The Modulation of Phosphatase Expression Impacts the Proliferation Efficiency of HSV-1 in Infected Astrocytes

Herpes Simplex Virus 1 (HSV-1) is a major pathogen that causes human neurological diseases, including herpes simplex encephalitis (HSE). Previous studies have shown that astrocytesare involved in HSV-1 systemic pathogenesis in the central nervous system (CNS), although the mechanism remains unclear. In this study, a high-throughput RNAi library screening method was used to analyze the effect of host phosphatasegene regulation on HSV-1 replication using Macaca mulatta primary astrocytesin an in vitro culture system. The results showed that the downregulation of five phosphatasegenes (PNKP, SNAP23, PTPRU, LOC714621 and PPM1M) significantly inhibited HSV-1 infection, suggesting that these phosphataseswere needed in HSV-1 replication in rhesus astrocytes. Although statistically significant, the effect of downregulation of these phosphataseson HSV-1 replication in a human astrocytomacell line appears to be more limited. Our results suggest that the phosphatasegenes in astrocytesmay regulate the immunological and pathological reactions caused by HSV-1 CNS infection through the regulation of HSV-1 replication or of multiple signal transduction pathways.