Mechanism of action of the suppression of herpes simplex virus type 2 replication by pterocarnin A. – PubMed

Mechanism of action of the suppression of herpes simplex virus type 2 replication by pterocarnin A. - PubMed

Mechanism of action of the suppression of herpes simplex virus type 2 replication by pterocarnin A. - PubMed
A recent study of men co-infected with herpes simplex virus type 2 (HSV-2) and HIV revealed that drugs used to suppress HSV decrease the levels of HIV in the blood and rectal secretions, which may make patients less likely to transmit the virus. Earlier studies from this laboratory have shown that infection of vascular cells with herpes simplex virus 1 or 2 (HSV-1, HSV-2) results in the differential suppression of extracellular matrix proteins including fibronectin (FN), type IV collagen, thrombospondin (TSP) and Factor VIII von Willebrand protein. In this study, we proposed that imiquimod has an IFN-independent antiviral effect in nonimmune cells. It suppresses CD1d expression primarily by inhibiting its recycling to the cell surface after endocytosis. It also actively suppressed HSV-2 multiplication in Vero cells even when added 12 h after infection. Lymphoproliferation, in the presence of increasing amounts of H238 CM, resulted in a greater degree of suppression of [3H]thymidine ([3H]Tdr) uptake, in both human and mouse systems. Additional studies demonstrate that the 217–414 aa domain of US1 is critical for the suppression of IFN-β production.

From these observations, it was concluded that pterocarnin A suppressed both early and late in the replication cycle of HSV-2. This junction is important because of the roles it plays in cellular communication, nutrient exchange and absorption, and other skin functions.

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