VAGINAL AND RECTAL INFECTION OF CATS WITH FELINE IMMUNODEFICIENCY VIRUS

The objective of this study was to examine the potential of vaginal an d rectal mucosal routes for feline immunodeficiency virus (FIV) uptake and infection, as a model of mucosal HIV infection, and to determine the fate of virus at these mucosal sites following transmission of inf ection. SPF cats were exposed to FIV isolates (PET, GL-8, T637), admin istered as either cell-associated or cell-free inocula, via the rectum or vagina. Establishment of infection was confirmed by isolation of i nfectious FIV from peripheral blood mononuclear cells (PBMC), and by p resence of FIV proviral DNA in PBMC, using a nested polymerase chain r eaction. Fate of virus in tissue taken at necropsy from, cats infected for 6-48 weeks was assessed by localizing FIV core and envelope prote ins, p24 and gp41, using a biotin-streptavidin linked immunoperoxidase (IP) technique. Cells susceptible to infection were identified by an in situ hybridization technique for FIV viral DNA and RNA. Cell-free, as well as cell-associated, virus was infectious across intact vaginal and rectal mucosal surfaces. Transmission was most successful using c ell-associated inocula, and via the rectal route. Cells infected with FIV were detected by IP staining in the colon of 6/9 rectally challeng ed cats and 1/5 vaginally challenged cats. Virus was predominantly loc alized within the epithelium at the base of the colonic crypts associa ted with lymphoid aggregates (follicle associated epithelium; FAE), an d within the lymphoid follicle itself. Occasional infected cells were also noted within the lamina propria. The distribution of FIV DNA posi tive cells in the colon was similar to that for FIV antigen whilst FIV RNA positive cells were found more extensively, including within the lamina propria and lymphoid follicle. FIV infected cells were not dete cted within the vagina, or colonic and ileac lymph nodes. Similar patt erns of infected cells were seen in all of the positive cats, indicati ng that colonic tissues remain persistently actively infected with FIV . We conclude that the FIV/cat model of rectal and vaginal mucosal inf ection should prove useful for characterizing the mechanism by which H IV infects mucosal surfaces and as challenge system for the design of vaccines effective at preventing HIV infection via rectal and vaginal routes.