Chapter 9 Feline Immunodeficiency Virus
ETIOLOGY
• Feline immunodeficiency virus (FIV) is a member of the lentivirus subfamily of retroviruses. It is an RNA virus with outer envelope and nucleocapsid. FIV originally was isolated in 1986 from a cattery in northern California; however, retrospective assays of stored cat sera have shown that FIV has been widely distributed worldwide since at least the 1960s.
• FIV causes a lifelong infection and gradually progressive decline in immune function that leads to an acquired immunodeficiency syndrome. Manifestations include chronic weight loss, opportunistic infections, chronic inflammatory conditions, and increased risk for malignant neoplasia.
• At least 5 FIV subtypes (clades A through E) have been identified based on genetic differences. Subtypes vary in regional distribution and influence cell tropism and pathogenicity. Subtype A predominates in the Western United States, and subtype B is seen most often in the Eastern United States.
• Numerous wild feline species are susceptible to various subtypes of FIV, including lions, tigers, jaguars, snow leopards, panthers, and bobcats.
Epidemiology
Prevalence
• The prevalence in a 1991 IDEXX survey of 27,976 sick and high-risk cats in the United States presenting to veterinarians was 7.4%. This included sick cats that had a prevalence of 11.6% and asymptomatic high-risk cats (defined as outdoor pet cats, cats exposed to outdoor cats, or cats in large multicat households) that had a prevalence of 4%.
Age and Gender Distribution
• FIV affects cats of all ages (reported range is 2 months to 18 years); however, the incidence increases with age, and FIV is most prevalent in cats 6 years of age and older.
High-Risk Factors
• Sexually intact males are at increased risk for fighting behavior that can lead to bite-wound transmission.
• Cats in high-density habitats are at increased risk for territorial fighting that can lead to bite-wound transmission.
Public Health Risks
• FIV is a feline host-specific virus, and there is no evidence that it causes human infection. People who have had intimate contact with infected cats or direct exposure to FIV through cat bites or lab accidents do not develop antibodies, illness, or any other evidence of infection.
Transmission
• FIV is shed in saliva and transmitted primarily through direct bite-wound inoculation during territorial fights (hence the higher prevalence in males). Experimentally, a single-tooth puncture wound from a FIV-infected cat is an efficient method of transmitting FIV.
• Transmission through intimate contact during cohabitation is unlikely but not impossible. In a study that confined FIV-positive and FIV-negative cats together in the same cages for 2 years, only 1 of 20 negative sentinel cats became infected. Contact transmission has been suspected in rare cases in catteries, but the mode of transmission in most of these cases is undetermined. Fomite transmission is highly unlikely.
• Transmucosal transmission of FIV can occur experimentally through direct atraumatic contact of FIV with oral, vaginal, or rectal mucosa and through artificial insemination; however, these routes are unlikely to be important under natural conditions.
• Experimentally, acute and chronically infected queens may transmit FIV vertically to their kittens in utero or during passage through the birth canal (congenital infection) or postnatally through ingestion of infected milk (lactogenic infection). However, transmission from mother to offspring in these ways is infrequent under natural conditions. More commonly, infected queens pass colostral FIV antibodies to their nursing kittens, causing a false-positive FIV antibody test (e.g., ELISA or Western blot) for up to 6 months (see “Diagnosis”).
Pathogenesis
• FIV has a primary tropism for lymphocytes but also infects macrophages, salivary glands, and the central nervous system.
• FIV primarily infects and gradually destroys subpopulations of T lymphocytes. This cytopathic effect causes a progressive loss of CD4+ lymphocytes, inversion of the CD4/CD8 ratio, and eventual loss of CD8+ lymphocytes in the late stages of infection. Cell-mediated immunity is impaired to a greater extent than antibody-mediated immunity.
• In addition, impaired production and dysregulation of various cytokines plays a role in the pathogenesis of disease.
• After a prolonged, clinically silent latent period that can extend for years, the progressive loss of T lymphocytes results in an immunodeficiency syndrome characterized by chronic and recurrent infections. FIV infection is lifelong and eventually fatal. The natural incubation period for FIV averages 5 years, corresponding to this lengthy latency.
