Abstract
To determine the influence of route of virus exposure on early pathogenesis of feline immunodeficiency virus (FIV) infection, cats were exposed to either of two FIV isolates (FIV-B-2542 or FIV-A-PPR) by vaginal or intravenous (IV) inoculation. Exposure to either virus clade by either route of inoculation resulted in vaginal and systemic infection. Peak plasma viremia and tissue proviral burden were 1-3 log(10) greater in cats infected with FIV-B-2542 vs. FIV-A-PPR, irrespective of inoculation route. Plasma RNA levels paralleled provirus titers in FIV-B-2542-infected cats and were highest in those exposed IV. In contrast, plasma RNA titers were higher in cats infected vaginally with FIV-A-PPR than in those infected IV. Despite early differences, PBMC provirus titers were similar in all groups by 9 weeks postinfection. In cats infected IV, but not vaginally, CD4(+) lymphocyte counts declined significantly independent of the magnitude of viremia. Mitogen-induced lymphoproliferation was decreased in all infected cats regardless of CD4(+) cell counts; this decline correlated with the magnitude of peak plasma viremia in FIV-B-2542, but not FIV-A-PPR, infected cats. These results establish that the kinetics of early FIV infection differ with route of exposure as well as virus isolate and that properties extrapolated from one virus isolate may not be universal.
Published Version
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