Leary K, Connor J R, Morahan P S
J Gen Virol. 1985 May;66 ( Pt 5):1123-9. doi: 10.1099/0022-1317-66-5-1123.
The mechanism of resistance of murine macrophages (M phi) to infection by herpes simplex virus type 1 (HSV-1) was examined. Infection of bone marrow-derived M phi (BMDM phi) and resident peritoneal M phi (Res-M phi) was compared with infection of permissive Vero cells. In contrast to HSV-1 infection in Vero cells, no infectious virus was produced from either M phi cell type. However, marked cytopathic effect (c.p.e.) was evident in BMDM phi at 48 h post-infection, while there was no c.p.e. at any time post-infection in the Res-M phi. Cloned EcoRI subgenomic fragments representing the entire HSV-1 genome were used as probes in DNA :DNA hybridization experiments to determine the viral genome content in the infected cell types. In Res-M phi, HSV-1 DNA was present at early times post-infection but declined rapidly. In BMDM phi, the virus genome was always detected and increased with time after infection. The results suggest that Res-M phi restrict HSV-1 production at a point prior to viral DNA synthesis, whereas the block in HSV production in BMDM phi occurs at a later stage in the viral replicative cycle.