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Molecular evidence of SARS-CoV-2 in New York before the first pandemic wave.

ABSTRACT: Numerous reports document the spread of SARS-CoV-2, but there is limited information on its introduction before the identification of a local case. This may lead to incorrect assumptions when modeling viral origins and transmission. Here, we utilize a sample pooling strategy to screen for previously undetected SARS-CoV-2 in de-identified, respiratory pathogen-negative nasopharyngeal specimens from 3,040 patients across the Mount Sinai Health System in New York. The patients had been previously evaluated for respiratory symptoms or influenza-like illness during the first 10 weeks of 2020. We identify SARS-CoV-2 RNA from specimens collected as early as 25 January 2020, and complete SARS-CoV-2 genome sequences from multiple pools of samples collected between late February and early March, documenting an increase prior to the later surge. Our results provide evidence of sporadic SARS-CoV-2 infections a full month before both the first officially documented case and emergence of New York as a COVID-19 epicenter in March 2020.

SUBMITTER: Hernandez MM

PROVIDER: S-EPMC8187428 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a novel coronavirus that was first reported in Wuhan, China in December of 2019 and has since caused a global pandemic resulting in millions of deaths and tens of millions of patients testing positive for infection. Analysis of different viral strains has identified a D614G change in the spike protein that is correlated with the virus becoming more transmissible. While studies have shown G614 viruses to be more transmissible, the effects of this mutation on the host response, especially on the cellular level, are yet to be fully elucidated. In this experiment we infected NHBE cells with the Washington (D614) strain or the New York (G614) strains of SARS-CoV-2. We generated RNA sequencing data at three different time points to improve our understanding of how the intracellular host response differs between infections with these two strains. We analyzed these data with a bioinformatics pipeline that identifies differentially expressed genes, enriched Gene Ontology terms and dysregulated signaling pathways. We detected over 2,000 differentially expressed genes, over 600 Gene Ontology terms, and 29 affected pathways between the two treatments. Many of these entities play a role in immune signaling and response. When comparing the different strains and different time points we found more overall similarities between matched time points than across different time points with the same strain. When specifically comparing the affected pathways, we saw that the 24hr time point of the New York strain was more similar to the 12hr time point of the Washington strain with a large number of pathways related to translation being inhibited in both strains at these time points. These results suggest that D614G substitution in the spike protein, combined with other nonsynonymous changes in the viral gene products cause distinct responses in infected host cells, especially relating to how quickly translation is dysregulated after infection. These observed differences in the intracellular host response to infection could play a role in driving the increase in pathogenicity and mortality seen in the New York outbreaks versus the Washington outbreaks at the beginning of the SARS-CoV-2 pandemic.

Project description:BackgroundAs the COVID-19 pandemic continues to unfold, the infection-fatality risk (ie, risk of death among all infected individuals including those with asymptomatic and mild infections) is crucial for gauging the burden of death due to COVID-19 in the coming months or years. Here, we estimate the infection-fatality risk of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in New York City, NY, USA, the first epidemic centre in the USA, where the infection-fatality risk remains unclear.MethodsIn this model-based analysis, we developed a meta-population network model-inference system to estimate the underlying SARS-CoV-2 infection rate in New York City during the 2020 spring pandemic wave using available case, mortality, and mobility data. Based on these estimates, we further estimated the infection-fatality risk for all ages overall and for five age groups (<25, 25-44, 45-64, 65-74, and ≥75 years) separately, during the period March 1 to June 6, 2020 (ie, before the city began a phased reopening).FindingsDuring the period March 1 to June 6, 2020, 205 639 people had a laboratory-confirmed infection with SARS-CoV-2 and 21 447 confirmed and probable COVID-19-related deaths occurred among residents of New York City. We estimated an overall infection-fatality risk of 1·39% (95% credible interval 1·04-1·77) in New York City. Our estimated infection-fatality risk for the two oldest age groups (65-74 and ≥75 years) was much higher than the younger age groups, with a cumulative estimated infection-fatality risk of 0·116% (0·0729-0·148) for those aged 25-44 years and 0·939% (0·729-1·19) for those aged 45-64 years versus 4·87% (3·37-6·89) for those aged 65-74 years and 14·2% (10·2-18·1) for those aged 75 years and older. In particular, weekly infection-fatality risk was estimated to be as high as 6·72% (5·52-8·01) for those aged 65-74 years and 19·1% (14·7-21·9) for those aged 75 years and older.InterpretationOur results are based on more complete ascertainment of COVID-19-related deaths in New York City than other places and thus probably reflect the true higher burden of death due to COVID-19 than that previously reported elsewhere. Given the high infection-fatality risk of SARS-CoV-2, governments must account for and closely monitor the infection rate and population health outcomes and enact prompt public health responses accordingly as the COVID-19 pandemic unfolds.FundingNational Institute of Allergy and Infectious Diseases, National Science Foundation Rapid Response Research Program, and New York City Department of Health and Mental Hygiene.

Project description:Objective Estimate the seroprevalence of SARS-CoV-2 antibodies among New York City Health and Hospitals (NYC H+H) healthcare workers during the first wave of the COVID-19 pandemic, and describe demographic and occupational factors associated with SARS-CoV-2 antibodies among healthcare workers. Design Descriptive, observational, cross-sectional study using a convenience sample of data from SARS-CoV-2 serological tests accompanied by a demographic and occupational survey administered to healthcare workers. Setting A large, urban public healthcare system in NYC. Participants Participants were employed by NYC H+H and either completed serological testing at NYC H+H between 30 April 2020 and 30 June 2020, or completed SARS-CoV-2 antibody testing outside of NYC H+H and were able to self-report results from the same time period. Primary outcome measure SARS-CoV-2 serostatus, stratified by key demographic and occupational characteristics reported through the demographic and occupational survey. Results Seven hundred and twenty-seven survey respondents were included in analysis. Participants had a mean age of 46 years (SD=12.19) and 543 (75%) were women. Two hundred and fourteen (29%) participants tested positive or reported testing positive for the presence of SARS-CoV-2 antibodies (IgG+). Characteristics associated with positive SARS-CoV-2 serostatus were Black race (25% IgG +vs 15% IgG−, p=0.001), having someone in the household with COVID-19 symptoms (49% IgG +vs 21% IgG−, p<0.001), or having a confirmed COVID-19 case in the household (25% IgG +vs 5% IgG−, p<0.001). Characteristics associated with negative SARS-CoV-2 serostatus included working on a COVID-19 patient floor (27% IgG +vs 36% IgG−, p=0.02), working in the intensive care unit (20% IgG +vs 28% IgG−, p=0.03), being employed in a clinical occupation (64% IgG +vs 78% IgG−, p<0.001) or having close contact with a patient with COVID-19 (51% IgG +vs 62% IgG−, p=0.03). Conclusions Results underscore the significance that community factors and inequities might have on SARS-CoV-2 exposure for healthcare workers.

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Molecular evidence of SARS-CoV-2 in New York before the first pandemic wave.

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