Prior Virus Exposure Alters the Long-Term Landscape of Viral Replication during Feline Lentiviral Infection

Viruses

Xin Zheng¹  Scott Carver¹  Ryan M. Troyer¹  Julie A. Terwee¹ 

[1] Department of Microbiology, Immunology and Pathology, 1619 Campus Delivery, Colorado State University, Fort Collins, CO 80523, USA

关键词: FIV;    HIV;    co-infection;    lentivirus;    feline;    tropism;    reservoir;    immunodeficiency;    interferon-gamma;    innate immunity;   

DOI  :  10.3390/v3101891

来源: mdpi

【 摘 要 】

We developed a feline model of lentiviral cross-species transmission using a puma lentivirus (PLV or FIV_Pco) 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.

【 授权许可】

CC BY   
This is an open access article distributed under the Creative Commons Attribution License (CC BY) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.