HIV-1 with gag processing defects activates cGAS sensing.


Journal

Retrovirology
ISSN: 1742-4690
Titre abrégé: Retrovirology
Pays: England
ID NLM: 101216893

Informations de publication

Date de publication:
23 May 2024
Historique:
received: 08 04 2024
accepted: 07 05 2024
medline: 23 5 2024
pubmed: 23 5 2024
entrez: 22 5 2024
Statut: epublish

Résumé

Detection of viruses by host pattern recognition receptors induces the expression of type I interferon (IFN) and IFN-stimulated genes (ISGs), which suppress viral replication. Numerous studies have described HIV-1 as a poor activator of innate immunity in vitro. The exact role that the viral capsid plays in this immune evasion is not fully understood. To better understand the role of the HIV-1 capsid in sensing we tested the effect of making HIV-1 by co-expressing a truncated Gag that encodes the first 107 amino acids of capsid fused with luciferase or GFP, alongside wild type Gag-pol. We found that unlike wild type HIV-1, viral particles produced with a mixture of wild type and truncated Gag fused to luciferase or GFP induced a potent IFN response in THP-1 cells and macrophages. Innate immune activation by Gag-fusion HIV-1 was dependent on reverse transcription and DNA sensor cGAS, suggesting activation of an IFN response by viral DNA. Further investigation revealed incorporation of the Gag-luciferase/GFP fusion proteins into viral particles that correlated with subtle defects in wild type Gag cleavage and a diminished capacity to saturate restriction factor TRIM5α, likely due to aberrant particle formation. We propose that expression of the Gag fusion protein disturbs the correct cleavage and maturation of wild type Gag, yielding viral particles that are unable to effectively shield viral DNA from detection by innate sensors including cGAS. These data highlight the crucial role of capsid in innate evasion and support growing literature that disruption of Gag cleavage and capsid formation induces a viral DNA- and cGAS-dependent innate immune response. Together these data demonstrate a protective role for capsid and suggest that antiviral activity of capsid-targeting antivirals may benefit from enhanced innate and adaptive immunity in vivo.

Sections du résumé

BACKGROUND BACKGROUND
Detection of viruses by host pattern recognition receptors induces the expression of type I interferon (IFN) and IFN-stimulated genes (ISGs), which suppress viral replication. Numerous studies have described HIV-1 as a poor activator of innate immunity in vitro. The exact role that the viral capsid plays in this immune evasion is not fully understood.
RESULTS RESULTS
To better understand the role of the HIV-1 capsid in sensing we tested the effect of making HIV-1 by co-expressing a truncated Gag that encodes the first 107 amino acids of capsid fused with luciferase or GFP, alongside wild type Gag-pol. We found that unlike wild type HIV-1, viral particles produced with a mixture of wild type and truncated Gag fused to luciferase or GFP induced a potent IFN response in THP-1 cells and macrophages. Innate immune activation by Gag-fusion HIV-1 was dependent on reverse transcription and DNA sensor cGAS, suggesting activation of an IFN response by viral DNA. Further investigation revealed incorporation of the Gag-luciferase/GFP fusion proteins into viral particles that correlated with subtle defects in wild type Gag cleavage and a diminished capacity to saturate restriction factor TRIM5α, likely due to aberrant particle formation. We propose that expression of the Gag fusion protein disturbs the correct cleavage and maturation of wild type Gag, yielding viral particles that are unable to effectively shield viral DNA from detection by innate sensors including cGAS.
CONCLUSIONS CONCLUSIONS
These data highlight the crucial role of capsid in innate evasion and support growing literature that disruption of Gag cleavage and capsid formation induces a viral DNA- and cGAS-dependent innate immune response. Together these data demonstrate a protective role for capsid and suggest that antiviral activity of capsid-targeting antivirals may benefit from enhanced innate and adaptive immunity in vivo.

Identifiants

pubmed: 38778414
doi: 10.1186/s12977-024-00643-0
pii: 10.1186/s12977-024-00643-0
doi:

Substances chimiques

cGAS protein, human EC 2.7.7.-
gag Gene Products, Human Immunodeficiency Virus 0
Nucleotidyltransferases EC 2.7.7.-
Antiviral Restriction Factors 0
Tripartite Motif Proteins 0
TRIM5 protein, human EC 2.3.2.27
Ubiquitin-Protein Ligases EC 2.3.2.27
Carrier Proteins 0
DNA, Viral 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

10

Subventions

Organisme : Biotechnology and Biological Sciences Research Council
ID : BB/T006501/1
Pays : United Kingdom
Organisme : Wellcome Trust
ID : 108183
Pays : United Kingdom
Organisme : European Research Council
ID : FP7/2007-2013
Pays : International

Informations de copyright

© 2024. The Author(s).

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Auteurs

Rebecca P Sumner (RP)

Division of Infection and Immunity, University College London, 90 Gower Street, London, WC1E 6BT, UK. rebecca.sumner@surrey.ac.uk.
Department of Microbial Sciences, University of Surrey, Guildford, GU2 7XH, UK. rebecca.sumner@surrey.ac.uk.

Henry Blest (H)

Division of Infection and Immunity, University College London, 90 Gower Street, London, WC1E 6BT, UK.

Meiyin Lin (M)

Division of Infection and Immunity, University College London, 90 Gower Street, London, WC1E 6BT, UK.

Carlos Maluquer de Motes (C)

Department of Microbial Sciences, University of Surrey, Guildford, GU2 7XH, UK.

Greg J Towers (GJ)

Division of Infection and Immunity, University College London, 90 Gower Street, London, WC1E 6BT, UK.

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