Heat-shock protein 90α is involved in maintaining the stability of VP16 and VP16-mediated transactivation of α genes from herpes simplex virus-1.

ABSTRACT:

Background

Numerous host cellular factors are exploited by viruses to facilitate infection. Our previous studies and those of others have shown heat-shock protein 90 (Hsp90), a cellular molecular chaperone, is involved in herpes simplex virus (HSV)-1 infection. However, the function of the dominant Hsp90 isoform and the relationship between Hsp90 and HSV-1 α genes remain unclear.

Methods and results

Hsp90α knockdown or inhibition significantly inhibited the promoter activity of HSV-1 α genes and downregulated virion protein 16(VP16) expression from virus and plasmids. The Hsp90α knockdown-induced suppression of α genes promoter activity and downregulation of α genes was reversed by VP16 overexpression, indicating that Hsp90α is involved in VP16-mediated transcription of HSV-

SUBMITTER: Wang Y 

PROVIDER: S-EPMC6303900 | biostudies-literature | 2018 Dec

REPOSITORIES: biostudies-literature