Targeting the host transcription factor HSF1 prevents human cytomegalovirus replication in vitro and in vivo.

ABSTRACT: FDA-approved antivirals against HCMV have several limitations, including only targeting the later stages of the viral replication cycle, adverse side effects, and the emergence of drug-resistant strains. Antivirals targeting host factors specifically activated within infected cells and necessary for viral replication could address the current drawbacks of anti-HCMV standard-of-care drugs. In this study, we found HCMV infection stimulated the activation of the stress response transcription factor heat shock transcription factor 1 (HSF1). HCMV entry into fibroblasts rapidly increased HSF1 activity and subsequent relocalization from the cytoplasm to the nucleus, which was maintained throughout viral replication and in contrast to the transient burst of activity induced by canonical heat shock

SUBMITTER: Akter D 

PROVIDER: S-EPMC12700004 | biostudies-literature | 2025 May

REPOSITORIES: biostudies-literature