Maurernoer2793

Whereas the magnitude of the early CD4+ T cell immune response is determined by the severity of initial infection (participants requiring hospitalization or intensive care), pre-existing lung disease was significantly associated with higher long-term SARS-CoV2-specific CD8+ T cell responses, independent of initial disease severity or age. Neutralizing antibody levels were strongly correlated with SARS-CoV-2-specific CD4+ T but not CD8+ T cell responses. Importantly, we did not identify substantial differences in long-term virus-specific T cell or antibody responses between participants with and without COVID-19-related symptoms that persist months after initial infection.

We previously reported and validated a risk prediction tool based on COVID-19 hospitalizations prior to June 2020. Here, we report performance of that model on subsequent data from 6 hospitals and among individual patient subgroups.

We included individuals age 18 or older hospitalized at one of 2 academic medical centers and 4 community hospitals from 6/7/2020 through 1/22/2021 with positive PCR test for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) within 5 days of admission. Coefficients from our previously reported least absolute shrinkage and selection operator (Lasso) risk models were applied to estimate probability of a mortality, as well as a composite severe illness outcome, including admission to the ICU, mechanical ventilation or mortality.

Overall model performance for mortality included AUC of 0.83 (95% CI0.80-0.87) for mortality, with a PPV 0.55 and NPV of 0.95 when using a cutoff corresponding to the highest 20% of predicted risk derived in the training set. For all adverse outcomes, AUC was 0.79 (95% CI0.75-0.81) and PPV 0.48 and NPV 0.98 in the top 20% risk group. Model discrimination was generally similar between genders and race/ethnicity groups, but markedly poorer for younger age groups.

Although the population of individuals hospitalized for COVID-19 has shifted and outcomes have improved overall, prediction models derived earlier in the pandemic may maintain utility.

Although the population of individuals hospitalized for COVID-19 has shifted and outcomes have improved overall, prediction models derived earlier in the pandemic may maintain utility.

Physical activity has been proposed as a protective factor for COVID-19 hospitalization. However, the mechanisms underlying this association are unclear. Here, we examined the association between physical activity and COVID-19 hospitalization and whether this relationship was explained by other risk factors for severe COVID-19.

We used data from adults aged 50 years and older from the Survey of Health, Ageing and Retirement in Europe. The outcome was self-reported hospitalization due to COVID-19 measured before August 2020. The main exposure was usual physical activity, self-reported between 2004 and 2017. Data were analyzed using logistic regression models.

Among the 3139 participants included in the study (69.3 ± 8.5 years, 1763 women), 266 were tested positive for COVID-19 and 66 were hospitalized. Results showed that individuals who engaged in physical activity more than once a week had lower odds of COVID-19 hospitalization than individuals who hardly ever or never engaged in physical activity (odds ratios = 0.41, 95% confidence interval = 0.22-0.74,

= .004). This association between physical activity and COVID-19 hospitalization was explained by muscle strength, but not by other risk factors.

These findings suggest that, after 50 years of age, engaging in physical activity more than once a week is associated with lower odds of COVID-19 hospitalization. The protective effect of physical activity on COVID-19 hospitalization is explained by muscle strength.

These findings suggest that, after 50 years of age, engaging in physical activity more than once a week is associated with lower odds of COVID-19 hospitalization. The protective effect of physical activity on COVID-19 hospitalization is explained by muscle strength.As highlighted by the ongoing COVID-19 pandemic, vaccination is critical for infectious disease prevention and control. Obesity is associated with increased morbidity and mortality from respiratory virus infections. While obese individuals respond to influenza vaccination, what is considered a seroprotective response may not fully protect the global obese population. In a cohort vaccinated with the 2010-2011 trivalent inactivated influenza vaccine, baseline immune history and vaccination responses were found to significantly differ in obese individuals compared to healthy controls, especially towards the 2009 pandemic strain of A/H1N1 influenza virus. Young, obese individuals displayed responses skewed towards linear peptides versus conformational antigens, suggesting aberrant obese immune response. Overall, these data have vital implications for the next generation of influenza vaccines, and towards the current SARS-CoV-2 vaccination campaign.

Obese individuals have altered baseline and post-vaccination influenza antibody repertoires.

Obese individuals have altered baseline and post-vaccination influenza antibody repertoires.The emergence and rapid rise in prevalence of three independent SARS-CoV-2 "501Y lineages, B.1.1.7, B.1.351 and P.1, in the last three months of 2020 has prompted renewed concerns about the evolutionarily capacity of SARS-CoV-2 to adapt to both rising population immunity, and public health interventions such as vaccines and social distancing. Viruses giving rise to the different 501Y lineages have, presumably under intense natural selection following a shift in host environment, independently acquired multiple unique and convergent mutations. As a consequence all have gained epidemiological and immunological properties that will likely complicate the control of COVID-19. Here, by examining patterns of mutations that arose in SARS-CoV-2 genomes during the pandemic we find evidence of a major change in the selective forces acting on immunologically important SARS-CoV-2 genes (such as N and S) that likely coincided with the emergence of the 501Y lineages. JQ1 In addition to involving continuing sequence diversification, we find evidence that a significant portion of the ongoing adaptive evolution of the 501Y lineages also involves further convergence between the lineages. Our findings highlight the importance of monitoring how members of these known 501Y lineages, and others still undiscovered, are convergently evolving similar strategies to ensure their persistence in the face of mounting infection and vaccine induced host immune recognition.Sensitive, accessible, and biosafe sampling methods for COVID-19 reverse-transcriptase polymerase chain reaction (RT-PCR) assays are needed for frequent and widespread testing. We systematically evaluated diagnostic yield across different sample collection and transport workflows, including the incorporation of a viral inactivation buffer. We prospectively collected nasal swabs, oral swabs, and saliva, from 52 COVID-19 RT-PCR-confirmed patients, and nasopharyngeal (NP) swabs from 37 patients. Nasal and oral swabs were placed in both viral transport media (VTM) and eNAT™, a sterilizing transport buffer, prior to testing with the Xpert Xpress SARS-CoV-2 (Xpert) test. link2 The sensitivity of each sampling strategy was compared using a composite positive standard. Overall, swab specimens collected in eNAT showed superior sensitivity compared to swabs in VTM (70% vs 57%, P=0.0022). Direct saliva 90.5%, (95% CI 82%, 95%), followed by NP swabs in VTM and saliva in eNAT, was significantly more sensitive than nasal swabs in VTM (50%, P less then 0.001) or eNAT (67.8%, P=0.0012) and oral swabs in VTM (50%, P less then 0.0001) or eNAT (56%, P less then 0.0001). Saliva and use of eNAT buffer each increased detection of SARS-CoV-2 with the Xpert test; however, no single sample matrix identified all positive cases.Hospitalizations for acute cardiac conditions have markedly declined during the coronavirus disease 2019 (COVID-19) pandemic, yet the cause of this decline is not clear. Using remote monitoring data of 4,029 patients with implantable cardiac defibrillators (ICDs) living in New York City and Minneapolis/Saint Paul, we assessed changes in markers of cardiac status among these patients and compared thoracic impedance and arrhythmia burden in 2019 and 2020 from January through August. We found no change in several key disease decompensation markers among patients with implanted ICD devices during the first phase of COVID-19 pandemic, suggesting that the decrease in cardiovascular hospitalizations in this period is not reflective of a true population-level improvement in cardiovascular health.Nationwide public health restrictions due to the coronavirus disease 2019 (COVID-19) pandemic have disrupted people's routine physical activities, yet little objective information is available on the extent to which physical activity has changed among patients with pre-existing cardiac diseases. link3 Using remote monitoring data of 9,924 patients with pacemakers and implantable cardiac defibrillators (ICDs) living in New York City and Minneapolis/Saint Paul, we assessed physical activity patterns among these patients in 2019 and 2020 from January through October. We found marked declines in physical activity among patients with implantable cardiac devices during COVID-19-related restrictions and the reduction was consistent across age and sex subgroups. Moreover, physical activity among these vulnerable patients did not return to pre-restrictions levels several months after COVID-19 restrictions were eased. Our findings highlight the need to consider the unintended consequences of mitigation strategies and develop approaches to encourage safe physical activity during the pandemic.

Individuals with obesity show alterations in smell and taste abilities. Smell and taste loss are also the most prominent neurological symptoms of COVID-19, yet how chemosensory ability present in individuals with obesity with a positive COVID-19 diagnosis is unknown.

In this secondary analysis of a cross-sectional global dataset, we compared self-reported chemosensory ability in participants with a respiratory illness reporting a positive (C19+; n = 5156) or a negative (C19-; n = 659) COVID-19 laboratory test outcome, who also self-reported to be obese (C19+; n = 433, C19-; n = 86) or non-obese.

Compared to the C19- group, C19+ exhibited a greater decline in smell, taste, and chemesthesis during illness, though these symptoms did not differ between participants with obesity and without obesity. In 68% of participants who reported recovery from respiratory illness symptoms (n=3431 C19+ and n= 539 C19-), post-recovery chemosensory perception did not differ in C19+ and C19- diagnosis, and by self-reported obesity. Finally, we found that all chemosensory and other symptoms combined predicted the C19+ diagnosis in participants with obesity with a moderately good estimate (63% accuracy). However, in C19+ participants with obesity, we observed a greater relative prevalence of non-chemosensory symptoms, including respiratory as respiratory and GI symptoms.

We conclude that despite a presumed lower sensitivity to chemosensory stimuli, COVID-19 respondents with obesity experience a similar self-reported chemosensory loss as those without obesity, and in both groups self-reported chemosensory symptoms are similarly predictive of COVID-19.

We conclude that despite a presumed lower sensitivity to chemosensory stimuli, COVID-19 respondents with obesity experience a similar self-reported chemosensory loss as those without obesity, and in both groups self-reported chemosensory symptoms are similarly predictive of COVID-19.