Feline immunodeficiency virus

FIV was first isolated in 1986, by Niels C Pedersen and Janet K. Yamamoto at the UC Davis School of Veterinary Medicine in a colony of cats that had a high prevalence of opportunistic infections and degenerative conditions and was originally called Feline T-lymphotropic virus.

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.

FIV may also be transmitted from pregnant females to their offspring in utero; however, this vertical transmission is considered to be relatively rare, based on the small number of FIV-infected kittens and adolescents.

The initial stage, or acute phase, is accompanied by mild symptoms such as lethargy, anorexia, fever, and lymphadenopathy (swelling of the lymph nodes).

[10] Veterinarians will check a cat's history, look for clinical signs, and possibly administer a blood test for FIV antibodies.

[citation needed] Cats that have been vaccinated will test positive for the FIV antibody for the rest of their lives owing to seroconversion, even though they are not infected.

[citation needed] In 2006, the United States Department of Agriculture issued a conditional license for a new treatment aid termed Lymphocyte T-Cell Immunomodulator (LTCI).

Purification of protein from bovine-derived stromal cell supernatants produces a substantially homogeneous factor, free of extraneous materials.

[citation needed] As with HIV, the development of an effective vaccine against FIV is difficult because of the high number of, and differences between, variations of the virus strains.

It has the typical genomic structure of retroviruses and includes LTR, vif, pol, gag, orfA, env, and rev genes.

[28][29] FIV vectors could potentially be used to treat neurological disorders like Parkinson's disease, and have already been used for transfer RNAi, which may find use as gene therapy for cancer.

Fossil records indicate extant felids arose from a common ancestor in Asia approximately 10.8 million years ago, and since then thirty eight species from eight distinct evolutionary lineages have spread and successfully inhabited every continent but Antarctica.

The earliest migration across the Bering Strait into North America occurred approximately 4.5 million years ago during a period of low sea levels.

[35] These migrations events increased opportunities for FIV transmission among felids and established infections globally for felidae species.

[37] In the late Pleistocene, pumas fell victim to the ice age, went extinct in North America except for a small inbred population in Florida, and did not re-emerge until 10–12,000 years ago.

[40] Approximately 2 million years ago, African lions arose and dispersed throughout Africa, Asia, and North, Central, and South America.

[43] Currently, FIV has been documented in over nineteen wild felid species due to its transmission through blood and saliva, which often occurs during aggressive interactions.

[43][44] FIV is more rampant in non-Panthera lineages, such as lynxes, bobcats, cheetahs, and pumas, compared to Panthera species like lions, leopards, jaguars, and tigers.

[42] Studies indicate that lynxes are more susceptible to FIV due to higher levels of the A3Z3 protein, part of the APOBEC3 family, which limits virus replication in felids.

However, A3Z3 mutations do not significantly alter viral genes, suggesting that other genetic or environmental factors may influence the virus's effects.

[42] Members of the Panthera genus exhibit higher levels of protective protein expression, potentially mitigating the severity of infection.

Many live without advanced symptoms, while severe cases are rarely observed in the wild due to rapid mortality or predation.

Infected lions exhibit reduced T-cell counts, inflammation, and systemic complications, but the disease's progression often occurs beyond reproductive age, limiting its population-level effects.

[44] Behavioral changes have been observed in infected felids, such as reduced hunting ability and impaired social interactions, may hinder survival.

[43] These behavioral and physiological effects highlight the multifaceted challenges posed by FIV, influenced by genetics, ecological dynamics, and interspecies interactions.

While it has been connected to immunological complications, current evidence and studies have not conclusively proven that FIV has a significant increase of mortality rates across populations.

[43][44] However, its effects on individual fitness and survival, driven by genetic susceptibility, ecological interactions, and strain diversity, are undeniable.

A study conducted in Colorado on native puma populations found no definitive correlation between human hunting and the spread of FIV.

The interplay of genetic diversity, environmental factors, and interspecies interactions shapes health outcomes and informs efforts to ensure the survival of affected species[44] In domestic cats, FIV-Fca is pathogenic and can lead to feline AIDS symptoms and subsequent death.

Phylogenetic analysis shows FIV to be a monophyletic branch that diverges into three subtypes A, B, and C.[27] Domestic cats arose more recently than other felidae species approximately around 10,000 years ago from a subspecies of wildcat Felis silvestris which inhabited East Asia.

Genome structure of FIV based on available data 2013