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Single-base m 6 A epitranscriptomics reveals novel HIV-1 host interaction targets in primary CD4 + T cells
Journal article   Open access   Peer reviewed

Single-base m 6 A epitranscriptomics reveals novel HIV-1 host interaction targets in primary CD4 + T cells

Siyu Huang, Yutao Zhao, Stacia Phillips, Julia E Warrick, Michael G Kearse, Chuan He and Li Wu
Journal of virology, Vol.99(11), e01536-25
11/25/2025
DOI: 10.1128/jvi.01536-25
PMCID: PMC12645991
PMID: 41085277
url
https://doi.org/10.1128/jvi.01536-25View
Published (Version of record) Open Access

Abstract

N6-methyladenosine (m6A) plays a critical role in regulating RNA stability, localization, and gene expression. m6A modification is also important for modulating the expression of viral and cellular genes during HIV-1 infection. However, the function of m6A modification in regulating HIV-1 infection of primary CD4+ T cells remains unclear. Here, we demonstrate that HIV-1 infection of activated primary CD4+ T cells promotes the interaction between the m6A writer complex subunits methyltransferase-like 3 and 14 (METTL3/METTL14). Using single-base m6A-specific RNA sequencing, we identified differentially m6A-modified cellular mRNAs in HIV-1-infected primary CD4+ T cells, including perilipin 3 (PLIN3). We also identified 30 m6A sites in HIV-1 RNA from infected primary CD4+ T cells. HIV-1 infection increased PLIN3 mRNA level and nuclear accumulation but decreased PLIN3 protein expression in primary CD4+ T cells. Polysome profiling revealed that PLIN3 mRNA was less actively translated during HIV-1 infection of primary CD4+ T cells. Furthermore, PLIN3 knockdown in primary CD4+ T cells significantly reduced HIV-1 release but enhanced virion infectivity. Our results highlight the importance of m6A RNA modification during HIV-1 infection and suggest PLIN3 as a regulatory protein of HIV-1 replication in primary CD4+ T cells.
Translation N6-methyladenosine (m6A) HIV-1 infection polysome fractionation m6A-SAC-seq perilipin 3 (PLIN3) primary CD4+T cells

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