#ACE #gene #polymorphism and severe #lung #injury in patients with #COVID19 (Am J Pathol., abstract)

[Source: American Journal of Pathology, full page: (LINK). Abstract, edited.]

ACE gene polymorphism and severe lung injury in patients with COVID-19

Haoyi Zheng, MD, PhD, J. Jane Cao, MD, MPH

Published: July 28, 2020 | DOI: https://doi.org/10.1016/j.ajpath.2020.07.009

 

Abstract

COVID-19 has markedly varied clinical presentations, with the majority of patients being asymptomatic or having mild symptoms. However, severe acute respiratory disease caused by SARS-CoV-2 is common and associated with mortality in patients who require hospitalization. The etiology of susceptibility to severe lung injury remains unclear. Angiotensin II, converted by angiotensin-converting enzyme (ACE) from angiotensin I and metabolized by angiotensin converting enzyme 2 (ACE2), plays a pivotal role in the pathogenesis of lung injury. ACE2 is identified as an essential receptor for SARS-COV-2 to enter the cell. The binding of ACE2 and SARS-COV-2 leads to the exhaustion of ACE2 and down-regulation of ACE2. The interaction and imbalance between ACE and ACE2 result in an unopposed angiotensin II. Considering that the ACE insertion/deletion (I/D) gene polymorphism contributes to the ACE level variability in general population, in which mean ACE level in DD carriers are approximately twice that in II carriers, we propose a hypothesis of genetic predisposition to severe lung injury in patients with COVID-19. It is plausible that the ACE inhibitors and ACE receptor blockers (ARBs) may have the potential to prevent and to treat the acute lung injury after SARS-COV-2 infection especially for those with the ACE genotype associated with high ACE level.

Keywords: SARS-CoV-2; COVID-19; Genetics.

——

#Haplotype #networks of #SARS-CoV-2 infections in the #DiamondPrincess #cruiseship #outbreak (Proc Natl Acad Sci USA, abstract)

[Source: Proceedings of the National Academy of Sciences of the United States of America, full page: (LINK). Abstract, edited.]

Haplotype networks of SARS-CoV-2 infections in the Diamond Princess cruise ship outbreak

Tsuyoshi Sekizuka, Kentaro Itokawa, Tsutomu Kageyama, Shinji Saito, Ikuyo Takayama, Hideki Asanuma, Naganori Nao, Rina Tanaka, Masanori Hashino,  Takuri Takahashi, Hajime Kamiya,  Takuya Yamagishi,  Kensaku Kakimoto, Motoi Suzuki, Hideki Hasegawa, Takaji Wakita, and Makoto Kuroda

PNAS first published July 28, 2020 https://doi.org/10.1073/pnas.2006824117

Edited by Y. Kawaoka, University of Wisconsin–Madison, Madison, WI, and approved July 2, 2020 (received for review April 10, 2020)

 

Significance

On February 5, 2020, the Diamond Princess cruise ship was put under quarantine offshore Yokohama, Japan, after a passenger who disembarked in Hong Kong was confirmed to have coronavirus disease 2019. Whole-genome sequencing of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and a network/phylogeny analysis of the outbreak suggested that there was a single introduction of SARS-CoV-2, which disseminated among passengers on the ship through possible mass-gathering events in the recreational areas. These findings provide information useful for preventing future outbreaks on cruise ships and emphasize the importance of genome-based network/phylogeny analysis to elucidate possible transmission routes in outbreak situations.

 

Abstract

The Diamond Princess cruise ship was put under quarantine offshore Yokohama, Japan, after a passenger who disembarked in Hong Kong was confirmed as a coronavirus disease 2019 case. We performed whole-genome sequencing of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) directly from PCR+ clinical specimens and conducted a phylogenetic analysis of the outbreak. All tested isolates exhibited a transversion at G11083T, suggesting that SARS-CoV-2 dissemination on the Diamond Princess originated from a single introduction event before the quarantine started. Although further spreading might have been prevented by quarantine, some progeny clusters could be linked to transmission through mass-gathering events in the recreational areas and direct transmission among passengers who shared cabins during the quarantine. This study demonstrates the usefulness of haplotype network/phylogeny analysis in identifying potential infection routes.

SARS-CoV-2 – COVID-19 – Diamond Princess – haplotypes

 

Footnotes

1 To whom correspondence may be addressed. Email: makokuro@niid.go.jp.

Author contributions: T.W. and M.K. designed research; T.S., K.I., T.K., S.S., I.T., H.A., N.N., R.T., M.H., T.T., H.K., T.Y., K.K., M.S., H.H., and M.K. performed research; T.S. and K.I. contributed new reagents/analytic tools; T.S., K.I., and T.T. analyzed data; and M.K. wrote the paper.

The authors declare no competing interest.

This article is a PNAS Direct Submission.
This article contains supporting information online at https://www.pnas.org/lookup/suppl/doi:10.1073/pnas.2006824117/-/DCSupplemental.

Data Availability. Whole-genome sequence (fasta) data have been deposited in the Global Initiative on Sharing All Influenza Data database (GISAID; https://www.gisaid.org/epiflu-applications/next-hcov-19-app/) with accession IDs EPI_ISL_416565 to EPI_ISL_416634 (Dataset S1) and GenBank under accession nos. LC570961–LC571041.

Copyright © 2020 the Author(s). Published by PNAS. This open access article is distributed under Creative Commons Attribution License 4.0 (CC BY).

Keywords: SARS-CoV-2; COVID-19; Genetics; Japan.

——

Presence of #Genetic #Variants Among Young #Men With #Severe #COVID19 (JAMA, abstract)

[Source: JAMA, full page: (LINK). Abstract, edited.]

Presence of Genetic Variants Among Young Men With Severe COVID-19

Caspar I. van der Made, MD1,2,3,4; Annet Simons, PhD1; Janneke Schuurs-Hoeijmakers, MD, PhD1; Guus van den Heuvel, MD5; Tuomo Mantere, PhD1; Simone Kersten, MSc1,2,3; Rosanne C. van Deuren, MSc1,2,3; Marloes Steehouwer, BSc1; Simon V. van Reijmersdal, BSc1; Martin Jaeger, PhD2,3; Tom Hofste, BSc1; Galuh Astuti, PhD1; Jordi Corominas Galbany, PhD1; Vyne van der Schoot, MD, PhD6; Hans van der Hoeven, MD, PhD7; Wanda Hagmolen of ten Have, MD, PhD5; Eva Klijn, MD, PhD8; Catrien van den Meer, MD9; Jeroen Fiddelaers, MD10; Quirijn de Mast, MD, PhD2,3,4; Chantal P. Bleeker-Rovers, MD, PhD2,4,11; Leo A. B. Joosten, PhD2,3,4; Helger G. Yntema, PhD1,12; Christian Gilissen, PhD1,3; Marcel Nelen, PhD1; Jos W. M. van der Meer, MD, PhD2,3,4; Han G. Brunner, MD, PhD1,6,12,13; Mihai G. Netea, MD, PhD2,3,4,14; Frank L. van de Veerdonk, MD, PhD2,3,4; Alexander Hoischen, PhD1,2,3,4

Author Affiliations: 1 Department of Human Genetics, Radboud University Medical Center, Nijmegen, the Netherlands; 2 Radboud University Medical Center Center for Infectious Diseases (RCI), Department of Internal Medicine, Radboud University Medical Center, Nijmegen, the Netherlands; 3 Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, the Netherlands; 4 Radboud Expertise Center for Immunodeficiency and Autoinflammation and Radboud Center for Infectious Disease (RCI), Radboud University Medical Center, Nijmegen, the Netherlands; 5 Pulmonology Department, Radboud University Medical Center, Nijmegen, the Netherlands; 6 Department of Clinical Genetics, Maastricht University Medical Center, Maastricht, the Netherlands; 7 Department of Intensive Care, Radboud University Medical Center Center for Infectious Diseases (RCI), Radboud University Medical Center, Nijmegen, the Netherlands; 8 Department of Intensive Care, Erasmus Medical Center, Rotterdam, the Netherlands; 9 Department of Intensive Care, Ziekenhuis Rivierenland, Tiel, the Netherlands; 10 Department of Pulmonology, Admiraal de Ruyter Ziekenhuis, Goes, the Netherlands; 11 Radboud Institute Health Sciences, Radboud University Medical Center, Nijmegen, the Netherlands; 12 Donders Institute for Brain, Cognition and Behaviour, Radboud University Medical Center, Nijmegen, the Netherlands; 13 GROW School of Oncology and developmental biology, and MHeNs School of Mental Health and Neuroscience, Maastricht University, the Netherlands; 14 Immunology and Metabolism, Life and Medical Sciences Institute (LIMES), University of Bonn, Bonn, Germany

JAMA. Published online July 24, 2020. doi:10.1001/jama.2020.13719

 

Key Points

  • Question  – Are genetic variants associated with severe coronavirus disease 2019 (COVID-19) in young male patients?
  • Findings  – In a case series that included 4 young male patients with severe COVID-19 from 2 families, rare loss-of-function variants of the X-chromosomal TLR7 were identified, with immunological defects in type I and II interferon production.
  • Meaning  – These findings provide insights into the pathogenesis of COVID-19.

 

Abstract

Importance  

Severe coronavirus disease 2019 (COVID-19) can occur in younger, predominantly male, patients without preexisting medical conditions. Some individuals may have primary immunodeficiencies that predispose to severe infections caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).

Objective  

To explore the presence of genetic variants associated with primary immunodeficiencies among young patients with COVID-19.

Design, Setting, and Participants  

Case series of pairs of brothers without medical history meeting the selection criteria of young (age <35 years) brother pairs admitted to the intensive care unit (ICU) due to severe COVID-19. Four men from 2 unrelated families were admitted to the ICUs of 4 hospitals in the Netherlands between March 23 and April 12, 2020. The final date of follow-up was May 16, 2020. Available family members were included for genetic variant segregation analysis and as controls for functional experiments.

Exposure  

Severe COVID-19.

Main Outcome and Measures  

Results of rapid clinical whole-exome sequencing, performed to identify a potential monogenic cause. Subsequently, basic genetic and immunological tests were performed in primary immune cells isolated from the patients and family members to characterize any immune defects.

Results  

The 4 male patients had a mean age of 26 years (range, 21-32), with no history of major chronic disease. They were previously well before developing respiratory insufficiency due to severe COVID-19, requiring mechanical ventilation in the ICU. The mean duration of ventilatory support was 10 days (range, 9-11); the mean duration of ICU stay was 13 days (range, 10-16). One patient died. Rapid clinical whole-exome sequencing of the patients and segregation in available family members identified loss-of-function variants of the X-chromosomal TLR7. In members of family 1, a maternally inherited 4-nucleotide deletion was identified (c.2129_2132del; p.[Gln710Argfs*18]); the affected members of family 2 carried a missense variant (c.2383G>T; p.[Val795Phe]). In primary peripheral blood mononuclear cells from the patients, downstream type I interferon (IFN) signaling was transcriptionally downregulated, as measured by significantly decreased mRNA expression of IRF7, IFNB1, and ISG15 on stimulation with the TLR7 agonist imiquimod as compared with family members and controls. The production of IFN-γ, a type II IFN, was decreased in patients in response to stimulation with imiquimod.

Conclusions and Relevance  

In this case series of 4 young male patients with severe COVID-19, rare putative loss-of-function variants of X-chromosomal TLR7 were identified that were associated with impaired type I and II IFN responses. These preliminary findings provide insights into the pathogenesis of COVID-19.

Keywords: SARS-CoV-2; COVID-19; Genetics; Immunodeficiency; Viral pathogenesis; Interferons.

——

#ACE2, #TMPRSS2 , and #Furin variants and #SARS‐CoV‐2 infection in #Madrid, #Spain (J Med Virol., abstract)

[Source: Journal of Medical Virology, full page: (LINK). Abstract, edited.]

ACE2, TMPRSS2 , and Furin variants and SARS‐CoV‐2 infection in Madrid, Spain

Laura Torre‐Fuentes,  Jorge Matías‐Guiu,  Laura Hernández‐Lorenzo,  Paloma Montero‐Escribano,  Vanesa Pytel,  Jesús Porta‐Etessam,  Ulises Gómez‐Pinedo,  Jordi A. Matías‐Guiu

First published: 21 July 2020 | DOI:  https://doi.org/10.1002/jmv.26319

This article has been accepted for publication and undergone full peer review but has not been through the copyediting, typesetting, pagination and proofreading process, which may lead to differences between this version and the Version of Record. Please cite this article as doi: 10.1002/jmv.26319

 

Abstract

Introduction

It has been suggested that some individuals may present genetic susceptibility to SARS‐CoV‐2 infection, with particular research interest in variants of the ACE2 and TMPRSS2 genes, involved in viral penetration into cells, in different populations and geographic regions, although insufficient information is currently available. This study addresses the apparently reasonable hypothesis that variants of these genes may modulate viral infectivity, making some individuals more vulnerable than others.

Material and methods

Through whole‐exome sequencing, the frequency of exonic variants of the ACE2 , TMPRSS2, and Furin genes was analysed in relation to presence/absence of SARS‐CoV‐2 infection in a familial multiple sclerosis cohort including 120 individuals from Madrid.

Results

The ACE2 gene showed a low level of polymorphism, and none variant was significantly associated with SARS‐CoV‐2 infection. These variants have previously been detected in Italy. While TMPRSS2 is highly polymorphic, the variants found do not coincide with those described in other studies, with the exception of rs75603675, which may be associated with SARS‐CoV‐2 infection. The synonymous variants rs61735792 and rs61735794 showed a significant association with infection.

Conclusions

Despite the limited number of patients with SARS‐CoV‐2 infection, some variants, especially in TMPRSS2 , may be associated with COVID‐19.

This article is protected by copyright. All rights reserved.

Keywords: SARS-CoV-2; COVID-19; ACE2; Genetics; Spain.

——

#Host / #genetic #factors associated with #COVID19 call for precision medicine (Prec Clin Med., abstract)

[Source: Precision Clinical Medicine, full page: (LINK). Abstract, edited.]

Host/genetic factors associated with COVID-19 call for precision medicine

Alain R Thierry

Precision Clinical Medicine, pbaa026, https://doi.org/10.1093/pcmedi/pbaa026

Published: 21 July 2020

 

Abstract

If the current rates of infection are to be better managed, and future waves of infection kept at bay, it is absolutely necessary that the conditions and mechanisms of exposure to Severe Acute Respiratory Syndrome-Coronavirus 2 (SARS-CoV-2) be better understood, as well as the downstream severe or lethal clinical complications. While the identification of notable comorbidities has now helped to define broad risk groups, the idiosyncratic responses of individual patients can nonetheless generate unexpected clinical deterioration which is difficult to predict from initial clinical features. Thus, physicians caring for COVID-19 patients face clinical dilemmas on a daily basis. The ability to decipher individual predispositions to SARS-CoV-2 infection or severe illness, in light of variations in host immunological and inflammatory responses, in particular due to genetic variations, would be of great benefit in infection management. To this end, this work associates the description of COVID-19 clinical complications, comorbidities, sequelae and environmental and genetic factors. We also give examples of underlying genomic susceptibility to COVID-19, especially with regard to the newly reported link between the disease and the unbalanced formation of neutrophil extracellular traps. As a consequence, we propose that the host/genetic factors associated with COVID-19 call for precision medicine in its treatment. This is to our knowledge the first article describing elements towards precision medicine for COVID-19 patients.

Issue Section: Short Communication

This content is only available as a PDF.

© The Author(s) 2020. Published by Oxford University Press on behalf of the West China School of Medicine & West China Hospital of Sichuan University.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

Keywords: SARS-CoV-2; COVID-19; Genetics.

——

A #dynamic #nomenclature proposal for #SARS-CoV-2 #lineages to assist #genomic #epidemiology (Nat Microbiol., abstract)

[Source: Nature Microbiology, full page: (LINK). Abstract, edited.]

A dynamic nomenclature proposal for SARS-CoV-2 lineages to assist genomic epidemiology

Andrew Rambaut, Edward C. Holmes, Áine O’Toole, Verity Hill, John T. McCrone, Christopher Ruis, Louis du Plessis & Oliver G. Pybus

Nature Microbiology (2020)

 

Abstract

The ongoing pandemic spread of a new human coronavirus, SARS-CoV-2, which is associated with severe pneumonia/disease (COVID-19), has resulted in the generation of tens of thousands of virus genome sequences. The rate of genome generation is unprecedented, yet there is currently no coherent nor accepted scheme for naming the expanding phylogenetic diversity of SARS-CoV-2. Here, we present a rational and dynamic virus nomenclature that uses a phylogenetic framework to identify those lineages that contribute most to active spread. Our system is made tractable by constraining the number and depth of hierarchical lineage labels and by flagging and delabelling virus lineages that become unobserved and hence are probably inactive. By focusing on active virus lineages and those spreading to new locations, this nomenclature will assist in tracking and understanding the patterns and determinants of the global spread of SARS-CoV-2.

Keywords: SARS-CoV-2; COVID-19; Epidemiology.

——

Rapid implementation of #SARS-CoV-2 #sequencing to investigate cases of #healthcare associated #COVID19: a prospective #genomic #surveillance study (Lancet Infect Dis., abstract)

[Source: Lancet Infectious Diseases, full page: (LINK). Abstract, edited.]

Rapid implementation of SARS-CoV-2 sequencing to investigate cases of health-care associated COVID-19: a prospective genomic surveillance study

Luke W Meredith, PhD *, †, William L Hamilton, PhD *, †, Ben Warne, MB Bchir, Charlotte J Houldcroft, PhD, Myra Hosmillo, PhD, Aminu S Jahun, PhD, Martin D Curran, PhD, Surendra Parmar, PhD, Laura G Caller, PhD, Sarah L Caddy, PhD, Fahad A Khokhar, BSc, Anna Yakovleva, BSc, Grant Hall, BS, Theresa Feltwell, Sally Forrest, BSc, Sushmita Sridhar, BS, Michael P Weekes, PhD, Prof Stephen Baker, PhD, Nicholas Brown, MD, Elinor Moore, MBBS, Ashley Popay, BSc, Iain Roddick, BSc, Mark Reacher, MD, Theodore Gouliouris, PhD, Prof Sharon J Peacock, FRCP, Prof Gordon Dougan, PhD, M Estée Török, FRCP  *, ‡, Prof Ian Goodfellow, PhD  *, ‡

Published: July 14, 2020 | DOI: https://doi.org/10.1016/S1473-3099(20)30562-4

 

Summary

Background

The burden and influence of health-care associated severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections is unknown. We aimed to examine the use of rapid SARS-CoV-2 sequencing combined with detailed epidemiological analysis to investigate health-care associated SARS-CoV-2 infections and inform infection control measures.

Methods

In this prospective surveillance study, we set up rapid SARS-CoV-2 nanopore sequencing from PCR-positive diagnostic samples collected from our hospital (Cambridge, UK) and a random selection from hospitals in the East of England, enabling sample-to-sequence in less than 24 h. We established a weekly review and reporting system with integration of genomic and epidemiological data to investigate suspected health-care associated COVID-19 cases.

Findings

Between March 13 and April 24, 2020, we collected clinical data and samples from 5613 patients with COVID-19 from across the East of England. We sequenced 1000 samples producing 747 high-quality genomes. We combined epidemiological and genomic analysis of the 299 patients from our hospital and identified 35 clusters of identical viruses involving 159 patients. 92 (58%) of 159 patients had strong epidemiological links and 32 (20%) patients had plausible epidemiological links. These results were fed back to clinical, infection control, and hospital management teams, leading to infection-control interventions and informing patient safety reporting.

Interpretation

We established real-time genomic surveillance of SARS-CoV-2 in a UK hospital and showed the benefit of combined genomic and epidemiological analysis for the investigation of health-care associated COVID-19. This approach enabled us to detect cryptic transmission events and identify opportunities to target infection-control interventions to further reduce health-care associated infections. Our findings have important implications for national public health policy as they enable rapid tracking and investigation of infections in hospital and community settings.

Funding

COVID-19 Genomics UK funded by the Department of Health and Social Care, UK Research and Innovation, and the Wellcome Sanger Institute.

Keywords: SARS-CoV-2; COVID-19; Nosocomial outbreaks; Diagnostic tests; UK; Genetics.

——

Making sense of #mutation: what D614G means for the #COVID19 pandemic remains unclear (Cell, abstract)

[Source: Cell, full page: (LINK). Abstract, edited.]

Making sense of mutation: what D614G means for the COVID-19 pandemic remains unclear

Nathan D. Grubaugh, William P. Hanage, Angela L. Rasmussen

Published: July 02, 2020 | DOI: https://doi.org/10.1016/j.cell.2020.06.040

 

Abstract

Korber et al. (2020) found that a SARS-CoV-2 variant in the spike protein, D614G, rapidly became dominant around the world. While clinical and in vitro data suggest that D614G changes the virus phenotype, the impact of the mutation on transmission, disease, and vaccine and therapeutic development are largely unknown.

In Press Accepted Manuscript

Identification DOI: https://doi.org/10.1016/j.cell.2020.06.040

Copyright © 2020 Elsevier Inc.

Keywords: SARS-CoV-2; COVID-19; Genetics.

——-

Tracking #changes in #SARS-CoV-2 #Spike: evidence that D614G increases #infectivity of the #COVID19 virus (Cell, abstract)

[Source: Cell, full page: (LINK). Abstract, edited.]

Tracking changes in SARS-CoV-2 Spike: evidence that D614G increases infectivity of the COVID-19 virus

B. Korber, W.M. Fischer, S. Gnanakaran, H. Yoon, J. Theiler, W. Abfalterer, N. Hengartner, E.E. Giorgi, T. Bhattacharya, B. Foley, K.M. Hastie, M.D. Parker, D.G. Partridge, C.M. Evans, T.M. Freeman, T.I. de Silva, C. McDanal, L.G. Perez, H. Tang, A. Moon-Walker, S.P. Whelan, C.C. LaBranche, E.O. Saphire, D.C. Montefiori on behalf of the Sheffield COVID-19 Genomics Group

Published: July 02, 2020 | DOI: https://doi.org/10.1016/j.cell.2020.06.043

 

Highlights:

  • A SARS-CoV-2 variant with Spike G614 has replaced D614 as the dominant pandemic form
  • The consistent increase of G614 at regional levels may indicate a fitness advantage
  • G614 is associated with lower RT PCR Ct’s, suggestive of higher viral loads in patients
  • The G614 variant grows to higher titers as pseudotyped virions

 

Summary

A SARS-CoV-2 variant carrying the Spike protein amino acid change D614G has become the most prevalent form in the global pandemic. Dynamic tracking of variant frequencies revealed a recurrent pattern of G614 increase at multiple geographic levels: national, regional and municipal. The shift occurred even in local epidemics where the original D614 form was well established prior to the introduction of the G614 variant. The consistency of this pattern was highly statistically significant, suggesting that the G614 variant may have a fitness advantage. We found that the G614 variant grows to higher titer as pseudotyped virions. In infected individuals G614 is associated with lower RT-PCR cycle thresholds, suggestive of higher upper respiratory tract viral loads, although not with increased disease severity. These findings illuminate changes important for a mechanistic understanding of the virus, and support continuing surveillance of Spike mutations to aid in the development of immunological interventions.

Accepted: June 26, 2020 – Received in revised form: June 10, 2020 – Received: April 29, 2020

Publication stage In Press Accepted Manuscript

#Members of Sheffield COVID-19 Genomics Group: Adrienne Angyal, Rebecca L. Brown, Laura Carrilero, Luke R. Green, Danielle C. Groves, Katie J Johnson, Alexander J Keeley, Benjamin B Lindsey, Paul J Parsons, Mohammad Raza, Sarah Rowland-Jones, Nikki Smith, Rachel M. Tucker, Dennis Wang, Matthew D. Wyles

Identification DOI: https://doi.org/10.1016/j.cell.2020.06.043

Copyright © 2020 Published by Elsevier Inc.

Keywords: SARS-CoV-2; COVID-19; Virology.

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#Genomic and #phylogenetic characterization of an imported case of #SARS-CoV-2 in #Amazonas State, #Brazil (Mem Inst Oswaldo Cruz, abstract)

[Source: Memorias do Instituto Oswaldo Cruz, full page: (LINK). Abstract, edited.]

Genomic and phylogenetic characterization of an imported case of SARS-CoV-2 in Amazonas State, Brazil

[ACCEPTED ARTICLES / PRELIMINARY VERSION]

Valdinete Alves do Nascimento1,2, André Lima Guerra Corado1,2, Fernanda Oliveira do Nascimento1,3, Ágatha Kelly Araújo da Costa1,3, Debora Camila Gomes Duarte1, Michele Silva de Jesus 1, Sérgio Luiz Bessa Luz1,3, Luciana Mara Fé Gonçalves4, Cristiano Fernandes da Costa4, Edson Delatorre5, Felipe Gomes Naveca1,2,3,6,+

1 Instituto Leônidas e Maria Deane, Fiocruz, Amazonas, Brasil; 2 Programa de Pós-Graduação em Biologia Celular e Molecular Fundação, Instituto Oswaldo Cruz, Fiocruz, Rio de Janeiro, Brasil; 3 Programa de Pós-Graduação em Biologia da Interação Patógeno-Hospedeiro, Instituto Leônidas e Maria Deane, Amazonas, Brasil; 4 Fundação de Vigilância em Saúde do Amazonas, Amazonas, Brasil; 5 Departamento de Biologia, Centro de Ciências Exatas, Naturais e da Saúde, Universidade Federal do Espírito Santo, Espírito Santo, Brasil; 6 Rede Genômica em Saúde do Estado do Amazonas, Amazonas, Brasil

DOI: 10.1590/0074-02760200310

 

ABSTRACT

A new coronavirus (SARS-CoV-2) is currently causing a life-threatening pandemic. In this study, we report the complete genome sequencing and genetic characterization of a SARS-CoV-2 detected in Manaus, Amazonas, Brazil, and the protocol we designed to generate high-quality SARS-CoV-2 full genome data. The isolate was obtained from an asymptomatic carrier returning from Madrid, Spain. Nucleotide sequence analysis showed a total of nine mutations in comparison with the original Human case in Wuhan, China, and support this case as belonging to the recently proposed lineage A.2. Phylogeographic analysis further confirmed the likely European origin of this case. To our knowledge, this is the first SARS-CoV-2 genome obtained from the North Brazilian Region. We believe that the information generated in this study may contribute to the ongoing efforts toward the SARS-CoV-2 emergence.

key words: SARS-CoV-2 genome COVID-19 Coronavirus Brazil Amazon region

+ Corresponding author: felipe.naveca@fiocruz.br

Received 14 June 2020 – Accepted 15 June 2020

Keywords: SARS-CoV-2; COVID-19; Brazil; Genetics.

——