Epitranscriptomic m⁶A modifications during reactivation of HIV-1 latency in CD4⁺ T cells.

ABSTRACT: Despite effective antiretroviral therapy reducing HIV-1 viral loads to undetectable levels, the presence of latently infected CD4⁺ T cells poses a major barrier to HIV-1 cure. N⁶-methyladenosine (m⁶A) modification of viral and cellular RNA has a functional role in regulating HIV-1 infection. m⁶A modification of HIV-1 RNA can affect its stability, translation, and splicing in cells and suppresses type-I interferon induction in macrophages. However, the function of m⁶A modification in regulating HIV-1 latency reactivation remains unknown. We used the Jurkat T cell line-derived HIV-1 latency model (J-Lat cells) to investigate changes in m⁶A levels of cellular RNA in response to latency reversal. We observed a significant

SUBMITTER: Mishra T 

PROVIDER: S-EPMC11559067 | biostudies-literature | 2024 Nov

REPOSITORIES: biostudies-literature