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HSF1 Activation Can Restrict HIV Replication

ABSTRACT: Host protein folding stress responses can play important roles in RNA virus replication and evolution. Intriguingly, prior work revealed a complicated interplay between the cytosolic proteostasis stress response, controlled by its master regulator heat shock factor 1 (HSF1) and human immunodeficiency virus-1 (HIV-1). We sought to isolate HSF1 transcription factor activity from proteostasis stress and elucidate the function of HSF1 in HIV-1 lifecycle in absence of cellular stress. We used chemical genetic, stress-independent control of HSF1 activity to establish whether and how HSF1 influences HIV-1 replication. Stress-independent HSF1 induction decreased both the total quantity and infectivity of HIV-1 virions. Moreover, HIV-1 was unable to escape HSF1-mediated restriction over the course of several serial passages. These results promote continued consideration of the heat shock response as a potential target for antiviral drugs.

ORGANISM(S): Homo sapiens

PROVIDER: GSE137591 | GEO | 2022/01/30

REPOSITORIES: GEO

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Sivery2016 - A mammalian heat shock response model

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2012-06-19 | E-GEOD-38000 | biostudies-arrayexpress

HSF1 Activation Can Restrict HIV Replication

Project description:HSF1 Activation Can Restrict HIV Replication

| PRJNA565977 | ENA

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