Replication of equine herpesvirus type 1 in freshly isolated equine peripheral blood mononuclear cells and changes in susceptibility following mitogen stimulation.

In the present study, the outcome of an inoculation of equine peripheral blood mononuclear cells (PBMC) with equine herpesvirus type 1 (EHV-1) was studied in vitro. Cytoplasmic and plasma membrane expression of viral antigens, intra- and extracellular virus titres, and plaque formation in co-culture were determined. EHV-1 replicated in monocytes, although in a highly restricted way. Viral antigens were found at maximum levels (8.7% of the monocytes) at 12 h post-infection. The infection was productive in 0.16% of the monocytes. The virus yield was 10(0.7) TCID(50) per productive cell. In a population of resting lymphocytes, 0.9% of cells were infected and less than 0.05% produced infectious virus. After prestimulation with different mitogens, the number of infected lymphocytes increased four to twelve times. The susceptible lymphocytes were T-lymphocytes. In mitogen-stimulated lymphocytes, clear expression of viral antigens was found on the plasma membrane.

In vivo and in vitro interferon (IFN) studies with the porcine reproductive and respiratory syndrome virus (PRRSV).

Some of the interactions between the porcine reproductive and respiratory syndrome virus (PRRSV) and the porcine interferon-alpha (IFN-alpha) system were studied. In a first experiment, it was shown that pretreatment of primary porcine alveolar macrophages (AMs) with recombinant porcine (rPo) IFN-alpha 1 resulted in significant reductions of PRRSV yield and numbers of antigen expressing cells. In a second experiment, sensitivity of PRRSV to IFN-alpha was confirmed in vivo. In pigs inoculated with porcine respiratory coronavirus (PRCV)--a potent inducer of endogenous IFN-alpha in the lungs of pigs--followed 2 days later by PRRSV--lung PRRSV titers were 1.7 to 2.9 log10 TCID50 reduced compared to those in singly PRRSV inoculated pigs. It was concluded therefore that PRRSV has a fairly good sensitivity to the antiviral effects of IFN-alpha. A third experiment documented that in vivo PRRSV infection generally does not affect PRCV-induced IFN-alpha production in the lungs of pigs. In addition, it was shown that the IFN-inducing capacity of PRRSV is at least 159 times lower than that of PRCV. This finding suggests that cells other than AMs may be responsible for IFN production in the lungs of pigs.