Category: Corona Virus Vaccine

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President Joe Biden tests positive for COVID-19 while campaigning in Las Vegas – El Paso Inc.

July 18, 2024

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President Joe Biden tests positive for COVID-19 while campaigning in Las Vegas - El Paso Inc.

What Doctors Want You to Know About the Latest COVID-19 Variant, LB.1 – Prevention Magazine

July 11, 2024

While government data that tracks COVID-19 isnt as robust as it used to be, its clear that were in the middle of a summer wave. Contributing to the uptick is the newest COVID variant, LB.1.

Right now, emergency room visits due to the virus are up more than 23% than they were during the previous week and hospitalizations are up more than 13%, according to data from the Centers for Disease Control and Prevention (CDC).

The latest variant hasnt gotten a lot of attention so far, but its been steadily causing issues in the U.S. since late spring.

Meet the experts: Thomas Russo, M.D., professor and chief of infectious disease at the University at Buffalo in New York, Amesh A. Adalja, M.D., infectious disease expert and senior scholar at the Johns Hopkins Center for Health Security.

So, what is LB.1 and does it have unique symptoms? Infectious disease experts break it down.

LB.1 is the third most common COVID-19 variant in the U.S. right now, per CDC data. Its a descendant of JN.1, along with common variants KP.2 and KP.3, according to the Infectious Diseases Society of America (IDSA).

LB.1 is another Omicron variant, says Amesh A. Adalja, M.D., infectious disease expert and senior scholar at the Johns Hopkins Center for Health Security. Its also a FLiRT variant, along with KP.2, KP.3, and KP.1.1, he points out.

Its a little bit different from KP.2 and KP.3 in that it has a deletion in the spike protein, says Thomas Russo, M.D., professor and chief of infectious disease at the University at Buffalo in New York. (In case youre not familiar with it, the spike protein is what SARS-CoV-2, the virus that causes COVID-19, uses to attach itself to your cells and infect you.)

LB.1 first emerged as a blip on the CDCs radar back in April but has become more dominant over the past few weeks.

Its hard to say at this point. There is some lab data to suggest it may be more infectious than KP.2 and perhaps KP.3, Dr. Russo says. It appears to be more immune-evasive.

But Dr. Adalja points out that there seem to be fewer COVID-19 cases caused by LB.1 in the latest CDC surveillance data released than in the previous round of data.

It seems to be more common in the East and Southeast, Dr. Russo says.

There is chatter online about people having a really intense sore throat with COVID-19 lately, and its possible thats due to LB.1 (although tricky to know for sure). But doctors say that COVID-19 symptoms are largely the same as theyve been over the past year or two.

Theres not enough data to report any differences in symptoms, Dr. Adalja says. Each variant has certain symptoms anecdotally attributed to it, but they are mostly all still part of the same spectrum of illness of all versions of the virus.

According to the CDC, those symptoms may include:

It depends on how you look at it. Dr. Russo notes that the COVID-19 vaccine is imperfect at keeping people from getting the virus. However, it can help lower the risk youll end up getting seriously ill, being hospitalized, and dying from the virus.

Dr. Adalja agrees. The current vaccine is not very effective at durable protection against infectionand that has been the case for some timewith the current slew of variants, though it is protective against severe disease, he said.

Thats why Dr. Russo still recommends getting the updated COVID-19 vaccine, if you havent already. It will afford more protection than not being vaccinated, he says.

The best way to lower your risk of getting LB.1 is the same as its always been, although the steps to take really depend on your risk tolerance, Dr. Adalja says.

High-risk individuals should keep up to date with vaccinations and the extremely high-risk immunocompromised individuals should discuss the monoclonal antibody Pemgarda with their physician, he says.

If youre high risk for getting sickmeaning youre pregnant, an older adult, immunocompromised, or have certain underlying health conditionsits also a good idea to mask up in crowded indoor settings, like when you go to the grocery store, Dr. Russo says. Youll also want to avoid indoor settings where you cant wear a mask, like restaurants, until were on the back side of this wave, he adds.

Dr. Rusos says its likely that the summer wave wont die down until the end of the season. Soon after, a new COVID-19 vaccine thats better targeted to the FLiRT variants like LB.1 should be available.

Korin Miller is a freelance writer specializing in general wellness, sexual health and relationships, and lifestyle trends, with work appearing in Mens Health, Womens Health, Self, Glamour, and more. She has a masters degree from American University, lives by the beach, and hopes to own a teacup pig and taco truck one day.

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What Doctors Want You to Know About the Latest COVID-19 Variant, LB.1 - Prevention Magazine

New COVID-19 variant growing in Tennessee. What to know about KP.3 variant and its symptoms – Tennessean

July 11, 2024

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New COVID-19 variant growing in Tennessee. What to know about KP.3 variant and its symptoms - Tennessean

Summer 2024 Covid-19 Surge Occurring With FLiRT Variants Taking Over – Forbes

July 11, 2024

Data suggests that the U.S. has been experiencing a Covid-19 Summer surge since early June. Here ... [+] people visit The Edge observation deck for New York City's 48th annual Macy's 4th of July fireworks on July 4, 2024. (Photo by Noam Galai/Getty Images)

You could say that the U.S. is more than flirting with yet another Covid-19 surge. Chances are that a surge has already been occurring for at least a monthsince early June. And the FLiRT variants of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) have been front-and-center of this surge.

Now, the U.S. still doesnt have a comprehensive surveillance system that can catch surges before they happen or soon after they start happening even though its been over four and a half years since the the SARS-CoV-2 first surged in the U.S. Plus, nowadays, you dont see the public health alerts about Covid-19 surges that you saw during the first three years of the pandemic. So, these days if you want to know whether Covid-19 is surging, you have to rely on checking Covid-19-related emergency room visits, hospitalizations and deaths to see if a surge has already been occurring with an emphasis on the words has already been.

Indeed, emergency room visits due to Covid-19 from June 16 through June 22thats two weeks agowere up 23.3% from the previous week, according to data posted on the Centers for Disease and Control and Prevention. Also, Covid-19-related hospitalizations during the week of June 9 through 15 were 13.3% higher than they were than the week before. Recall that it can take a week or two after someone gets infected to develop symptoms severe enough to require an emergency room visit or a hospitalization. All of this suggests that Covid-19 cases were rising throughout most of June.

It shouldnt be too surprising that yet another Covid-19 Summer surge has been happening. Many political and business leaders are not advocating for Covid-19 precautions such as face mask use and indoor air filtration and purification. And take a wild guess as to what may happen to a virus thats still spreading and mutating when you dont really do much to prevent its spread. The answer is not that it will go away on its own. Moreover, its been about 10 months since the last Covid-19 vaccine update was rolled out last fall, and protection offered by the vaccine tends to wane significantly after four to six months.

Then there are the FLiRT variants, a new group of SARS-CoV-2 omicron variants that have two key mutations in their spike proteins. If you recall, the spike proteins are what makes the virus looks like a spiky ball and help the virus latch on to your cells to then invade them. The name FLiRT is derived from the actual amino acid changes that result from the pair of mutations: a switch of a phenylalanine (F) for a leucine (L) at position 456 and arginine (R) for threonine (T) at position 346 in the spike protein.

These FLiRTs are descendants of the JN.1 variant that was dominant in the United States earlier this year and encompass a group of variants with names that begin with the letters JN and KP. In the first week of June, KP.3 accounted for an estimated 33.1% of SARS-CoV-2 infections in the U.S., KP.2 for an estimated 20.8% and KP.1.1 for an estimated 9%. And these percentages have been growing, which is not surprising since preliminary data has suggested that the Rethe effective reproduction numberfor KP.2 may be 1.22 times higher than the Re for JN.1.

Whenever new variants emerge, the big question is whether they will be able to evade the existing protection that you may have from vaccination or previous Covid-19 infections. Well, the two mutations in the FLiRT variants do affect important locations in the spike proteinnamely where antibodies against the virus typically bind. Nevertheless, so far, theres no indication that vaccination will not be effective against the FLiRT variants. Butand this is big but, one cannot liemore data are needed to determine how effective vaccination will be against the FLiRT variants.

Covid-19 is less of a concern now than it was in the earlier days of the pandemic. Your immune system is probably more used to the spike protein and the virus now. You are likely less likely to get hospitalized and suffer more severe consequences when infected with SARS-CoV-2. But the risks of more severe outcomes are still there. There is still a significant chance of suffering long Covid. Therefore, it is a good idea to maintain appropriate precautions such as making sure that indoor locations are well-ventilated and wearing a face mask when you may come into close sustained contact with others who may be infected. And a summer surge does increase the latter possibility.

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Summer 2024 Covid-19 Surge Occurring With FLiRT Variants Taking Over - Forbes

New study highlights impact of sleep disturbances on COVID-19 and long COVID – News-Medical.Net

July 11, 2024

In a recent study published in eClinicalMedicine, researchers examined the influence of pre-existing sleep disturbances on coronavirus disease 2019 (COVID-19) susceptibility, severity, and long-term effects.

The study found that pre-existing sleep disturbances elevated the risk of susceptibility to COVID-19, as well as hospitalization, mortality, and long COVID, with age and sex playing a role.

Study:Pre-existing sleep disturbances and risk of COVID-19: a meta-analysis. Image Credit:PeopleImages.com - Yuri A/Shutterstock.com

The COVID-19 pandemic has caused significant global morbidity and mortality, with long COVID emerging as a major concern, affecting at least 65 million people worldwide.

Long COVID encompasses a range of symptoms and new-onset diseases, posing ongoing health and economic burdens. Sleep disturbances, such as insomnia and obstructive sleep apnea (OSA), were prevalent during the pandemic, affecting 40.49% of the global population. These disturbances are known to be linked to immune deficiency and inflammation, exacerbating the impact of COVID-19.

While previous studies have shown that OSA increases the severity and mortality of COVID-19, other sleep disturbances and their role in long COVID remain less explored.

Conflicting evidence exists regarding the relationship between sleep disturbances and long COVID, with some studies indicating a positive association between conditions like OSA and insomnia, while others find no significant link.

Comprehensive research is needed to understand these connections and effectively address long COVID. Therefore, researchers in the present meta-analysis aimed to examine the effect of pre-existing sleep disturbances on COVID-19 outcomes.

A total of 48 relevant observational studies with 8,664,026 participants were included from databases including Web of Science, PubMed, and Embase. The studies investigated COVID-19 susceptibility (22), hospitalization (12), mortality (16), and long COVID (11).

Case reports, brief communications, letters, reviews, and preprints were excluded. Most studies were conducted in the United States of America, and up to 72% of the participants were male. The studies focused on four sleep disturbances: OSA, insomnia, abnormal sleep duration, and night-shift work.

Two researchers extracted and assessed data. They collected basic information (author, year, study design, region, sample size, age, gender), types of sleep disturbances, and COVID-19 outcomes.

Odds ratios (ORs) were calculated from available data or other ratios if necessary. Quality was evaluated using the Agency for Healthcare Research and Quality for cross-sectional studies and the NewcastleOttawa Scale for cohort/case-control studies.

Statistical methods included pooled ORs, heterogeneity assessment, subgroup analysis, sensitivity analyses, Egger's test, and the trim-and-fill method for publication bias evaluation.

Participants with pre-existing sleep disturbances were more susceptible to COVID-19 (OR = 1.12). Specific disturbances like OSA, abnormal sleep duration, and night shift work also increased COVID-19 occurrence.

Higher susceptibility was found in low- and middle-income countries compared to high-income countries and in studies with unadjusted ORs. Younger individuals with sleep disturbances showed increased susceptibility (OR = 1.20), while older individuals did not.

Further, patients with pre-existing sleep disturbances had a higher risk of COVID-19 hospitalization (OR = 1.25), with all sleep disturbances except insomnia contributing to this increased risk. The association was stronger in patients younger than 60 years.

Pre-existing sleep disturbances were also found to increase COVID-19 mortality (OR = 1.45), mainly due to OSA. This risk was higher in older patients and males. Diabetes was found to be a significant source of heterogeneity, with a stronger association between sleep disturbances and COVID-19 mortality in diabetic patients as compared to the general population.

Moreover, pre-existing sleep disturbances significantly increased the risk of developing long COVID (OR = 1.36). The association was stronger for long COVID defined as symptoms lasting 3 months compared to 1 month.

Subgroup analysis confirmed that OSA increased long COVID risk in both definitions (3-month: OR = 1.75, 1-month: OR = 1.12). Therefore, OSA may be a potential risk factor for long COVID, but further research is warranted to confirm these findings.

Asymmetric funnel plots indicated potential publication bias for COVID-19 susceptibility, hospitalization, and mortality studies. Subgroup and sensitivity analyses aligned with the main findings, confirming the robustness of the study.

The study highlights the importance of addressing sleep disturbances in COVID-19 management and prevention strategies. It is the first meta-analysis to investigate the impact of all sleep disturbances (not only OSA) on the total clinical course of COVID-19. However, the study is limited by high heterogeneity among outcomes, the observational nature of all included studies, and the inability to confirm causal relationships.

In conclusion, sleep disturbances, particularly OSA, significantly heightened the risks of COVID-19 susceptibility, hospitalization, death, and long COVID, with these effects influenced by age and gender.

Therefore, the study urges healthcare professionals to conduct early examinations and timely intervention for patients with sleep disturbances to alleviate the immediate and long-term impact of COVID-19.

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New study highlights impact of sleep disturbances on COVID-19 and long COVID - News-Medical.Net

COVID-19 cases slightly up, but new vaccine is on the way – Spectrum News

July 11, 2024

RALEIGH, N.C. New vaccines are on the horizon in North Carolina, just as COVID-19 cases are slightly up and schoolhouse doors are getting ready to reopen.

COVID-19 isnt getting more dangerous. Its getting more catchy, which makes sense, said Dr. David Wohl, an infectious disease physician with the UNC medical system.

However, the consequences of catching the virus are not the same as they were at the beginning of the pandemic.

For ... most of us, catching COVID-19 doesnt mean that we are going to end up on oxygen or a ventilator, Wohl said.

A Centers for Disease Control and Prevention-contracted wastewater testing site for Swain and Jackson counties revealed percentiles of COVID-19 ranging from 80-100% in the last two weeks.

Masking, handwashing and social distancing are all still regarded as great tools to stay well, but better indoor ventilation for cleaner air circulations is more of an emphasis, Wohl also said.

COVID-19 is not as deadly as it once was, because most people are immunized, either through infection or a vaccine, but the virus itself is equally, if not more transmissible, Wohl explained.

And there will be updated shots very soon that will target the variants circulating now, he said.

Wohl added this is good timing with year-round schools coming back from their shorter summer break.

How the virus is tracked in North Carolina is changing shape too and shifting away from state-run dashboards. Wohl said wastewater monitoring still provides a great tool for following how the virus may be changing.

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COVID-19 cases slightly up, but new vaccine is on the way - Spectrum News

Second gentleman Doug Emhoff tests positive for COVID. Vice President Harris has tested negative – ABC News

July 11, 2024

Second Gentleman Doug Emhoff has tested positive for COVID-19 after experiencing mild symptoms, his office announced Sunday, but his wife, Vice President Kamala Harris, has tested negative and remains asymptomatic

July 7, 2024, 2:25 PM ET

1 min read

WASHINGTON -- Second Gentleman Doug Emhoff has tested positive for COVID-19 after experiencing mild symptoms, his office announced Sunday, but his wife, Vice President Kamala Harris, has tested negative and remains asymptomatic.

Emhoff spokesperson Liza Acevedo said in a statement that the second gentleman is fully vaccinated and three times boosted and that he is currently asymptomatic, continuing to work remotely, and remaining away from others at home.

Acevedo said Harris was tested for COVID on Saturday out of an abundance of caution and the result was negative. She is scheduled to campaign in Las Vegas for President Joe Biden 's reelection on Tuesday.

Emhoff previously tested positive for COVID in March of 2022, and Harris tested positive for the virus the following month.

Biden tested positive for COVID in July of 2022, then tested positive again slightly more than three days after he was cleared to exit coronavirus isolation in a rare case of rebound following treatment with an anti-viral drug.

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Second gentleman Doug Emhoff tests positive for COVID. Vice President Harris has tested negative - ABC News

Complex patterns of multimorbidity associated with severe COVID-19 and long COVID – Nature.com

July 11, 2024

Here, we systematically investigate the risk conferred by the presence and potential causal relevance of 1448 diseases for COVID-19 severity (hospitalisation, severe respiratory failure, and death) and Long COVID (Fig.1), based on medical disorder concepts14,16 defined and collated from >12 million medical records from primary (general practice), secondary care (hospital admissions), and disease registry (cancer registry), death certificates, and patient-reported conditions among 502,460 UKB participants (Fig.1 and Supplementary Data1). Incorporating primary care data more than doubled case numbers for more than half (n=817; 56.4%) of the diseases we considered (Supplementary Data1).

Scheme of the study design and analysis done, illustrating our workflow to define disease mechanisms that may causally contribute to severe COVID-19 or Long COVID. SNPs Single nucleotide polymorphisms; SPA = saddle point approximation; MAF = minor allele frequency; *COVID-19 HGI=COVID-19 Host Genetic Initiative, but excluding contributions from UK Biobank

We identified 1128 significant (p<1.1105) disease COVID-19 outcome associations, including almost half (n=679) of the diseases considered with at least one of the four COVID-19 outcomes derived (Fig.2 and Supplementary Data2). Pre-existing diseases were almost exclusively associated with a higher risk for COVID-19 endpoints (median hazard ratio (HR): 2.39, range: 0.5917.3), only two diseases (benign neoplasm of skin and varicella infection) were associated with a decreased risk. Associated diseases spanned almost all chapters of the ICD-10 (17 out of 18) but were consistently enriched in the chapters respiratory (odds ratio [OR]: 5.96; p-value: 2.7x108), circulatory (OR: 2.95; p-value: 3.5x107), and endocrine/metabolic diseases (OR: 2.76; p-value: 9.1104) when associated with severe COVID-19. In contrast, pre-existing disease-codes classified as symptoms were more than 13-fold enriched among diseases associated with an increased risk for Long COVID (OR: 13.2; p-value: 3.6x108) but also hospitalisation (OR: 5.53; p-value: 9.9x105) and death (OR: 3.06; p-value: 7.3x103).

Each panel contains association statistics, p-values (triangles), from Cox-proportional hazard models (two-sided) testing for an association between the disease on the x-axis and three different COVID-19 outcomes, as well as Long COVID. Disease associations passing the multiple testing correction (dotted line, p<1.1105) are depicted by larger triangles of which facing up ones indicate positive, e.g., increased disease risk, associations and downward facing vice versa. The diseases are ordered by ICD-10 chapters (colours) and the top ten for each endpoint annotated. Underlying sample numbers and statistics can be found in Supplementary Data1 and 2.

For COVID-19 requiring hospitalisation, we replicated and refined known associations with serious pre-existing diseases that have been previously used to identify clinically extremely vulnerable people. This included respiratory diseases like pseudomonal pneumonia (HR: 7.53, 95%-CI: 4.7411.97; p-value<1.2x1017), acute renal failure (HR: 4.02, 95%-CI: 3.744.32, p-value: <10300) or type 2 diabetes with renal complications (HR: 7.44; 95%-CI: 5.679.76; p-value: 1.5x1047), as well as immune deficiencies (e.g., deficiency of humoral immunity HR: 6.02; 95%-CI: 4.368.31; p-value: 1.3x1027) or patients under immune suppression (e.g., liver transplants HR: 7.25 95%-CI: 4.5111.68, p-value: 3.4x1016). However, we further observed strong associations with so far less recognized pre-existing mental health and psychiatric diseases and conditions with effect sizes comparable to those previously considered to identify extremely vulnerable people. This included symptoms of malaise and fatigue (HR: 2.17, 95%-CI: 2.072.27, p-value: 4.4x10222) or suicide attempts (HR 5.33, 95%-CI: 4.456.39, p-value: 3.6x1073). Most diseases (n=641, 95.5%, phetero>103) associated with similar magnitude across all three different definitions of COVID-19 severity, with different forms of dementias (phetero<2.1x1024) being among the few exceptions, associating with hospitalisation (HR: 3.83; 95%-CI: 3.384.34; p-value: 2.3x1097) and death (HR: 10.82; 95%-CI: 9.1512.80; p-value: 1.4x10170), but not severe respiratory failure (HR: 1.15; 95%-CI: 0.512.57; p-value: 0.74) due to COVID-19.

In contrast, pre-existing diseases associated with an increased risk for Long COVID only partially overlapped with those increasing the risk for severe COVID-19. Most notably, we replicated associations with anxiety disorders28 (HR: 2.59; 95%-CI: 2.093.20; p-value:1.8x1018) and other mental health symptoms, but most prominently with symptoms of malaise and fatigue (HR: 2.78; 95%-CI: 2.293.37; p-value:1.5x1025) that are hallmarks of Long COVID and were also strongly associated with severe COVID-19.

Almost all significant associations (99.8%, n=1126) were consistent when considering all-cause death as a competing event (Supplementary Data3), and more than half (63.6%; n=718) remained statistically significant (p<4.4x105) when accounting for a large set of potential confounders in multivariable Cox-models (Supplementary Data3). This suggests that potentially unreported associations, such as the increased risk for severe COVID-19 among patients reporting symptoms of malaise and fatigue (adjusted HR: 1.66, 95%-CI: 1.58 - 1.74, p-value=7.3x1092), are not just a reflection of a general disease burden or other chronic diseases associated with a greater risk for severe COVID-19.

We observed limited evidence for effect modifications by sex (n=7), non-European ancestry (n=1), or age (n=8), but not social deprivation, with 16 disease COVID 19 pairings showing evidence of significant differences (Supplementary Data4; p<3.6x106). All included stronger effects in women compared to men, e.g., gout for hospitalised COVID-19 (women: HR: 2.56, 95%-CI 2.212.96, p-value: 1.3x1036; men: HR: 1.46, 95%-CI: 1.341.58, p-value: 2.1x1019), among Europeans reporting vitamin D deficiencies (Europeans: HR: 2.31, 95%-CI: 2.132.51, p-value: 2.1x1087; non-Europeans: HR: 1.31, 95%-CI: 1.081.60, p-value=5.5x103), or among younger participants, e.g., disorders of magnesium metabolism and death with COVID-19 as a likely result of renal failure (age 65 years: HR: 42.98, 95%-CI: 20.1091.90, p-value: 3.0x1022; age >65 years: HR: 5.35, 95%-CI: 3.518.16, p-value: 5.9x1015).

We next derived a disease-disease network18 (Fig.3a) to understand, whether the large set of diseases associated with an increased risk for severe COVID-19 act independently or rather reflect an increased risk among participants suffering from multiple pre-existing conditions, i.e., multimorbidity. The network contained a total of 1381 diseases connected through 5212 edges based on non-random co-occurrence (Supplementary Data 5a, b). Diseases segregated into 31 communities being more strongly connected to each other compared to the rest of the network (Fig.3b, c).

a Disease disease network based on significant (p<4.8x108) positive partial correlations (two-sided). Nodes (diseases) are coloured by ICD-10 chapters and strength of partial correlation depicted by width of the edges. The underlying data can be found in Supplementary Data 5ac Same network, but only highlighting two disease communities strongly enriched for associations with severe COVID-19. d Hub score for the 30 diseases with highest values and associated association statistics, hazard ratios (rectangle) with 95%-confidence intervals (lines), from Cox-proportional hazard models (two-sided). Significant associations are indicated by filled boxes. Colours according to ICD-10 chapters. All underlying data can be found in Supplementary Data2 and 5b.

Two disease communities were consistently and strongly enriched for diseases associated with severe COVID-19. The first (e.g., OR: 5.20; p-value=2.2x1010; for severe respiratory failure) community was strongly enriched for circulatory (OR: 17.6; p-value: 4.4x1039) and respiratory (OR: 10.3; p-value: 7.8x1016) diseases, closely resembling the cardio-respiratory risk profile already described above (Fig.3b). The second community consisted of diverse endocrine (OR: 6.19; p-value: 1.9x1013) and circulatory disease (OR: 3.75; p-value: 5.4x108), and largely reflected the renal-diabetic risk profile (Fig.3c). Accordingly, for each disease acquired during lifetime within the latter disease community, participants risk increased by 18% and 20% to be hospitalised (HR: 1.18; 95%-CI: 1.171.18; p-value: p<10300) or die with COVID-19 (HR: 1.20; 1.191.20; p-value<10300), respectively.

Diseases increasing the risk for severe COVID-19, but not Long COVID further significantly correlated with hub status (e.g., hospitalisation: r=0.59; p-value: 2.8x10124) in the disease-disease network (Fig.3d), that is, diseases that connect a large cluster of diseases to the rest of the network and might hence be considered as multimorbidity hotspots. For example, acute renal failure, strongly associated with severe COVID-19 (Fig.3d), showed strong partial correlations with 30 other diseases and patients are hence prone to complex multimorbidity. However, the imperfect correlation between hub status and disease-association profiles indicates that certain forms of multimorbidity, such those related to secondary malignancies of lymph nodes, are possibly less related to severe COVID-19.

We next systematically characterised whether diseases identified to be associated with COVID-19 severity or Long COVID shared genetic similarity with host genetic susceptibility to severe COVID-19 to understand potential underlying causal mechanisms. We computed genetic correlation estimates for all 1128 disease COVID-19 outcome pairs and observed 75 pairs (6.6%) that showed evidence for significant (p<4.4x105) and directionally consistent genetic correlations (Fig.4 and Supplementary Data6), indicating a putatively causal link of any of 57 unique diseases on severe COVID-19. We did not observe evidence of convergence for Long COVID, which might likely be explained by the still low statistical power for the respective genome-wide association study13.

The first three panels show association statistics, hazard ratios (rectangle) and 95%-confidence interval (lines), for 57 diseases with evidence of convergence with genetic correlation analysis, that are shown in the last two panels (rectangle genetic correlation; lines 95%-confidence intervals). Disease have been grouped by ICD-10 chapters and coloured accordingly (see Figs.2 or 3 for legend). NOS = not elsewhere specified; All underlying data can be found in Supplementary Data1 (sample numbers), 2 and 6.

The diseases with consistent evidence from survival and genetic analysis included well-described risk-increasing effects of pre-existing endocrine (e.g., type 2 diabetes), respiratory (e.g., respiratory failure), or renal (e.g., chronic kidney disease) diseases, but also digestive (e.g., gastritis and duodenitis), or musculoskeletal (e.g., rheumatoid arthritis) diseases, and further symptoms of malaise and fatigue (rG=0.26; p-value=4.7106) and abdominal pain (rG=0.33; p=2.51011), as well as adverse reactions to drugs (e.g., poisoning by antibiotics: rG=0.38; p-value=2.2x106). Findings that collectively demonstrated the need for a comprehensive assessment of disease-risk beyond few, selected common chronic conditions.

Among the 41 diseases for which we had sufficient genetic instruments to perform more stringent Mendelian randomization (MR) analyses to assess causality, we observed only nominally significant (p<0.05) evidence for gout and hospitalisation (OR: 1.03; 95%-CI: 1.011.05, p-value: 0.03), as well as arthropathy not elsewhere specified (OR: 1.28; 95%-CI: 1.061.55; p-value: 0.02) and unspecified monoarthrtitis (OR: 1.21; 95%-CI: 1.041.41; p-value: 0.02) for severe COVID-19 (Supplementary Data7). While we might have been still underpowered for many diseases, this leaves the possibility that convergence of survival and genetic correlation analysis might, in part, be explained by shared risk factors.

To finally understand possible molecular mechanisms linking the diseasome to COVID-19, we systematically profiled disease associations across 49 independent genomic regions linked to COVID-19 or Long COVID. We observed strong and robust evidence of a genetic signal shared between severe COVID-19 and a total of 33 diseases at nine loci (posterior probability (PP)>80%) (Fig.5a and Supplementary Data8). Apart from known pleiotropic loci, such as ABO and FUT2 coding for blood group types, this included respiratory risk loci, albeit with contradicting effect estimates for three loci (Fig.5b). While COVID-19 risk increasing alleles at LZTFL1 and TRIM4 were consistently associated with a higher risk for viral pneumonia and post-inflammatory pulmonary fibrosis, respectively, risk-increasing alleles at MUC5B, NPNT, and PSMD3 were inversely associated with post-inflammatory pulmonary fibrosis and asthma. An observation that extended even beyond shared loci (Fig.5c) illustrating a general trend of phenotypic divergence of genetic effects on diseases that share pathological features with severe COVID-19.

a Network representation of significant (PP>80%) colocalization results. Loci are depicted as white rectangles and diseases as coloured nodes according to ICD-10 chapters. Edges represent strong evidence for colocalization, and solid lines indicate a risk-increasing effect of the COVID-19 risk increasing allele, whereas dashed lines indicate protective effects. Underlying data can be found in Supplementary Data8. b Forest plot displaying hazard ratios (rectangle) with 95%-confidence intervals (lines) for each variant and different COVID-19 and colocalising disease outcomes. Effect estimates for COVID-19 have been obtained from the COVID-19 Host Genetic Initiative and effect estimates for diseases in the present study. All estimates are derived from logistic regression models. c Heatmap of effect estimates across 49 independent genetic loci associated with increased risk for sever COVID-19 and corresponding effects on six selected traits that showed evidence of colocalization at least one other locus. Black rectangles indicate genome-wide significant effects (p<5108). NOS not elsewhere specified; All underlying data can be found in Supplementary Data1 and 8 or is given in the data availability statement.

A notable observation was the TYK2 locus that has previously been suggested to indicate the efficacy of successfully repurposed drugs for severe COVID-1929. Briefly, TYK2 encodes for tyrosine kinase 2 (TYK2) a protein partially targeted by Janus kinase (JAK) inhibitors like baricitinib, that have been approved for rheumatoid arthritis and successfully repurposed for severe COVID-19, although predating possible evidence from genetic studies30,31,32. Accordingly, we observed that the same genetic variant, rs34536443 (PP=99.8%), associated with the risk for severe COVID-19 was also associated with, amongst others, the risk of rheumatoid arthritis, but in opposing effect directions (Fig.5b). Rs34536443 is a loss-of-function missense variant (p.Pro1104Ala) for TYK2 and the functionally impairing minor C allele was associated with a 50% increased risk for severe COVID-19 (odds ratio: 1.50; 95%-CI: 1.40 1.62, p-value= 4.3x1029) but a 23% reduced risk for rheumatoid arthritis (odds ratio: 0.77; 95%-CI: 0.720.83; p-value=2.4x1012) as well as other autoimmune diseases, in particular psoriasis (Supplementary Data8). While the discrepancy between the success of the drug and genetic inference might be explained by the rather weak affinity of baricitinib for TYK233, patients undergoing trials with TYK2-inhibitors for psoriasis34 might be at an elevated risk for severe COVID-19. This observation seemingly aligns with studies on Tyk2-/- mouse models reporting an impaired immune response to viral infections35.

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Complex patterns of multimorbidity associated with severe COVID-19 and long COVID - Nature.com

Health officials warn of new COVID variants, increased hospitalizations in New York – Spectrum News

July 11, 2024

COVID-19 hospitalizations are on the rise in New York, and health officials are reminding everyone to continue following precautions to stay safe.

Eden Di Bianco just got over having COVID-19 for a third time. It came as a surprise after being very cautious due to being immunocompromised.

I tested positive on a home test when I started to feel some symptoms, but it was definitely a way rougher go than my second bout, Di Bianco said.

While the rest of her family stayed healthy, Di Bianco said she believes she was exposed to the disease at a baseball game they attended, keeping her bedridden for eight days.

It started with a headache and a sore throat, and Im hearing from a lot of other friends who've had it recently that the sore throat was really killer, and that was definitely my experience as well," Di Bianco said. "I had really intense sweats for about three days. I lost five pounds in a week. I had nausea, congestion, sneezing, which I have not had before, and just a general full body ache like someone threw me down a flight of stairs."

Di Bianco isnt sure which strain of COVID she may have had, but health expertssaynew strains of omicron, called the FLiRT variants, are spreading.

There's a surge that we knew would be coming, and we can't forget that this is kind of a cyclical thing that has been happening for the past few years, so we need to be prepared, said Neal Smoller, holistic pharmacist and owner of Village Apothecary.

Smoller said hes sold 30 times thenumberof COVID-19 tests in the past week than the one prior.

For the people that want to, again, be vigilant, to make sure that they are doing the best things wellness-wise for themselves. They are practicing all of the things that we've talked about since this started in 2020. Handwashing, social distancing, don't go into big crowds if you're nervous, wear masks and of course, get vaccinated as soon as you're eligible, Smoller said.

According to Gov. Kathy Hochuls office, COVID-19 hospitalization rates in New York are higher than this time last year but below what was experienced at this time in 2022.

Ive never been one to say that you can't live your life," Smoller said. "We have to live alongside COVID. I think that you should know that if you're going to get in an airplane, you run the risk of catching COVID. So, you might want to put a mask on, especially it's surging right now. But I don't think that that should deter anybody from their summer plans at all. I just think that you just need to be a little bit more cautious when you're out and about."

Di Bianco said her family plans on using caution throughout the rest of the summer with mostly outdoor activities planned.

Summer is actually a little bit more of a freeform time because we can enjoy being outdoors more, Di Bianco said.

Although Smoller said a new vaccine will be available in the fall, he said its still worth getting a booster now if those eligible havenot yetreceived one.

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Health officials warn of new COVID variants, increased hospitalizations in New York - Spectrum News

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