Molecular evidence of SARS-CoV-2 in New York before the first pandemic wave.
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ABSTRACT:
SUBMITTER: Hernandez MM
PROVIDER: S-EPMC8187428 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:During the first phase of the COVID-19 epidemic, New York City rapidly became the epicenter of the pandemic in the United States. While molecular phylogenetic analyses have previously highlighted multiple introductions and a period of cryptic community transmission within New York City, little is known about the circulation of SARS-CoV-2 within and among its boroughs. We here perform phylogeographic investigations to gain insights into the circulation of viral lineages during the first months of the New York City outbreak. Our analyses describe the dispersal dynamics of viral lineages at the state and city levels, illustrating that peripheral samples likely correspond to distinct dispersal events originating from the main metropolitan city areas. In line with the high prevalence recorded in this area, our results highlight the relatively important role of the borough of Queens as a transmission hub associated with higher local circulation and dispersal of viral lineages toward the surrounding boroughs.
| S-EPMC8136714 | biostudies-literature
Project description:Public health interventions such as social distancing and mask wearing decrease the incidence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, but it is unclear whether they decrease the viral load of infected patients and whether changes in viral load impact mortality from coronavirus disease 2019 (COVID-19). We evaluated 6923 patients with COVID-19 at six New York City hospitals from March 15-May 14, 2020, corresponding with the implementation of public health interventions in March. We assessed changes in cycle threshold (CT) values from reverse transcription-polymerase chain reaction tests and in-hospital mortality and modeled the impact of viral load on mortality. Mean CT values increased between March and May, with the proportion of patients with high viral load decreasing from 47.7% to 7.8%. In-hospital mortality increased from 14.9% in March to 28.4% in early April, and then decreased to 8.7% by May. Patients with high viral loads had increased mortality compared to those with low viral loads (adjusted odds ratio 2.34). If viral load had not declined, an estimated 69 additional deaths would have occurred (5.8% higher mortality). SARS-CoV-2 viral load steadily declined among hospitalized patients in the setting of public health interventions, and this correlated with decreases in mortality.
| S-EPMC8604305 | biostudies-literature
Project description:Occupational and non-occupational risk factors for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection have been reported in healthcare workers (HCWs), but studies evaluating risk factors for infection among physician trainees are lacking. We aimed to identify sociodemographic, occupational, and community risk factors among physician trainees during the first wave of coronavirus disease 2019 (COVID-19) in New York City. In this retrospective study of 328 trainees at the Mount Sinai Health System in New York City, we administered a survey to assess risk factors for SARS-CoV-2 infection between 1 February and 30 June 2020. SARS-CoV-2 infection was determined by self-reported and laboratory-confirmed IgG antibody and reverse transcriptase-polymerase chain reaction test results. We used Bayesian generalized linear mixed effect regression to examine associations between hypothesized risk factors and infection odds. The cumulative incidence of infection was 20.1%. Assignment to medical-surgical units (OR, 2.51; 95% CI, 1.18-5.34), and training in emergency medicine, critical care, and anesthesiology (OR, 2.93; 95% CI, 1.24-6.92) were independently associated with infection. Caring for unfamiliar patient populations was protective (OR, 0.16; 95% CI, 0.03-0.73). Community factors were not statistically significantly associated with infection after adjustment for occupational factors. Our findings may inform tailored infection prevention strategies for physician trainees responding to the COVID-19 pandemic.
| S-EPMC8156350 | biostudies-literature
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.
2022-09-06 | GSE207923 | GEO
Project description:BackgroundUnderstanding community transmission of SARS-CoV-2 variants of concern (VOCs) is critical for disease control in the post pandemic era. The Delta variant (B.1.617.2) emerged in late 2020 and became the dominant VOC globally in the summer of 2021. While the epidemiological features of the Delta variant have been extensively studied, how those characteristics shaped community transmission in urban settings remains poorly understood.MethodsUsing high-resolution contact tracing data and testing records, we analyze the transmission of SARS-CoV-2 during the Delta wave within New York City (NYC) from May 2021 to October 2021. We reconstruct transmission networks at the individual level and across 177 ZIP code areas, examine network structure and spatial spread patterns, and use statistical analysis to estimate the effects of factors associated with COVID-19 spread.ResultsWe find considerable individual variations in reported contacts and secondary infections, consistent with the pre-Delta period. Compared with earlier waves, Delta-period has more frequent long-range transmission events across ZIP codes. Using socioeconomic, mobility and COVID-19 surveillance data at the ZIP code level, we find that a larger number of cumulative cases in a ZIP code area is associated with reduced within- and cross-ZIP code transmission and the number of visitors to each ZIP code is positively associated with the number of non-household infections identified through contact tracing and testing.ConclusionsThe Delta variant produced greater long-range spatial transmission across NYC ZIP code areas, likely caused by its increased transmissibility and elevated human mobility during the study period. Our findings highlight the potential role of population immunity in reducing transmission of VOCs. Quantifying variability of immunity is critical for identifying subpopulations susceptible to future VOCs. In addition, non-pharmaceutical interventions limiting human mobility likely reduced SARS-CoV-2 spread over successive pandemic waves and should be encouraged for reducing transmission of future VOCs.
| S-EPMC10621074 | biostudies-literature
Project description:Proteomic Ig-SEQ identification of SARS-COV-2 specific antibodies from serum of two convalescent patients during the first wave of the COVID-19 pandemic. Total IgG was isolated from serum, digested with IdeS protease to generate F(ab)2 fragments, and subjected to antigen affinity chromatography using agarose beads coupled with SARS-COV-2 spike protein. Purified F(ab)2 fragments were reduced, alkylated, and digested with trypsin prior to LC-MSMS analysis on an Orbitrap Fusion Lumos mass spectrometer. Resulting peptide IDs were used to identify IgG clonotypes in antigen-specific and flow-through fractions.
2024-01-26 | PXD046829 | Pride
Project description:The spatiotemporal profiling of molecular transmission clusters (MTCs) using viral genomic data can effectively identify transmission networks in order to inform public health actions targeting SARS-CoV-2 spread. We used whole genome SARS-CoV-2 sequences derived from ten European regions belonging to eight countries to perform phylogenetic and phylodynamic analysis. We developed dedicated bioinformatics pipelines to identify regional MTCs and to assess demographic factors potentially associated with their formation. The total number and the scale of MTCs varied from small household clusters identified in all regions, to a super-spreading event found in Uusimaa-FI. Specific age groups were more likely to belong to MTCs in different regions. The clustered sequences referring to the age groups 50-100 years old (y.o.) were increased in all regions two weeks after the establishment of the lockdown, while those referring to the age group 0-19 y.o. decreased only in those regions where schools' closure was combined with a lockdown. The spatiotemporal profiling of the SARS-CoV-2 MTCs can be a useful tool to monitor the effectiveness of the interventions and to reveal cryptic transmissions that have not been identified through contact tracing.
| S-EPMC8001481 | biostudies-literature
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.
| S-EPMC7572090 | biostudies-literature
Project description:To evaluate the gene expression profiling of peripheral leukocytes in different outcomes of SARS-CoV-2 infections, whole blood samples were collected from individuals with positive SARS-CoV-2 nasopharyngeal swab by RT-PCR (54 patients) and healthy uninfected individuals (12 volunteers). Infected patients were classified into mild, moderate, severe and critical groups according to a modified statement in the Novel Coronavirus Pneumonia Diagnosis and Treatment Guideline. Blood were collected into EDTA tubes and the buffy coat samples were stored in TRIzol reagent at -80 °C until use for RNA extraction. Affymetrix Clariom S array was used to perform the high-throughput gene expression profiling. Microarray analyses were performed using APT Affymetrix software, R packages and Bioconductor libraries. This systemic view of SARS-CoV-2 infections through blood transcriptomics will foster the understanding about molecular mechanisms and immunopathological processes involved in COVID-19 disease and its different outcomes.
2022-04-29 | E-MTAB-11240 | biostudies-arrayexpress
Project description: Not available
| S-EPMC8360701 | biostudies-literature