Effects of the angiotensin II receptor antagonist losartan on herpes simplex virus-type 2 infection of cultured vero and cardiac neonatal myocytes.

Previous studies indicate that captopril, an angiotensin II converting enzyme inhibitor, attenuates cardiomyopathy in a murine viral myocarditis model. Accordingly, we investigated the ability of captopril as well as angiotensin II (AII) and losartan, a nonpeptide AII receptor antagonist, to alter infection or replication of herpes simplex virus- type 2 (HSV-2) in cultured cardiac and vero cells. Neither captopril nor AII influenced the ability of HSV-2 to replicate in either cell type. Losartan, however, caused a dose dependent decrease in pfu ability on vero cells with an ED50 of 1.35 mM. In cultured myocytes, losartan (400 microM) reduced significantly %LDH released (54.9 +/- 7.5 vs 29.1 +/- 4.2 in infected controls) and % pfu released (40.9 +/- 8.4 vs 14.8 +/- 3.8 in infected controls) into the media. These results suggest that losartan attenuates deleterious effects of the virus by preventing release of the virus by the cells.