HDAC6 Triggers the ATM-Dependent DNA Damage Response To Promote PRV Replication

Abstract

Pseudorabies virus (PRV) is a member of the subfamily Alphaherpesvirinae of the family Herpesviridae . PRV infection in swine can lead to high morbidity and mortality of swine, causing huge economic losses.

Alphaherpesvirus manipulates retinoic acid metabolism for optimal replication

“…P53 is a transcription factor highly inducible by many stress signals, such as the DNA damage response (DDR), oncogene activation and nutrient deprivation. 23 Because alphaherpesvirus induces DDR, 24 , 25 , 26 we hypothesized that DDR might be responsible for HSV-1-induced P53 activation and subsequent DHRS3 upregulation. Indeed, viral infection resulted in DDR, as indicated by immunofluorescence of phosphorylated H2AX (γ-H2AX), the most sensitive marker of DDR, 27 and by comet assays of DNA double-strand breaks 28 ( Figures 4 A and 4B).…”

For better or worse: crosstalk of parvovirus and host DNA damage response

“…Viruses utilize many strategies to manipulate the host pathways and hijack host types of machinery for efficient replication. Many DNA and RNA viruses are reported to interact with proteins involved in DDR, such as HIV-1 (16), pseudorabies (17), chikungunya virus (18), autographa californica multiple nucleopolyhedro (19), human papillomavirus (20) and porcine enteric coronavirus PEDV (21). Previous studies have shown that DNA damage signaling is required for parvovirus replication (22)(23)(24)(25)(26)(27), and NS1 plays an essential role in this process.…”