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Abstract
The mechanism of resistance of murine macrophages (Mϕ) to infection by herpes simplex virus type 1 (HSV-1) was examined. Infection of bone marrow-derived Mϕ (BMDMϕ) and resident peritoneal Mϕ (Res-Mϕ) was compared with infection of permissive Vero cells. In contrast to HSV-1 infection in Vero cells, no infectious virus was produced from either Mϕ cell type. However, marked cytopathic effect (c.p.e.) was evident in BMDMϕ at 48 h post-infection, while there was no c.p.e. at any time post-infection in the Res-Mϕ. 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-Mϕ, HSV-1 DNA was present at early times post-infection but declined rapidly. In BMDMϕ, the virus genome was always detected and increased with time after infection. The results suggest that Res-Mϕ restrict HSV-1 production at a point prior to viral DNA synthesis, whereas the block in HSV production in BMDMϕ occurs at a later stage in the viral replicative cycle.
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