Nef enhances HIV-1 replication and infectivity independently of SERINC5 in CEM T cells.


Journal

Virology
ISSN: 1096-0341
Titre abrégé: Virology
Pays: United States
ID NLM: 0110674

Informations de publication

Date de publication:
01 2023
Historique:
received: 23 09 2022
revised: 14 12 2022
accepted: 15 12 2022
pubmed: 29 12 2022
medline: 7 1 2023
entrez: 28 12 2022
Statut: ppublish

Résumé

A primary function of HIV-1 Nef is the enhancement of viral infectivity and replication. Whether counteraction of the antiretroviral proteins SERINC3 and SERINC5 is the cause of this positive influence on viral growth-rate and infectivity remains unclear. Here, we utilized CRISPR/Cas9 to knockout SERINC3 and SERINC5 in a leukemic CD4-positive T cell line (CEM) that displays nef-related infectivity and growth-rate phenotypes. Viral replication was attenuated in CEM cells infected with HIV-1 lacking Nef (HIV-1ΔNef). This attenuated growth-rate phenotype was observed regardless of whether the coding regions of the serinc3 or serinc5 genes were intact. Moreover, knockout of serinc5 alone or of both serinc5 and serinc3 together failed to restore the infectivity of HIV1ΔNef virions produced from infected CEM cells. Our results corroborate a similar study using another T-lymphoid cell line (MOLT-3) and indicate that the antagonism of SERINC3 and SERINC5 does not fully explain the virology of HIV-1 lacking Nef.

Identifiants

pubmed: 36577173
pii: S0042-6822(22)00219-7
doi: 10.1016/j.virol.2022.12.008
pmc: PMC10484624
mid: NIHMS1919722
pii:
doi:

Substances chimiques

Membrane Proteins 0
nef Gene Products, Human Immunodeficiency Virus 0
nef protein, Human immunodeficiency virus 1 0
SERINC5 protein, human 0

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

154-162

Subventions

Organisme : NIGMS NIH HHS
ID : K12 GM068524
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI129706
Pays : United States

Informations de copyright

Published by Elsevier Inc.

Déclaration de conflit d'intérêts

Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

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Auteurs

Peter W Ramirez (PW)

Department of Biological Sciences, California State University Long Beach, Long Beach, CA, USA. Electronic address: Peter.Ramirez@csulb.edu.

Thomas Vollbrecht (T)

Department of Medicine, University of California San Diego, La Jolla, CA, USA; VA San Diego Healthcare System, San Diego, CA, USA.

Francisco M Acosta (FM)

Department of Biological Sciences, California State University Long Beach, Long Beach, CA, USA.

Marissa Suarez (M)

VA San Diego Healthcare System, San Diego, CA, USA.

Aaron O Angerstein (AO)

Department of Medicine, University of California San Diego, La Jolla, CA, USA; VA San Diego Healthcare System, San Diego, CA, USA.

Jared Wallace (J)

Division of Microbiology and Immunology, Department of Pathology, The University of Utah, Salt Lake City, UT, USA.

Ryan M O' Connell (RM)

Division of Microbiology and Immunology, Department of Pathology, The University of Utah, Salt Lake City, UT, USA.

John Guatelli (J)

Department of Medicine, University of California San Diego, La Jolla, CA, USA; VA San Diego Healthcare System, San Diego, CA, USA.

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