Feline immunodeficiency virus (FIV) is a lentivirus that affects domesticated housecats worldwide and is the causative agent of feline AIDS. From 2.5% up to 4.4% of cats worldwide, and about 2.5% of cats in the USA, are infected with FIV. FIV differs taxonomically from two other feline retroviruses, feline leukemia virus (FeLV) and feline foamy virus (FFV), and is more closely related to human immunodeficiency virus HIV. Within FIV, five subtypes have been identified based on nucleotide sequence differences coding for the viral envelope (env) or polymerase (pol). FIV is the only non-primate lentivirus to cause an AIDS-like syndrome, but FIV is not typically fatal for cats, as they can live relatively healthily as carriers and transmitters of the disease for many years. A vaccine is available although its efficacy remains uncertain, and cats will test positive for FIV antibodies after vaccination. FIV was first discovered in 1986 in a colony of cats that had a high prevalence of opportunistic infections and degenerative conditions, and has since been identified as an endemic disease in domestic cat populations worldwide (Wiki: Feline Immunodeficincy Virus).
4. Microbial Pathogenesis
FIV can attack the immune system of cats, much like the human immunodeficiency virus (HIV) can attack the immune system of human beings. FIV infects many cell types in its host, including CD4+ and CD8+ T lymphocytes, B lymphocytes, and macrophages. FIV can be tolerated well by cats, but can eventually lead to debilitation of the immune system in its feline hosts by the infection and exhaustion of T-helper (CD4+) cells (Wiki: Feline Immunodeficincy Virus).
>gi|9626705|ref|NP_040975.1| hypothetical protein FIVgp4 [Feline immunodeficiency virus]
MEDIIVLFNRVTEKLEKELAIRIFVLAHQLERDKAIRLLQGLFWRYRFKKPRVDYCLCWWCCKFYYWQLQ
STLSITTA
Molecule Role :
Virmugen
Molecule Role Annotation :
Feline immunodeficiency virus (FIV) made defective in the accessory gene ORF-A were previously shown to be greatly attenuated in its ability to replicate in lymphocytes but to grow normally or near normally in other cell types. 3/9 vaccinees (cats) showed no evidence of the challenge virus over a 15-month observation period. In the other vaccinees, the challenge virus was predominant for various periods of time, but pre-existing viral loads and CD4 lymphocyte counts were either unaffected or altered only marginally and transiently (Pistello et al., 2005).
Molecule Role Annotation :
A vif mutant in feline immunodeficiency virus was attenuated and FIV-pPPRΔvif proviral DNA protected cats against challenge with the homologous FIV-PPR biological isolate. (Lockridge et al., 2000).
Vaccination Protocol:
Kittens, which were 12 weeks old, were randomized into groups of five for immunization. DNA was administered at four sites in the gastrocnemius and quadriceps muscles (100 μg of each DNA in a total of 200 μl of PBS at each site) (Hosie et al., 1998).
Vaccine Immune Response Type:
VO_0003057
Immune Response:
The bias toward CTL induction rather than antibody production in response to inoculation with FIVΔRT suggested that intramuscular administration of the FIVΔRT DNA generated primarily a Th1-type immune response (Hosie et al., 1998).
Challenge Protocol:
The cats were challenged with the homologous F-14 molecular clone of the FIV-PET isolate that had been subjected to titer determination by intraperitoneal inoculation of age-matched cats to calculate the 50% infectious dose (Hosie et al., 1998).
Efficacy:
At 6, 9, and 12 weeks postchallenge, one of five FIVΔRT vaccinates and three of five FIVΔRT-plus-IFN-γ vaccinates remained virus free. In contrast, virus was isolated consistently from all of the control cats (IFN-γ alone and no-DNA control groups) at 6, 9, and 12 weeks postchallenge (Hosie et al., 1998).
