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1.
PLoS One ; 17(12): e0279347, 2022.
Article in English | MEDLINE | ID: covidwho-2197088

ABSTRACT

BACKGROUND: Risk compensation, or matching behavior to a perceived level of acceptable risk, can blunt the effectiveness of public health interventions. One area of possible risk compensation during the SARS-CoV-2 pandemic is antibody testing. While antibody tests are imperfect measures of immunity, results may influence risk perception and individual preventive actions. We conducted a randomized control trial to assess whether receiving antibody test results changed SARS-CoV-2 protective behaviors. PURPOSE: Assess whether objective information about antibody status, particularly for those who are antibody negative and likely still susceptible to SARS-CoV-2 infection, increases protective behaviors. Secondarily, assess whether a positive antibody test results in decreased protective behaviors. METHODS: In September 2020, we enrolled 1076 undergraduate students, used fingerstick tests for SARS-CoV-2 antibodies, and randomized participants to receive their results immediately or delayed by 4 weeks. Two weeks later, participants completed a survey about their engagement in 4 protective behaviors (mask use, social event avoidance, staying home from work/school, ensuring physical distancing). We estimated differences between conditions for each of these behaviors, stratified by antibody status. For negative participants at baseline, we also estimated the difference between conditions for seroconversion over 8 weeks of follow-up. RESULTS: For the antibody negative participants (n = 1029) and antibody positive participants (n = 47), we observed no significant differences in protective behavior engagement between those who were randomized to receive test results immediately or after 4 weeks. For the baseline antibody negative participants, we also observed no difference in seroconversion outcomes between conditions. CONCLUSIONS: We found that receiving antibody test results did not lead to significant behavior change in undergraduate students whether the SARS-CoV-2 antibody result was positive or negative.


Subject(s)
COVID-19 , Humans , SARS-CoV-2 , Antibodies, Viral , Pandemics/prevention & control , Public Health
2.
Aging (Albany NY) ; 13(18): 21838-21854, 2021 09 16.
Article in English | MEDLINE | ID: covidwho-1417382

ABSTRACT

Senescent cells, which arise due to damage-associated signals, are apoptosis-resistant and can express a pro-inflammatory, tissue-destructive senescence-associated secretory phenotype (SASP). We recently reported that a component of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) surface protein, S1, can amplify the SASP of senescent cultured human cells and that a related mouse ß-coronavirus, mouse hepatitis virus (MHV), increases SASP factors and senescent cell burden in infected mice. Here, we show that SARS-CoV-2 induces senescence in human non-senescent cells and exacerbates the SASP in human senescent cells through Toll-like receptor-3 (TLR-3). TLR-3, which senses viral RNA, was increased in human senescent compared to non-senescent cells. Notably, genetically or pharmacologically inhibiting TLR-3 prevented senescence induction and SASP amplification by SARS-CoV-2 or Spike pseudotyped virus. While an artificial TLR-3 agonist alone was not sufficient to induce senescence, it amplified the SASP in senescent human cells. Consistent with these findings, lung p16INK4a+ senescent cell burden was higher in patients who died from acute SARS-CoV-2 infection than other causes. Our results suggest that induction of cellular senescence and SASP amplification through TLR-3 contribute to SARS-CoV-2 morbidity, indicating that clinical trials of senolytics and/or SASP/TLR-3 inhibitors for alleviating acute and long-term SARS-CoV-2 sequelae are warranted.


Subject(s)
COVID-19/virology , Cellular Senescence , SARS-CoV-2/pathogenicity , Toll-Like Receptor 3/metabolism , Aging , Animals , Apoptosis , COVID-19/metabolism , Cyclin-Dependent Kinase Inhibitor p16/metabolism , Humans , Inflammation , Lung/metabolism , Mice , Phenotype , Viral Proteins , COVID-19 Drug Treatment
3.
Science ; 373(6552)2021 07 16.
Article in English | MEDLINE | ID: covidwho-1262378

ABSTRACT

The COVID-19 pandemic has revealed the pronounced vulnerability of the elderly and chronically ill to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-induced morbidity and mortality. Cellular senescence contributes to inflammation, multiple chronic diseases, and age-related dysfunction, but effects on responses to viral infection are unclear. Here, we demonstrate that senescent cells (SnCs) become hyper-inflammatory in response to pathogen-associated molecular patterns (PAMPs), including SARS-CoV-2 spike protein-1, increasing expression of viral entry proteins and reducing antiviral gene expression in non-SnCs through a paracrine mechanism. Old mice acutely infected with pathogens that included a SARS-CoV-2-related mouse ß-coronavirus experienced increased senescence and inflammation, with nearly 100% mortality. Targeting SnCs by using senolytic drugs before or after pathogen exposure significantly reduced mortality, cellular senescence, and inflammatory markers and increased antiviral antibodies. Thus, reducing the SnC burden in diseased or aged individuals should enhance resilience and reduce mortality after viral infection, including that of SARS-CoV-2.


Subject(s)
Aging , Cellular Senescence/drug effects , Coronavirus Infections/mortality , Flavonols/therapeutic use , Pathogen-Associated Molecular Pattern Molecules/metabolism , Spike Glycoprotein, Coronavirus/metabolism , Animals , COVID-19/immunology , COVID-19/mortality , Cell Line , Coronavirus Infections/immunology , Dasatinib/pharmacology , Dasatinib/therapeutic use , Female , Flavonols/pharmacology , Gene Expression Regulation , Humans , Lipopolysaccharides , Male , Mice , Mice, Inbred C57BL , Murine hepatitis virus/immunology , Quercetin/pharmacology , Quercetin/therapeutic use , Receptors, Coronavirus/genetics , Receptors, Coronavirus/metabolism , Specific Pathogen-Free Organisms , COVID-19 Drug Treatment
4.
J Clin Apher ; 35(4): 378-381, 2020 Aug.
Article in English | MEDLINE | ID: covidwho-633842

ABSTRACT

As the COVID-19 pandemic continues to claim lives across the globe, insufficient data exists regarding the optimal treatment. It is well known that patients 55 years of age or older and patients with certain chronic diseases are at higher risk of severe illness, including acute respiratory distress syndrome and death. A potentially fatal pulmonary complication of sickle cell disease, acute chest syndrome, can be precipitated by acute infections, including respiratory viruses. We report the case of a patient with sickle cell disease (HbSC) who developed COVID-19 pneumonia and acute chest syndrome who was treated with emergent red blood cell exchange in order to avoid endotracheal intubation.


Subject(s)
Anemia, Sickle Cell/complications , Betacoronavirus , Coronavirus Infections/complications , Erythrocyte Transfusion/methods , Intubation, Intratracheal , Pandemics , Pneumonia, Viral/complications , Respiratory Insufficiency/therapy , Acute Chest Syndrome/etiology , Acute Chest Syndrome/therapy , Adult , Analgesics/therapeutic use , Antiviral Agents/therapeutic use , Azithromycin/therapeutic use , COVID-19 , Combined Modality Therapy , Contraindications, Procedure , Coronavirus Infections/drug therapy , Humans , Hydroxychloroquine/therapeutic use , Male , Methylprednisolone/therapeutic use , Oxygen Inhalation Therapy , Pneumonia, Viral/drug therapy , Respiration, Artificial , Respiratory Insufficiency/etiology , SARS-CoV-2
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