Cloning and Sequencing of the Gene Encoding the Spike Protein of the Coronavirus IBV

Abstract

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