We discovered that Human Cytomegalovirus (HCMV) infection of human fibroblasts led to an impressive rise in p38 mitogen-activated protein kinase (MAPK) phosphorylation. Lately, drug mediated inhibition of p38 continues to be shown to demonstrate anti-viral activity against Aids (Shapiro, L., Heidenreich, K.A., Meintzer, M.D. and Dinarello, C.A., 1998. Role of p38 mitogen-activated protein kinase in Aids type 1 production in vitro. Proc. Natl. Acad. Sci. USA. 95, 7422-7426). Therefore, we examined the consequence of specific p38 kinase inhibitor on HCMV infection. Inhibiting p38 activity in HCMV infected cells by treating cells with 4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)1H-imidazole (FHPI), a p38 inhibitor drug, avoided permissive HCMV infection as measured by plaque assay. In the existence of FHPI, HCMV immediate early gene expression was slightly lower at early occasions of infection, but there wasn’t any inhibition of expression from the early gene UL-84, an HCMV protein required for viral replication. However, FHPI inhibited HCMV DNA replication and late gene expression. The inhibitory aftereffect of FHPI was reversible, as shown through the induction of HCMV replication upon withdrawal of FHPI. Our data describes FHPI like a novel anti-HCMV compound that inhibits synthesis/activation of cellular and/or viral factors needed for initiation of HCMV DNA replication.

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