Homotypic and Heterotypic Protection and Risk of Reinfection Following Natural Norovirus Infection in a Highly Endemic Setting.


Journal

Clinical infectious diseases : an official publication of the Infectious Diseases Society of America
ISSN: 1537-6591
Titre abrégé: Clin Infect Dis
Pays: United States
ID NLM: 9203213

Informations de publication

Date de publication:
27 01 2021
Historique:
received: 08 07 2019
accepted: 08 01 2020
entrez: 27 1 2021
pubmed: 28 1 2021
medline: 29 4 2021
Statut: ppublish

Résumé

Norovirus is a leading cause of acute gastroenteritis worldwide, yet there is limited information on homotypic or heterotypic protection following natural infection to guide vaccine development. A total of 6020 stools collected from 299 Peruvian children between 2010 and 2014 were tested by norovirus real-time reverse-transcription polymerase chain reaction followed by sequence-based genotyping. Cox proportional hazards models were used to derive adjusted hazard ratios (HRs) of infection among children with vs without prior exposure. Norovirus was detected in 1288 (21.3%) samples. GII.4 (26%), GII.6 (19%), and GI.3 (9%) viruses accounted for 54% of infections. Homotypic protection for GI.3 (HR, 0.35; P = .015), GI.7 (HR, 0.19; P = .022), GII.4 (HR, 0.39; P < .001), and GII.6 (HR, 0.52; P = .006) infections was observed. Hazard analysis showed that children with prior GII.4 infection exhibited heterotypic protection with a 48% reduction of subsequent GI.3 infection (HR, 0.52; P = .005). Prior exposure to GI.3, GII.2, and GII.17 infections enhanced susceptibility to subsequent infections with several other norovirus genotypes. Children up to 2 years of age infected with GII.4 noroviruses demonstrated both homotypic and heterotypic protection to reinfection with other genotypes. These data support the need for ongoing vaccine development efforts with GII.4 as the main component and caution the inclusion of genotypes that may enhance susceptibility to infections.

Sections du résumé

BACKGROUND
Norovirus is a leading cause of acute gastroenteritis worldwide, yet there is limited information on homotypic or heterotypic protection following natural infection to guide vaccine development.
METHODS
A total of 6020 stools collected from 299 Peruvian children between 2010 and 2014 were tested by norovirus real-time reverse-transcription polymerase chain reaction followed by sequence-based genotyping. Cox proportional hazards models were used to derive adjusted hazard ratios (HRs) of infection among children with vs without prior exposure.
RESULTS
Norovirus was detected in 1288 (21.3%) samples. GII.4 (26%), GII.6 (19%), and GI.3 (9%) viruses accounted for 54% of infections. Homotypic protection for GI.3 (HR, 0.35; P = .015), GI.7 (HR, 0.19; P = .022), GII.4 (HR, 0.39; P < .001), and GII.6 (HR, 0.52; P = .006) infections was observed. Hazard analysis showed that children with prior GII.4 infection exhibited heterotypic protection with a 48% reduction of subsequent GI.3 infection (HR, 0.52; P = .005). Prior exposure to GI.3, GII.2, and GII.17 infections enhanced susceptibility to subsequent infections with several other norovirus genotypes.
CONCLUSIONS
Children up to 2 years of age infected with GII.4 noroviruses demonstrated both homotypic and heterotypic protection to reinfection with other genotypes. These data support the need for ongoing vaccine development efforts with GII.4 as the main component and caution the inclusion of genotypes that may enhance susceptibility to infections.

Identifiants

pubmed: 33501947
pii: 5699601
doi: 10.1093/cid/ciaa019
pmc: PMC7840104
doi:

Substances chimiques

RNA, Viral 0

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

222-229

Commentaires et corrections

Type : CommentIn

Informations de copyright

© The Author(s) 2020. Published by Oxford University Press for the Infectious Diseases Society of America.

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Auteurs

Preeti Chhabra (P)

Division of Viral Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia, USA.

Saba Rouhani (S)

Bloomberg School of Public Health, Johns Hopkins University, Baltimore, Maryland, USA.

Hannah Browne (H)

Oak Ridge Institute for Science and Education, Oak Ridge, Tennessee, USA.

Pablo Peñataro Yori (P)

Division of Infectious Diseases and International Health, University of Virginia, Charlottesville, Virginia, USA.
Investigaciones Biomédicas, AB PRISMA, Iquitos, Peru.

Mery Siguas Salas (M)

Investigaciones Biomédicas, AB PRISMA, Iquitos, Peru.

Maribel Paredes Olortegui (M)

Investigaciones Biomédicas, AB PRISMA, Iquitos, Peru.

Lawrence H Moulton (LH)

Bloomberg School of Public Health, Johns Hopkins University, Baltimore, Maryland, USA.

Margaret N Kosek (MN)

Division of Infectious Diseases and International Health, University of Virginia, Charlottesville, Virginia, USA.
Investigaciones Biomédicas, AB PRISMA, Iquitos, Peru.

Jan Vinjé (J)

Division of Viral Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia, USA.

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