strain, and what are the chances that it eventually mutates to cause severe illness.

"It's something that even as a scientific community, we don't understand yet," Dr. Abraham said. He is an assistant professor of microbiology at Harvard Medical School and runs the Abraham Lab, which studies how pathogens interact with the cells of their hosts.

Two questions that remain:

When will immunity significantly wane?

While each new variant appears to be better at infecting vaccinated people than the last, vaccines have still largely protected against severe illness from each of them.

The question of whether the SARS-CoV-2 virus could eventually evolve to cause more severe illness then depends, at least in part, on the level of immunity a population has.

"Overtime, we've seen this virus mutate and mutate, but the question is still when will the immunity we have either from vaccines or from prior exposure [wane,] and by then, will the virus have disappeared or will it have continued to mutate?" said Dr. Abraham.

If the virus continues to mutate over time and the population's immunity wanes significantly, more severe disease is a possibility, "but the question is really hard to separate from one of the infected host, which has some degree of immunity," he said.

In a vaccine-less world where there were no levels of immunity and a mutating virus, variants like omicron would likely cause severe illness. But in a world where most people have been vaccinated or previously infected, that's not the case.

Could the virus evolve to evade T-cell responses?

Even with the virus able to evade antibodies, there is evidence that T-cells a separate arm of the immune system's response play a role in maintaining immunity from COVID-19.

In someone with prior immunity from vaccination, infection or both, "I think most would believe T-cells probably account for why disease severity is not as significant when someone gets infected now," Dr. Abraham said.

"T-cells are really the work horses that may be protecting us from getting sicker," he said, but if the virus mutates in a way that allows it to evade both antibody and T-cell responses, that may be a recipe for more severe disease.

Some research has shown people who have COVID-19 generate T-cells that target at least 15 to 20 different fragments of SARS-CoV-2 virus' protein, according to a Nature report. The targeted protein fragments can vary widely among different people, meaning a population could generate a broad variety of T-cells against the virus.

"That makes it very hard for the virus to escape cell recognition," Dr. Alessandro Sette at the La Jolla Institute for Immunology in California, told the news outlet, adding its "unlike the situation for antibodies."

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2 questions a Harvard infectious disease expert still has about the coronavirus' evolution - Becker's Hospital Review