Great Britain Olympic swimmer Adam Peaty tested positive for COVID-19 on Monday, less than 24 hours after he won the silver medal in the mens 100-m breaststroke.
Peaty, 29, began feeling unwell before the final on Sunday, Team Great Britain said in a statement. In the hours after the race, his symptoms worsened, and he tested positive for COVID-19 early on Monday morning.
He is hopeful to be back in competition for the relay events later in the swimming programme, Team Great Britain said. As in any case of illness, the situation is being managed appropriately, with all usual precautions being taken to keep the wider delegation healthy.
Peaty confirmed his COVID-19 diagnosis in an Instagram post on Monday. Ill now be focusing on a fast, full recovery to give my best in the team relays later in the week, Peaty wrote in the caption of the post.
The mixed 4x100-m medley relay final is set to take place on Aug. 3, and the mens 4x100-m medley relay final will be held on Aug. 4. Peaty previously competed in the Tokyo and Rio de Janeiro Olympics.
Team Great Britain declined to specify what precautions Peaty and the team were taking or what treatment, if any, Peaty was receiving.
The Paris Games have significantly less stringent COVID-19 restrictions compared to the Tokyo Games in 2021; there are no mask mandates or isolation periods. The International Olympic Committee (IOC) did not respond to a request for comment about its guidelines or Peatys positive test. When five players on the Australian womens water polo team tested positive for the virus last week, the countrys Olympic team chief told Le Monde that affected players would be cleared for practice when they feel well enough to train, adding that affected athletes would be wearing masks and isolating from other team members outside of training.
Read More: Leon Marchands First Olympic Gold Will Only Fuel Michael Phelps Comparisons
Peaty shared a step on the podium with Team USA swimmer Nic Fink on Sunday night, after the two athletes tied for silver in the mens 100-m breaststroke.
Video footage also showed Peaty kissing Italian swimmer Nicolo Martinenghi, who won the gold medal for the race on Sunday, on the cheek that same night.
People who test positive for COVID-19 can continue to test positive for the virus for days or even weeks after, according to the U.S. Centers for Disease Control and Prevention.
Data sources and study cohorts
UK Biobank is a large-scale population-based prospective cohort study with deep phenotyping and genomic data, as detailed elsewhere51. Briefly, between 2006 and 2010, over 500,000 individuals aged 4069 years were recruited from 22 assessment centers across the United Kingdom at baseline, with collection of socio-demographic, lifestyle and health-related factors, a range of physical measures, and blood samples51. Follow-up information is obtained by linking health and medical records, including national primary and secondary care, disease and mortality registries52, with validated reliability, accuracy and completeness53. To identify cases of SARS-CoV-2 infection, polymerase chain reaction (PCR)-based test results were obtained by linking all participants to the Public Health Englands Second Generation Surveillance System, with dates of specimen collection and healthcare settings of testing54. Outbreak dynamics were validated to be broadly similar between UK Biobank participants and the general population of England54.
In this study, we included participants who were alive by March 1, 2020 and had a positive SARS-CoV-2 PCR test result between March 1, 2020 (date of the first recorded case in the UK Biobank), and March 1, 2022, with the date of first infection considered as index date (T0). For those diagnosed with COVID-19 in hospital, we defined T0 as the date of hospital admission minus a random number of 7 days. The major prevalent variants during the study period included wildtype, Alpha (B.1.1.7), Delta (B.1.617.2), and Omicron (B.1.1.529 BA.1). The calendar periods of dominant variants in the UK were based on pandemic data from the Office for National Statistics26. Participants with missing data on study exposures at baseline were excluded. We addressed missing data on covariates using the following approaches: (1) participants with missing values in age and sex (<0.1%) were excluded. (2) participants with missing values in ethnicity were classified as other ethnic groups. (3) participants with missing values in education level (0.9%) were classified as category I, which includes none of the above and prefer not to answer. (4) missing values in IMD (13.8%) were imputed with the mean value of the entire UK Biobank cohort. All participants included in this study provided written informed consent at recruitment. This study followed the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) reporting guidelines and received ethical approval from the UKBB ethics advisory committee. Study design, cohort construction, and timeline are provided in Supplementary Fig.1. All participants provided written informed consent at the UK Biobank cohort recruitment. This study received ethical approval from UK Biobank Ethics Advisory Committee (EAC) and was performed under the application of 65397.
Ten prespecified potentially modifiable lifestyle factors were assessed, including smoking, alcohol consumption, body mass index (BMI), physical activity, sedentary time, sleep duration, intake of fruit and vegetable, intake of oily fish, intake of red meat, and intake of processed meat. Selection and categorization of lifestyle factors was based on literature review, previous knowledge, and UK national health service guidelines55,56. Multiple lifestyle factors were measured by validated questionnaire for all participants at baseline recruitment. Detailed definitions on measurement and classification of lifestyle factors are provided in Supplementary Table1. Briefly, healthy lifestyle components including past or never smoker, moderate alcohol intake (4 times week), BMI<30kg/m2, at least 150min of moderate or 75min of vigorous physical activity per week, less sedentary time (<4h per day), healthy sleep duration (79h per day), adequate intake of fruit and vegetables (400g/day), adequate oily fish intake (1 portion/week), moderate intake of red meat (4 portion week) and processed meat (4 portion week) were defined, in accordance with previous evidence or UK national health service guidelines55,56.
A binary variable was created for each of the 10 factors, with 1 point assigned for those meeting the healthy criteria and 0 otherwise. A composite lifestyle score was then calculated for each participant by summing the total number of healthy lifestyle factors, ranging from 0 to 10. Based on the composite score, participants were classified into three lifestyle categories: unfavorable (05), intermediate (67), and favorable (810). The lifestyle score was also used as a continuous variable of number of healthy lifestyle factors. Similar methods of defining lifestyle score have been used in the same UK Biobank cohort57 as well as external cohorts16,28. Distributions of lifestyle score and categories are provided in Supplementary Table2.
The median [IQR] duration between baseline assessment of lifestyle factors and the date of infection was 12.5 [11.813.3] years. Part of participants took part in up to two further touchscreen interviews with lifestyle and health-related factors similarly measured. There were generally stable responses to lifestyle factors between baseline assessment and the latest repeat assessment (median time difference from baseline, 8 years) as shown in Supplementary Fig.2. 34.9% of participants with an unfavorable lifestyle, 48.6% with an intermediate lifestyle, and 73.7% with a favorable lifestyle at baseline remained in the same corresponding lifestyle category at the latest repeat assessment following a median of 8 years. Overall, the proportion of stable lifestyle categories is 60.6%.
The outcomes after COVID-19 were prespecified, including a set of multisystem sequelae, death, and hospital admission following the SARS-CoV-2 infection. The multisystem sequelae were selected and defined based on previous evidence of the long COVID, including 75 systemic diseases or symptoms in 10 organ systems: cardiovascular46, coagulation and hematologic46, metabolic and endocrine44, gastrointestinal48, kidney43, mental health45, musculoskeletal47, neurologic47, and respiratory disorders10,13,14, and general symptoms of fatigue and malaise3,4,42,49. Detailed definitions of multisystem sequelae are listed in the Supplementary Table3. Outcomes were identified as follows: individual sequela from the hospital inpatient ICD-10 (International Classification of Diseases 10th Revision) diagnosis codes, deaths from the records of national death registry, and hospital admission from hospital inpatient data from the Hospital Episode Statistics. Incident outcomes were assessed in participants with no history of the related outcome within one year before the date of the first infection.
As SARS-CoV-2 infection has been associated with both multisystem manifestations during its acute phase and with sequelae during its post-acute phase7,49, we conducted analyses stratified by phase of infection. We reported risk of each outcome during the acute phase (T0 to T0+30d), post-acute phase (T0+30d to T0+210d), and overall period following infection (T0 to T0+210d) to reflect the full spectrum of post-COVID conditions. The end of follow-up for the overall cohort was September 30, 2022, with the maximum follow-up period censored to 210 days.
We prespecified a list of covariates for adjustment or stratification based on literature review and prior knowledge: socio-demographic characteristics including age, sex, education level (mapped to the international standard for classification of education), index of multiple deprivation (IMD, a summary measure of crime, education, employment, health, housing, income, and living environment)58, and race and ethnicity; and infection related factors including healthcare settings of the testing (community/outpatient vs inpatient setting as proxy of severity of infection), COVID-19 vaccination status, and SARS-CoV-2 variants.
Baseline characteristics of the overall cohort of participants with SARS-CoV-2 infection and by composite healthy lifestyle categories were reported as mean and standard deviation or frequency and percentage, when appropriate. Multivariable cox proportional hazard (PH) model was used to assess the association between composite healthy lifestyle and risk of multisystem sequelae (composite or by organ systems), death, and hospital admission, with adjustment for age, sex, ethnicity, education level, and IMD. PH assumption across lifestyle categories was tested by Schoenfeld residuals with no violations observed for outcomes. Hazard ratio (HR) and absolute risk reduction (ARR, difference in incidence rate between lifestyle groups per 100 persons during the corresponding follow-up period) were estimated from the Cox model. We also assessed the association between individual lifestyle factor instead of composite categories (each component as a categorical variable with or without mutual adjustment for others, or the number of factors as continuous variables) and risk of outcomes.
We conducted causal mediation analysis59,60 to quantify the extent to which the habitual healthy lifestyle may affect COVID-19 sequelae through the potential pathway of relevant pre-infection medical conditions (mediator), with the proportion of direct and indirect effects estimated by quasi-Bayesian Monte Carlo methods with 1000 simulations for each. Detailed modeling procedures and a directed acyclic graph are provided in Supplementary Methods.
We examined the association between composite healthy lifestyle and the overall risk of multisystem sequelae in prespecified clinical subgroups by demographic and infection-related factors. The demographic factors included age (65 and >65 years), sex (male and female), and ethnicity (White and other ethnic groups). As the risk profile of COVID sequelae was related to vaccination and severity of infection, and may change with the evolving pandemic, infection-related factors including vaccine status (no or one-dose partial vaccination and two-dose full vaccination), test setting (inpatient and outpatient or community), dominant variants during the study period (wildtype, Alpha, Delta, and Omicron BA.1) were assessed. Multiplicative interactions between the composite healthy lifestyle and the stratification variables were tested, with P-value reported.
We conducted multiple sensitivity analyses to assess the robustness of primary findings. First, to reflect the multisystem and potentially comorbid nature of COVID sequelae, accounting for both the number of sequelae by an individual and the relative health impact of each sequela. Weights based on Global Burden of Disease study data and methodologies for general diseases and long COVID were assigned to each sequela (Supplementary Table1)61,62. The weighted score was calculated for each participant by summing the weights of all incident sequelae during the follow-up period. Zero inflated Poisson regression was then used to calculate relative risk (RR), with follow-up time set as the offset of the model and adjustment for covariates. Second, to further account for potential reverse causality and more accurately define incident cases, extending the washout period for outcomes from one year to two years. Third, defining events of post-acute sequelae 90 days after infection (follow-up period T0+90d to T0+210d), instead of 30 days in the main analyses. The adjustment was made as there is no uniform definition for long COVID, which is currently described as conditions occurring 3090 days after infection in existing guidelines27. Fourth, restricting the identification of outcomes to the first three ICD diagnoses, which are the main causes for each hospital admission. Fifth, reconstructing a composite lifestyle index without BMI and assessed its association with outcomes. Finally, we conducted quantitative sensitivity analysis to adjust for changes in lifestyle factors over time since the baseline assessment. We used odds ratios to quantify associations and assumed a sensitivity and specificity of 90% for each lifestyle component (Supplementary Methods).
As a healthy lifestyle is associated with a lower risk of chronic diseases and mortality among the general population predated pandemic, we conduct exploratory analysis to compare the effects of healthy lifestyle on adverse outcomes following COVID-19 with the effects among participants without infection. A random index date was assigned to the participants without infection based on the distribution of T0 among those with infection, and we repeated the main analyses with the maximum follow-up period censored to 210 days.
Statistical significance was determined by a 95% confidence interval (CI) that excluded 1 for ratios and 0 for rate differences. All analyses and data visualizations were conducted using R statistical software (version 4.2.2).
Further information on research design is available in theNature Portfolio Reporting Summary linked to this article.
Diabetes is a chronic disease affecting hundreds of millions worldwide and has multiple risk factors. The more the risk factors present, the higher the likelihood of developing diabetes. Understanding these factors is essential for prevention. A new study published inThe Lancet Diabetes and Endocrinologydescribes a link between COVID-19 and diabetes.
From databases of tens of millions of people in England registered with their general practitioners, researchers examined the risk of developing diabetes following COVID-19. They found a four-fold increase in risk during the first month post-infection. The risk remained elevated in two-thirds of these individuals in the second year.
Early indications came in 2020 when doctors across the world noted a surprisingly high occurrence of diabetes in previously healthy individuals following a diagnosis of COVID-19. Some required high doses of insulin. A paper published in theJournal of Family Medicine and Primary Carein October 2022 from Telangana reported similar findings.
However, observations based on small numbers of patients are not always definitive. For instance, steroid use for COVID-19 raises blood sugar levels on its own. Besides, in any population, diabetes exists undetected in a significant proportion of individuals. This might have been unearthed only because of the medical attention they received after contracting COVID. A reverse causality has also been implicated, with people with diabetes being at greater risk for severe COVID-19. It was also unclear whether the rise in blood sugars would settle down after the immediate stress of COVID passed. Thus, the link remained a matter of debate, necessitating larger studies over an extended period of time.
The new study also examined health records from before and after the vaccine rollout, enabling researchers to investigate the impact of vaccination on diabetes risk. With a follow-up period exceeding a year, they could assess the persistence of newly diagnosed diabetes. Since the study relied on well-maintained databases from before the pandemic, the findings are unlikely to be due to increased testing alone. The persistence of diabetes into the second year indicates that steroid use alone was not responsible.
Two key observations linked the severity of COVID-19 to an increased risk of diabetes. Firstly, the risk was significantly higher among hospitalised patients. Secondly, vaccinated individuals, who experienced less severe COVID-19, had a lower risk of developing diabetes.
When comparing vaccinated and unvaccinated populations, it is important to address demographic differences. For instance, unvaccinated people in England tended to be younger, healthier, and more likely to be of South Asian or Black ethnicity. Although South Asians have a higher baseline risk of diabetes, younger age lowers the overall risk in a population. To ensure accurate conclusions, the researchers adjusted for these factors, eliminating any inaccuracies from comparing unequal populations.
The increased diabetes risk following COVID-19 is believed to involve at least two mechanisms. The receptors used by the virus to attach and enter human cells are also found in the insulin-producing beta cells in the pancreas. Therefore it is possible the virus might have damaged these cells. Additionally, the widespread inflammation caused by COVID-19 leads to insulin resistance. Besides adding to the body of evidence connecting chronic diseases and viral infections, the study enhances our understanding of the various mechanisms involved in the development of diabetes. In summary, COVID-19 has increased the burden of chronic diseases among survivors in several ways, with diabetes being one of them.
(RajeevJayadevanisco-chairmanof the National IMA COVID task Force)
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Sydney, Australia:
Covid-19 is still driving Australia's above-average mortality rate, research showed on Monday, with experts predicting the disease's impact will continue to be felt for years to come.
The Australian Actuaries Institute found that five per cent more people died than would be expected in 2023, amounting to 8,400 excess deaths.
Experts measured the number of people who had died as a direct or indirect result of Covid and found the excess mortality rate was still higher than pre-pandemic levels.
About 4,600 deaths were directly attributed to Covid-19, the ninth leading cause of death last year.
Non-Covid-19 excess deaths, meanwhile, were "particularly apparent" in Australians over 75 years old -- with previous infections and interruptions in healthcare related to Covid increasing risks related to heart disease, stroke, diabetes and dementia.
Delays in routine or emergency care and undiagnosed Covid-19 were cited as possible reasons for the higher-than-usual death rate.
Still, the excess mortality rate was lower in 2023 than it was in 2022, according to experts.
"It's encouraging that each successive Covid-19 wave has, so far, resulted in fewer deaths than the previous one," Actuary Institute spokeswoman Karen Cutter said.
"However, we think that Covid-19 is likely to cause some excess mortality for several years to come, either as a direct cause of death or a contributing factor to other causes such as heart disease."
She added the "new normal" level of mortality was likely higher than it would be had the pandemic not occurred.
The report also found Australia's excess mortality was lower than the global average -- with Ecuador, Mexico and Russia showing the highest rates of unexplained deaths.
New Zealand had the lowest excess mortality rate of the 40 countries for which data was available.
(Except for the headline, this story has not been edited by NDTV staff and is published from a syndicated feed.)
Delhi Coaching Centre Deaths: Cops Send Notice To Civic Body
Researchers have just discovered a process in fruit flies which links inflammation with impaired motor function, providing researchers with a potential target for treating the persistent muscle fatigue that follows many infections.
Of long COVID's numerous symptoms, an intolerance to exertion could be considered one of the more debilitating.
"This is more than a lack of motivation to move because we don't feel well," says Washington University developmental biologist Aaron Johnson. "These processes reduce energy levels in skeletal muscle, decreasing the capacity to move and function normally."
With every new infection of the SARS-CoV-2 virus, our risk of experiencing long COVID increases. Almost 18 million adult Americans have now faced this lingering malaise and its exhausting physical symptoms.
Many of these symptoms are familiar, including the frustrating loss of energy that hits around half of all long COVID sufferers. Muscle fatigue is also present in other post-viral conditions, as well as in people suffering from neurodegenerative diseases like Alzheimer's and Parkinson's.
The thing all these conditions have in common is inflammation of our central nervous system. Chemical markers associated with brain injuries have also been identified in COVID patients.
So Washington University developmental biologist Shuo Yang and colleagues used animal models to explore how inflamed neurons can lead to malfunctioning muscles. They identified a signaling pathway between the brain cells and muscles in both flies and mice that leads that leads to a loss of muscle function.
"Flies and mice that had COVID-associated proteins in the brain showed reduced motor function the flies didn't climb as well as they should have, and the mice didn't run as well or as much as control mice," explains Johnson.
"We saw similar effects on muscle function when the brain was exposed to bacterial-associated proteins and the Alzheimer's protein amyloid beta. We also see evidence that this effect can become chronic. Even if an infection is cleared quickly, the reduced muscle performance remains many days longer in our experiments."
In humans, inflammation causes neurons to release the immune cytokine interleukin-6 (IL-6). The team found a comparable protein in their test animals traveled to their muscles via the bloodstream and activated a cellular program called JAK-STAT. JAK-STAT then turned down the amount of energy produced by the muscle tissues' mitochondria power plants.
"We're not sure why the brain produces a protein signal that is so damaging to muscle function across so many different disease categories," says Johnson.
"If we want to speculate about possible reasons this process has stayed with us over the course of human evolution, despite the damage it does, it could be a way for the brain to reallocate resources to itself as it fights off disease. We need more research to better understand this process and its consequences throughout the body.
Yang and team then used drugs to block this pathway in flies to confirm the process can be reversed, as has been shown in previous mouse studies. IL-6 inhibitors have already successfully been used to treat autoimmune diseases such as rheumatoid arthritis, and have shown promise in a few severe COVID-19 cases so far.
"It seems likely that the brain-muscle axis is activated by respiratory infections via the CSF [cerebrospinal fluid] and continues to signal long after the initial infection is cleared," the researchers write in their paper. "Long-COVID may therefore be caused by chronic cytokine signaling."
Some parts of this puzzle remain unclear, the researchers caution, like how SARS-CoV-2 gets into the central nervous system in humans to trigger this inflammation. But this new information could lead to some much needed relief for those suffering from a range of chronic conditions.
By altering chemicals secreted by our neurons, it is now clear how brain inflammation caused by many different conditions can have such a profound physical impact on our entire bodies.
This research is published in Science Immunology.
NANTERRE, France (AP) Less than 24 hours after claiming a swimming silver medal at the Paris Olympics, British star Adam Peaty tested positive for COVID-19.
The British Olympic committee announced Peatys condition on Monday, saying he first began feeling ill a day earlier ahead of the 100-meter breaststroke final.
The two-time defending Olympic champion in that event, Peaty just missed out on a third straight gold when he touched two-hundreds of a second behind the winner, Italys Nicolo Martinenghi. Peaty tied for the runner-up spot with American Nic Fink.
In the hours after the final, his symptoms became worse and he was tested for COVID early on Monday morning, Team GB said in a statement. He tested positive at that point.
The 29-year-old Peaty hopes to recover in time to take part in the relays, the statement said. The mixed 4x100 medley relay is set for Friday, while the mens 4x100 medley relay will be held Saturday and Sunday.
As in any case of illness, the situation is being managed appropriately, with all usual precautions being taken to keep the wider delegation healthy, Team GB said.
AP Summer Olympics: https://apnews.com/hub/2024-paris-olympic-games
Just hours after winning silver in the mens 100 breaststroke, Adam Peaty of Great Britain has tested positive for COVID-19, Team GB sent out in a statement Monday afternoon.
Adam Peaty began feeling unwell on Sunday, ahead of his Mens 100 breaststroke final. In the hours after the final, his symptoms became worse and he was tested for COVID early on Monday morning. He tested positive at that point, Team GB said in their release.
He is hopeful to be back in competition for the relay events later in the swimming program. As in any case of illness, the situation is being damaged appropriately, with all usual precautions being taken to keep the wider delegation healthy.
Peaty was the two-time defending Olympic Champion and was in search for a Three-Peaty on Sunday night. He came up just 0.02 seconds short, swimming a 59.05 for silver, tying with Nic Fink of the US. The two went on to share the podium step together.
His time in finals was slightly off his time from semifinals as he led the way through semifinals swimming a 58.86, a time that would have won gold Sunday night as Nicolo Martinenghi charged home to touch first in a 59.03.
Peaty is the World Record holder in the mens 100 breast as his best time stands at a 56.88 from 2019.
He was the fastest swimmer for Great Britain in the 100 breast by over half a second as James Wilby did not advance to the final as he swam a 59.49 in semifinals for 11th.
The good news for the British relay is that the mixed medley relay and mens medley relay do not occur until the end of the meet. Prelims of the mixed medley are scheduled for August 2nd with finals on August 3rd. The mens 4100 medley relay has prelims scheduled for August 3rd and the final on August 4th, the final night of competition.
This is not the first case of COVID for athletes in the village at the Paris Games as Australia had five members of its womens water polo team test positive last week, before the Games even began.
British Olympic swimmer Adam Peaty has tested positive for COVID-19 at the Paris Games, hours after winning the silver medal in the mens 100m breaststroke final Sunday.
Peaty, now a six-time Olympic medalist, began feeling unwell on Sunday before the event, and his symptoms became worse afterward, the British Olympic Association said in a statement Monday.
In the hours after the final, his symptoms became worse and he was tested for Covid early on Monday morning. He tested positive at that point, the British Olympic Associations statement read, according to The Guardian.
The British Olympic Association added Monday that Peaty is hopeful to be back in competition for the relay events later in the swimming programme [sic].
As in any case of illness, the situation is being managed appropriately, with all usual precautions being taken to keep the wider delegation healthy, the statement continued.
Peaty was seeking a three-peat in the mens 100m breaststroke at the Paris Games following gold medal wins at the 2016 Rio Olympics and the Tokyo Games in 2021.
He was edged out by Italys Nicol Martinenghi by 0.02 seconds.
I gave my absolute all there and I executed it as well as I could, Peaty said, per Team GB.
It doesnt matter what the time says on the board, I know that in my heart Ive already won.
Peaty, who previously took a break from the sport to focus on his mental health, added Sunday that he wasnt crying because of a second-place finish, but because it took so much to get here.
Everything Ive done to this point has happened for a reason and Im so happy that I can race the best in the world and still get joint second, the 29-year-old said.
In my heart Ive won and these are happy tears because I said to myself that I would give my absolute best every single day and I have.
Nic Fink of Team USA placed third in Sundays event.
With rising case numbers, COVID-19 seems to be everywhere right now. But did you know the virus might also be literally lurking in your back yard? A new study from scientists at Virginia Tech found SARS-CoV-2 in six of Virginias most recognizable animal species, many of which can be found across the United States.
Weve known for a while that a COVID-afflicted human can pose a risk to their pets. Two domestic cats were the first pets to test positive for the virus in the US way back in early 2020, and the most recent guidance from the Centers for Disease Control and Prevention (CDC) suggests that dogs, hamsters, and ferrets could also be at risk.
Numerous wild species and others held in zoos and sanctuaries have also been reported to be infected, leading the team at Virginia Tech to question just how widespread this virus could be within the local fauna.
This study was really motivated by seeing a large, important gap in our knowledge about SARS-CoV-2 transmission in a broader wildlife community, explained Assistant Professor of Biological Sciences Joseph Hoyt, one of the corresponding authors, in a statement.
They sampled 23 species and detected SARS-CoV-2 RNA in six of them: the deer mouse, Virginia opossum, raccoon, groundhog, Eastern cottontail rabbit, and Eastern red bat. A total of 798 nasal and oral swabs were collected between May 2022 and September 2023, from either wild-caught animals that were later released or animals that were being treated in rehabilitation centers. A further 126 blood samples were also collected from six species.
The researchers wanted to compare animals found in areas with different levels of human contact, from remote rural locations to right in our back yards. The data suggests that the virus has spread into wildlife populations in places with high human activity.
The virus can jump from humans to wildlife when we are in contact with them, like a hitchhiker switching rides to a new, more suitable host, said co-corresponding author and Professor of Biological Sciences Carla Finkielstein. The goal of the virus is to spread in order to survive. The virus aims to infect more humans, but vaccinations protect many humans. So, the virus turns to animals, adapting and mutating to thrive in the new hosts.
We often speak about the risks of viruses spilling over from animals into the human population not least when discussing the origins of COVID itself but rarely do we stop to think about the opposite scenario. A recent study found that viruses jump from humans to animals more often than the other way round, and now this data is showing that we have helped spread SARS-CoV-2 into more animal species than we might think.
I think the big take home message is the virus is pretty ubiquitous, said first author Amanda Goldberg.
Its not clear exactly how the animals caught the infection from humans, but the authors believe that garbage and discarded food are the most likely sources. Two of the mice sampled from the same location on the same day during the study were found to be infected with the exact same variant of the virus, meaning they either caught it from the same human or one infected the other.
Understanding how the virus is spreading in different animal populations is important to gain a more detailed picture of how it is evolving. How might it be spreading from one species to another? Which wild species might serve as reservoirs for human-pathogenic strains?
The black "root" of this evolutionary tree is the original Wuhan SARS-CoV-2 sequence isolated at the end of 2019. Arranged on the tree are 90 different virus sequences isolated in humans since then, and highlighted in red are nine wild animal isolates from species included in this study.
Image credit: figure courtesy of Carla Finkielstein/Virginia Tech
We understood the critical importance of sequencing the genome of the virus infecting those species, said Finkielstein, praising the work of the multidisciplinary team who came together for this study. One result, from an opossum, revealed virus mutations that have previously been unreported, underlining the wealth of useful data that these types of studies can provide.
Finkielstein said, The virus is indifferent to whether its host walks on two legs or four. Its primary objective is survival, adding that SARS-CoV-2 is not only a human problem.
The study is published in Nature Communications.
