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Abstract
We developed a feline model of lentiviral cross-species transmission using a puma lentivirus (PLV or FIVPco) which infects domestic cats but does not cause disease. Infection with PLV protects cats from CD4+ T-cell decline caused by subsequent infection with virulent feline immunodeficiency virus (FIV). Previous studies implicate innate immune and/or cellular restriction mechanisms for FIV disease attenuation in PLV-infected cats. In this study, we evaluated viral infection and cytokine mRNA transcription in 12 different tissue reservoirs approximately five months post infection. We quantitated tissue proviral load, viral mRNA load and relative transcription of IL-10, IL-12p40 and IFNγ from tissues of cats exposed to FIV, PLV or both viruses and analyzed these parameters using a multivariate statistical approach. The distribution and intensity of FIV infection and IFNγ transcription differed between single and co-infected cats, characterized by higher FIV proviral loads and IFNγ expression in co-infected cat tissues. Variability in FIV mRNA load and IFNγ was significantly more constrained in co-infected versus singly infected cat tissues. Single-infected:co-infected ratios of FIV mRNA load compared to FIV proviral load indicated that active viral transcription was apparently inhibited during co-infection. These results indicate that previous PLV infection increases activation of tissue innate immunity and constrains the ability of FIV to productively infect tissue reservoirs of infection for months, independent of FIV proviral load, supporting a model in which innate immunity and/or modulation of target cell susceptibility play a key role in PLV-induced protection from FIV disease.
Highlights
Feline immunodeficiency virus (FIV) is a lentivirus closely related to human immunodeficiency virus (HIV) and simian immunodeficiency virus (SIV) that naturally infects numerous wild and domestic feline species
Proviral load indicated that active viral transcription was apparently inhibited during co-infection. These results indicate that previous PLV infection increases activation of tissue innate immunity and constrains the ability of FIV to productively infect tissue reservoirs of infection for months, independent of FIV proviral load, supporting a model in which innate immunity and/or modulation of target cell susceptibility play a key role in PLV-induced protection from FIV disease
We determined PLV proviral load, FIV proviral load, FIV mRNA abundance and mRNA expression of IL-10, IL-12p40 and IFNγ for 12 different tissues from cats infected with FIV, PLV or both viruses
Summary
Feline immunodeficiency virus (FIV) is a lentivirus closely related to human immunodeficiency virus (HIV) and simian immunodeficiency virus (SIV) that naturally infects numerous wild and domestic feline species. Infection with the domestic cat (Felis catus) strain of FIV (FIVFca) results in CD4+. FIV infection and disease in domestic cats bears many similarities to HIV infection and AIDS in humans including similar routes of infection, cell and tissue tropism, clinical symptoms and course of disease [6,7]. FIV infection of nondomestic felid species has little measurable impact on survival of the natural host [2,10,11,12,13], but may be associated with long-term immune cell depletion and other disease sequelae [14,15,16,17]
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