Serial interval distribution of SARS-CoV-2 infection in Brazil.
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ABSTRACT:
SUBMITTER: Prete CA
PROVIDER: S-EPMC7454808 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Studies of novel coronavirus disease (COVID-19) have reported varying estimates of epidemiological parameters including serial interval distributions, i.e., the time between illness onset in successive cases in a transmission chain, and reproduction numbers. By compiling a line-list database of transmission pairs in mainland China, we show that mean serial intervals of COVID-19 have shortened substantially from 7.8 days to 2.6 days within a month (January 9 to February 13, 2020). This change is driven by enhanced non-pharmaceutical interventions, in particular case isolation. We also show that using real-time estimation of serial intervals allowing for variation over time, provides more accurate estimates of reproduction numbers than using conventionally fixed serial interval distributions. These findings could improve assessment of transmission dynamics, forecasting future incidence, and estimating the impact of control measures.
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Project description:We report mean severe acute respiratory syndrome coronavirus 2 serial intervals for Montana, USA, from 583 transmission pairs; infectors' symptom onset dates occurred during March 1-July 31, 2020. Our estimate was 5.68 (95% CI 5.27-6.08) days, SD 4.77 (95% CI 4.33-5.19) days. Subperiod estimates varied temporally by nonpharmaceutical intervention type and fluctuating incidence.
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Project description:IntroductionThe first detected case in Lebanon on 21 February 2020 engendered implementation of a nationwide lockdown alongside timely contact-tracing and testing.ObjectivesOur study aims to calculate the serial interval of SARS-CoV-2 using contact tracing data collected 21 February to 30 June 2020 in Lebanon to guide testing strategies.MethodsrRT-PCR positive COVID-19 cases reported to the Ministry of Public Health Epidemiological Surveillance Program (ESU-MOH) are rapidly investigated and identified contacts tested. Positive cases and contacts assigned into chains of transmission during the study time-period were verified to identify those symptomatic, with non-missing date-of-onset and reported source of exposure. Selected cases were classified in infector-infectee pairs. We calculated mean and standard deviation for the serial interval and best distribution fit using AIC criterion.ResultsOf a total 1788 positive cases reported, we included 103 pairs belonging to 24 chains of transmissions. Most cases were Lebanese (98%) and male (63%). All infectees acquired infection locally. Mean serial interval was 5.24 days, with a standard deviation of 3.96 and a range of - 4 to 16 days. Normal distribution was an acceptable fit for our non-truncated data.ConclusionTimely investigation and social restriction measures limited recall and reporting biases. Pre-symptomatic transmission up to 4 days prior to symptoms onset was documented among close contacts. Our SI estimates, in line with international literature, provided crucial information that fed into national contact tracing measures. Our study, demonstrating the value of contact-tracing data for evidence-based response planning, can help inform national responses in other countries.
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2013-07-31 | E-GEOD-47960 | biostudies-arrayexpress
Project description:HAE cultures were infected with SARS-CoV, SARS-ddORF6 or SARS-BatSRBD and were directly compared to A/CA/04/2009 H1N1 influenza-infected cultures. Cell samples were collected at various hours post-infection for analysis. Time Points = 0, 12, 24, 36, 48, 60, 72, 84 and 96 hrs post-infection for SARS-CoV. Time Points = 0, 24, 48, 60, 72, 84 and 96 hrs post-infection forSARS-ddORF6 and SARS-BatSRBD. Time Points = 0, 6, 12, 18, 24, 36 and 48 hrs post-infection for H1N1. Done in triplicate/quadruplicate for RNA Triplicates/quadruplicates are defined as 3/4 different wells, plated at the same time and using the same cell stock for all replicates. Time matched mocks done in triplicate from same cell stock as rest of samples. Culture medium (the same as what the virus stock is in) will be used for the mock infections. Infection was done at an MOI of 2.
2013-07-31 | E-GEOD-47961 | biostudies-arrayexpress
Project description:HAE cultures were infected with SARS-CoV, SARS-dORF6 or SARS-BatSRBD and were directly compared to A/CA/04/2009 H1N1 influenza-infected cultures. Cell samples were collected at various hours post-infection for analysis. Time Points = 0, 12, 24, 36, 48, 60, 72, 84 and 96 hrs post-infection for SARS-CoV, SARS-dORF6 and SARS-BatSRBD. Time Points = 0, 6, 12, 18, 24, 36 and 48 hrs post-infection for H1N1. Done in triplicate for RNA Triplicates are defined as 3 different wells, plated at the same time and using the same cell stock for all replicates. Time matched mocks done in triplicate from same cell stock as rest of samples. Culture medium (the same as what the virus stock is in) will be used for the mock infections. Infection was done at an MOI of 2 for SARS viruses and an MOI of 1 for H1N1.
2013-07-31 | E-GEOD-47962 | biostudies-arrayexpress
Project description:Interferon-induced transmembrane proteins (IFITMs) restrict infections by many viruses, but a subset of IFITMs enhance infections by specific coronaviruses through currently unknown mechanisms. We show that SARS-CoV-2 Spike-pseudotyped virus and genuine SARS-CoV-2 infections are generally restricted by human and mouse IFITM1, IFITM2, and IFITM3, using gain- and loss-of-function approaches. Mechanistically, SARS-CoV-2 restriction occurred independently of IFITM3 S-palmitoylation, indicating a restrictive capacity distinct from reported inhibition of other viruses. In contrast, the IFITM3 amphipathic helix and its amphipathic properties were required for virus restriction. Mutation of residues within the IFITM3 endocytosis-promoting Yxx? motif converted human IFITM3 into an enhancer of SARS-CoV-2 infection, and cell-to-cell fusion assays confirmed the ability of endocytic mutants to enhance Spike-mediated fusion with the plasma membrane. Overexpression of TMPRSS2, which increases plasma membrane fusion versus endosome fusion of SARS-CoV-2, attenuated IFITM3 restriction and converted amphipathic helix mutants into infection enhancers. In sum, we uncover new pro- and anti-viral mechanisms of IFITM3, with clear distinctions drawn between enhancement of viral infection at the plasma membrane and amphipathicity-based mechanisms used for endosomal SARS-CoV-2 restriction.
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