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1.
Science ; 371(6529)2021 02 05.
Article in English | MEDLINE | ID: covidwho-1388436

ABSTRACT

Analysis of 772 complete severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) genomes from early in the Boston-area epidemic revealed numerous introductions of the virus, a small number of which led to most cases. The data revealed two superspreading events. One, in a skilled nursing facility, led to rapid transmission and significant mortality in this vulnerable population but little broader spread, whereas other introductions into the facility had little effect. The second, at an international business conference, produced sustained community transmission and was exported, resulting in extensive regional, national, and international spread. The two events also differed substantially in the genetic variation they generated, suggesting varying transmission dynamics in superspreading events. Our results show how genomic epidemiology can help to understand the link between individual clusters and wider community spread.


Subject(s)
COVID-19/epidemiology , Genome, Viral , Phylogeny , SARS-CoV-2/genetics , Boston/epidemiology , COVID-19/transmission , Disease Outbreaks , Epidemiological Monitoring , Humans
2.
Cell ; 183(5): 1325-1339.e21, 2020 11 25.
Article in English | MEDLINE | ID: covidwho-838593

ABSTRACT

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a recently identified coronavirus that causes the respiratory disease known as coronavirus disease 2019 (COVID-19). Despite the urgent need, we still do not fully understand the molecular basis of SARS-CoV-2 pathogenesis. Here, we comprehensively define the interactions between SARS-CoV-2 proteins and human RNAs. NSP16 binds to the mRNA recognition domains of the U1 and U2 splicing RNAs and acts to suppress global mRNA splicing upon SARS-CoV-2 infection. NSP1 binds to 18S ribosomal RNA in the mRNA entry channel of the ribosome and leads to global inhibition of mRNA translation upon infection. Finally, NSP8 and NSP9 bind to the 7SL RNA in the signal recognition particle and interfere with protein trafficking to the cell membrane upon infection. Disruption of each of these essential cellular functions acts to suppress the interferon response to viral infection. Our results uncover a multipronged strategy utilized by SARS-CoV-2 to antagonize essential cellular processes to suppress host defenses.


Subject(s)
COVID-19/metabolism , Host-Pathogen Interactions , Protein Biosynthesis , RNA Splicing , SARS-CoV-2/metabolism , Viral Nonstructural Proteins/metabolism , A549 Cells , Animals , COVID-19/virology , Chlorocebus aethiops , HEK293 Cells , Humans , Interferons/metabolism , Protein Transport , RNA, Messenger/metabolism , RNA, Ribosomal, 18S/metabolism , RNA, Small Cytoplasmic/chemistry , RNA, Small Cytoplasmic/metabolism , Signal Recognition Particle/chemistry , Signal Recognition Particle/metabolism , Vero Cells , Viral Nonstructural Proteins/chemistry
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