Feline immunodeficiency virus

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Feline immunodeficiency virus
PDB 4fiv EBI.jpg
Virus classification e
(unranked): Virus
Realm: Riboviria
Kingdom: Pararnavirae
Phylum: Artverviricota
Class: Revtraviricetes
Order: Ortervirales
Family: Retroviridae
Genus: Lentivirus
Species:
Feline immunodeficiency virus

Feline immunodeficiency virus (FIV) is a Lentivirus that affects cats worldwide, with 2.5% to 4.4%[1][2] of felines being infected.

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.[3] It has since been identified in domestic cats.[4] It has been suggested FIV originated in Africa and has since spread to feline species worldwide.

Effects[edit]

FIV compromises the immune system of cats by infecting many cell types, 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.

FIV and HIV are both lentiviruses. However, humans cannot be infected by FIV, nor can cats be infected by HIV. FIV is transmitted primarily through deep bite wounds, where the virus present in the infected cat's saliva enters the body tissues of another cat. FIV+ cats can share water bowls, food bowls (for both wet and dry cat food), and use the same litter box with low danger of transmitting the disease. A vigilant pet owner who treats secondary infections can allow an infected cat to live a reasonably long life. The chance that an FIV-infected cat will pass the virus to other cats within a household is low, unless there is fighting between cats, or wounds present that could allow entry of the virus from infected to non-infected cat.

Newborn kittens may test positive for up to six months and most thereafter will gradually test negative. It is thought that this is due to antibodies transferred to the kittens via the mother's milk. However these antibodies are transient so subsequent testing will be negative. Once they have received vaccinations against FIV, they will, in the future, always test positive, as the various blood tests detect and show the antibodies that have developed in response to the vaccination.

FIV is known in other feline species, and in fact is endemic in some large wild cats, such as African lions. Three main clades of FIV are recognized as of 2006, FIV-Ple (lion), FIV-Fca (domestic cat), and FIV-Pco (puma).[5] The host boundaries are usually well-kept due to the limited types of APOBEC3 enzymes viral infectivity factor can neutralize.[6]

In the United States[edit]

Consensus in the United States on whether there is a need to euthanize FIV-infected cats has not been established. The American Association of Feline Practitioners (an organization in the United States), as well as many feral cat organizations, recommends against euthanizing FIV-positive cats, or even spending funds to test for the virus, as spaying or neutering cats seems to effectively control transmission (spayed/neutered cats are less likely to engage in territorial fights).[7]

Pathology[edit]

The virus gains entry to host cells through the interaction of its own envelope glycoproteins with the target cells' surface receptors. First, the SU glycoprotein binds to CD134, a receptor on the host cell. This initial binding changes the shape of the SU protein to one that facilitates interaction between SU and the chemokine receptor CXCR4.[8] This interaction causes the viral and cellular membranes to fuse, allowing the transfer of the viral RNA into the cytoplasm, where it is reverse transcribed and integrated into the cellular genome through nonhomologous recombination. Once integrated into the host cell's genome, the virus can lay dormant in the asymptomatic stage for extended periods of time without being detected by the immune system or can cause lysis of the cell.[9][10]

CD134 is predominantly found on activated T cells and binds to OX40 ligand, causing T-cell stimulation, proliferation, activation, and apoptosis (3). This leads to a significant drop in cells that have critical roles in the immune system. Low levels of CD4+ and other affected immune system cells cause the cat to be susceptible to opportunistic diseases once the disease progresses to feline acquired immune deficiency syndrome (FAIDS).[11]

Transmission[edit]

The primary mode of transmission is via deep bite wounds, in which the infected cat's saliva enters the other cat's tissues. 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.[12][11] This differs from FeLV, which may be spread by more casual, non-aggressive contact, such as mutual grooming and sharing of food bowls.[citation needed]

Risk factors for infection include male sex, adulthood, and outdoor access. One case study conducted in São Paulo found that 75% of FIV-infected cats were males. Higher rates of infection in males than females occurs due to biting being more frequently engaged in by males defending their territory.[10]

Disease stages[edit]

FIV progresses through similar stages to HIV. The initial stage, or acute phase, is accompanied by mild symptoms such as lethargy, anorexia, fever, and lymphadenopathy (swelling of the lymph nodes).[11] This initial stage is fairly short and is followed by the asymptomatic stage. Here the cat demonstrates no noticeable symptoms for a variable length of time. Some cats stay in this latent stage for only a few months, but for some it can last for years. Factors that influence the length of the asymptomatic stage include the pathogenicity of the infecting virus and FIV subtype (A–E), the age of the cat, and exposure to other pathogens. Finally, the cat progresses into the final stage (known as the feline acquired immune deficiency syndrome (FAIDS) stage), wherein the cat is extremely susceptible to secondary diseases that inevitably are the cause of death.[10]

Testing[edit]

Veterinarians will check a cat's history, look for clinical signs, and possibly administer a blood test for FIV antibodies. FIV affects 2–3% of cats in the US and testing is readily available. This testing identifies those cats that carry the FIV antibody but does not detect the actual virus.

"False positives" occur when the cat carries the antibody (which is harmless) but does not carry the virus. The most frequent occurrence of this is when kittens are tested after ingesting the antibodies from mother's milk (passive immunity), and when testing cats that have been previously vaccinated for FIV (active immunity). For this reason, neither kittens under eight weeks nor cats that have been previously vaccinated are tested. Kittens and young cats that test positive for the FIV antibody via passive immunity test negative later in life due to seroreversion, provided they have never been infected with FIV and have never been immunized with the FIV vaccine.

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. Therefore, testing of strays or adopted cats is inconclusive, since it is impossible to know whether or not they have been vaccinated in the past. For these reasons, a positive FIV antibody test by itself should never be used as a criterion for euthanasia.[13]

Tests can be performed in a vet's office with results in minutes, allowing for quick consultation. Early detection helps maintain the cat's health and prevents spreading infection to other cats. With proper care, infected cats can live long and healthy lives.

Treatment options[edit]

In 2006, the United States Department of Agriculture issued a conditional license for a new treatment aid termed Lymphocyte T-Cell Immunomodulator (LTCI).[14] Lymphocyte T-Cell Immunomodulator is manufactured and distributed exclusively by T-Cyte Therapeutics, Inc.[15]

Lymphocyte T-Cell Immunomodulator is intended as an aid in the treatment of cats infected with feline leukemia virus (FeLV) and/or feline immunodeficiency virus (FIV), and the associated symptoms of anemia (reduced oxygen-carrying ability in the blood), opportunistic infection, lymphocytopenia, granulocytopenia, or thrombocytopenia (low levels of lymphocytes, granulocytes, and platelets respectively, the first two are types of white blood cell). The absence of any observed adverse events in several animal species suggests that the product has a very low toxicity profile.

Lymphocyte T-Cell Immunomodulator is a potent regulator of CD-4 lymphocyte production and function.[16] It has been shown to increase lymphocyte numbers and Interleukin 2 production in animals.[17] It is a single-chain polypeptide and a strongly cationic glycoprotein, and is purified with cation exchange resin. Purification of protein from bovine-derived stromal cell supernatants produces a substantially homogeneous factor, free of extraneous materials. The bovine protein is homologous with other mammalian species and is a homogeneous 50 kDa glycoprotein with an isoelectric point of 6.5. The protein is prepared in a lyophilized (freeze-dried) 1 microgram dose. Reconstitution in sterile diluent produces a solution for subcutaneous injection.

Vaccine[edit]

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. "Single-strain" vaccines, i.e., vaccines that only protect against a single virus variant, have already demonstrated a good efficacy against homologous FIV strains. A dual-subtype vaccine for FIV released in 2002 called Fel-O-Vax made it possible to immunize cats against more FIV strains. It was developed using inactivated isolates of two of the five FIV subtypes (or clades): A Petaluma and D Shizuoka.[18] The vaccine was shown to be moderately protective (82% of cats were protected) against subtype A FIV,[19] but a later study showed it to offer no protection against subtype A.[20] It has shown 100% effectiveness against two different subtype B FIV strains.[21][22] Vaccination will cause cats to have positive results on FIV tests, making diagnosis more difficult. For these reasons the vaccine is considered "non-core", and the decision to vaccinate should be made after discussion with a veterinarian and consideration of the risks vs. the effectiveness.[23]

Structure[edit]

Genome structure of FIV based on available data 2013

FIV displays a similar structure to the primate and ungulate lentiviruses. The virion has a diameter from 80 to 100 nanometers and is pleomorphic. The viral envelope also has surface projections that are small, 8 nm, and evenly cover the surface.[9]

The FIV virus genome is diploid. It consists of two identical single-strands of RNA in each case about 9400 nucleotides existing in plus-strand orientation. It has the typical genomic structure of retroviruses and includes LTR, vif, pol, gag, orfA, env, and rev genes.[24][25][26] The Gag polyprotein is cleaved into matrix (MA), capsid (CA) and nucleocapsid (NC) proteins. Cleavage between CA and NC releases a nine amino acid peptide, while cleavage at the C-terminus of NC releases a 2kDa fragment (p2). The Pol polyprotein is translated by ribosomal frame-shifting, a feature shared with HIV. Cleavage of Pol by the viral protease releases the protease itself (PR), reverse transcriptase (RT), deoxyuridine triphosphatase (dUTPase or DU) and integrase (IN). The Env polyprotein consists of a leader peptide (L), surface (SU) and transmembrane (TM) glycoproteins. In common with other lentiviruses, the FIV genome encodes additional short open reading frames (ORFs) encoding the Vif and Rev proteins. An additional short ORF termed orfA (also known as orf2) precedes the env gene. The function of OrfA in viral replication is unclear, however the orfA-encoded product may display many of the attributes of HIV-1 accessory gene products such as Vpr, Vpu or Nef.

Among these subtypes, genetic sequences are mostly conserved; however, wide-ranging genetic differences exist between species specific FIV subtypes. Of FIV's genome, Pol is the most conserved across FIV strains along with gag. On the contrary, env, vif, orfa, and rev are the least conserved and exhibit the most genetic diversity among FIV strains.[27]

The capsid protein derived from the polyprotein Gag is assembled into a viral core (the protein shell of a virus) and the matrix protein also derived from Gag forms a shell immediately inside of the lipid bilayer. The Env polyprotein encodes the surface glycoprotein (SU) and transmembrane glycoprotein (TM). Both SU and TM glycoproteins are heavily glycosylated, a characteristic that scientists believe may mask the B-cell epitopes of the Env glycoprotein giving the virus resistance to the virus neutralizing antibodies.[9]

Lentiviral vector[edit]

Like HIV-1, FIV has been engineered into a viral vector for gene therapy.[28] Like other lentiviral vectors, FIV vectors integrate into the chromosome of the host cell, where it can generate long-term stable transgene expression. Furthermore, the vectors can be used on dividing and non-dividing cells.[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.[30]

Origin and spread[edit]

The exact origins and emergence of FIV in felids is unknown; however, studies of viral phylogenetics, felidae speciation, and FIV occurrence alludes to origins in Africa. Analysis of viral phylogenetics shows phylogenetic trees with a starbust phylogenetic pattern which is usually demonstrated by viruses that are a recent emergence with rapid evolution.[31] However, differences in topology, branch lengths, high genetic divergence suggest a more ancient origin in felidae species. 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.[24] Despite felidae origins in Asia, FIV is absent from felidae species in Asia except for the Mongolian Pallas cat; however, FIV is highly endemic in Africa with four out of five felids having seropositive PCR results.[32] Due to the widespread occurrence and interspecies divergence of FIV strains in Africa, it's suggested that FIV arose in Africa before disseminating worldwide. The high genetic diversity and divergence between FIV strains in African felidae species and the presence of hyena FIV-Ccr, is consistent with a long residence time giving rise to increased opportunities for inter-species transmission among species. Additionally, lentiviruses are also highly endemic in Africa infecting not only felids, but also primates, and ungulate species. This suggests to the origins of all lentiviruses and supports FIV origins in Africa; however, further research is needed.[33][34]

The spread of FIV from Africa might have occurred during two points of felidae migration. 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] Early felids in North America descended into seven species of the ocelot lineage, two species of the puma lineage, and four of the modern species of lynx.[36] The most recent migration of Asian lions and jaguars across Eurasia into North and South America occurred during the Pliocene/early Pleistocene.[35] These migrations events increased opportunities for FIV transmission among felids and established infections globally for felidae species.

Evolution[edit]

Wild felids[edit]

Comparisons of FIV subtypes illustrate rapid evolution and highlights divergence in FIV strains. FIV-Pco, which is specific to American pumas, has two highly divergent subtypes.[37] Several studies have demonstrated subtypes A and B to have long branch lengths and low geographic similarities which indicates the possibility of two separate FIV introductions into populations coupled with a long residence time.[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.[35][38] Phylogenetic analysis of FIV-Pco strains in Central, South, and North America show Central and South American strains are more closely related to North American strains than to each other.[37][39] This suggests FIV-Pco was already present in South American pumas which repopulated North America.[39] In African lions, FIV-Ple has diverged in to six subtypes A-F which exhibit distinct geographical endemicity to some degree.[40] Approximately 2 million years ago, African lions arose and dispersed throughout Africa, Asia, and North, Central, and South America. Modern lions currently reside only on the African continent except for a small population in India.[35] There is no documented disease association of FIV, but seroprevalence in free- ranging lion populations are estimated to be roughly 90%.[41] Phylogenetic analysis of FIV-Ple subtypes A, B, and C show high intra and interindividual genetic diversity and sequence divergence comparable to genetic differences to strains from other Felidae species.[25] These findings indicate these strains evolved in geographically distant lion populations; however, recent occurrences of these strains within populations in Serengeti National Park suggests recent convergence in the same population.

Domestic felids[edit]

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. Genetic analysis indicates lower genetic diversity of FIV in the domestic cat compared to wild Felidae species, higher evolutionary rates, and higher mortality rates when compared to FIV-Ple and FIV-Pco.[42] This suggests the emergence of FIV in domestic cats was recent since newly emerged viruses tend to have higher evolutionary rates with little to no co-adaption between virus and new host species occurring.[27] Additionally, seroprevalence studies show companion cats to have a 4–12% occurrence while feral cats have an 8–19% prevalence which is much lower compared to wild felidae species which supports the hypothesis of FIV's recent emergence in this species.[43][44]

Comparison with feline leukemia virus[edit]

FIV and feline leukemia virus (FeLV) are sometimes mistaken for one another though the viruses differ in many ways. Although they are both in the same retroviral subfamily (orthoretrovirinae), they are classified in different genera (FeLV is a gamma-retrovirus and FIV is a lentivirus like HIV-1). Their shapes are quite different: FeLV is more circular while FIV is elongated. The two viruses are also quite different genetically, and their protein coats differ in size and composition. Although many of the diseases caused by FeLV and FIV are similar, the specific ways in which they are caused actually differ. Also, while the feline leukemia virus may cause symptomatic illness in an infected cat, an FIV infected cat can remain completely asymptomatic its entire lifetime.[citation needed]

See also[edit]

References[edit]

  • Johnson (2005), Proceedings
  • Might, Jennifer Lynne (2004), Feline Immunodeficiency Virus (FIV), archived from the original on 2006-02-02, retrieved 2006-01-23
  • Wise (2005), Chapter
  • The Lion Research Center (2005), FIV in African Lions, archived from the original on 2008-08-01, retrieved 2008-07-22
  • Alley Cat Allies (2001), Should we release FIV+ cats?, retrieved 2014-06-17
  1. ^ Valéria Maria Lara; Sueli Akemi Taniwaki; João Pessoa Araújo Júnior (2008), "Occurrence of feline immunodeficiency virus infection in cats", Ciência Rural, 38 (8): 2245, doi:10.1590/S0103-84782008000800024.
  2. ^ Richards, J (2005), "Feline immunodeficiency virus vaccine: Implications for diagnostic testing and disease management", Biologicals, 33 (4): 215–7, doi:10.1016/j.biologicals.2005.08.004, PMID 16257536.
  3. ^ Pedersen NC; Ho EW; Brown ML; et al. (1987), "Isolation of a T-lymphotropic virus from domestic cats with an immunodeficiency-like syndrome", Science, 235 (4790): 790–793, Bibcode:1987Sci...235..790P, doi:10.1126/science.3643650, PMID 3643650.
  4. ^ Zislin, A (2005), "Feline immunodeficiency virus vaccine: A rational paradigm for clinical decision-making", Biologicals, 33 (4): 219–20, doi:10.1016/j.biologicals.2005.08.012, PMID 16257537.
  5. ^ Troyer, JL; Roelke, ME; Jespersen, JM; Baggett, N; Buckley-Beason, V; MacNulty, D; Craft, M; Packer, C; Pecon-Slattery, J; O'Brien, SJ (15 October 2011). "FIV diversity: FIV Ple subtype composition may influence disease outcome in African lions". Veterinary Immunology and Immunopathology. 143 (3–4): 338–46. doi:10.1016/j.vetimm.2011.06.013. PMC 3168974. PMID 21723622.
  6. ^ Konno, Y; Nagaoka, S; Kimura, I; Yamamoto, K; Kagawa, Y; Kumata, R; Aso, H; Ueda, MT; Nakagawa, S; Kobayashi, T; Koyanagi, Y; Sato, K (10 April 2018). "New World feline APOBEC3 potently controls inter-genus lentiviral transmission". Retrovirology. 15 (1): 31. doi:10.1186/s12977-018-0414-5. PMC 5894237. PMID 29636069.
  7. ^ Little, Susan; Levy, Julie; Hartmann, Katrin; Hofmann-Lehmann, Regina; Hosie, Margaret; Olah, Glenn; Denis, Kelly St (9 January 2020). "2020 AAFP Feline Retrovirus Testing and Management Guidelines". Journal of Feline Medicine and Surgery. 22 (1): 5–30. doi:10.1177/1098612X19895940. PMID 31916872.
  8. ^ Hu, Quiong-Ying (2012). "Mapping of Receptor Binding Interactions with the Fiv Surface Glycoprotein (SU); Implications Regarding Immune survelliance and cellular Targets of Infection". Retrovirology: Research and Treatment. 1 (11): 1–11. doi:10.4137/RRT.S9429. PMC 3523734. PMID 23255871.
  9. ^ a b c Lecollinet, Sylvie; Jennifer Richardson (12 July 2007), "Vaccination against the feline immunodeficiency virus: The road not taken", Comparative Immunology Microbiology & Infectious Disease, 31 (2–3): 167–190, doi:10.1016/j.cimid.2007.07.007, PMID 17706778, retrieved 15 November 2011
  10. ^ a b c Hartmann, Katrin (2011), "Clinical aspects of feline immunodeficiency and feline leukemia virus infection", Veterinary Immunology and Immunopathy, 143 (3–4): 190–201, doi:10.1016/j.vetimm.2011.06.003, PMC 7132395, PMID 21807418
  11. ^ a b c Yamamoto, Janet; Missa Sanou; Jeffrey Abbott; James Coleman (2010), "Feline immunodeficiency virus model for designing HIV/AIDS vaccines", Current HIV Research, 8 (1): 14–25, doi:10.2174/157016210790416361, PMC 3721975, PMID 20210778
  12. ^ American Association of Feline Practitioners (2002), "Feline Immunodeficiency Virus", Cornell Feline Health Center, Cornell University, College of Veterinary Medicine, retrieved 2008-11-12
  13. ^ Hosie, MJ; et al. (2009), "Feline immunodeficiency. ABCD guidelines on prevention and management", Journal of Feline Medicine & Surgery, 11 (7): 575–84, doi:10.1016/j.jfms.2009.05.006, PMC 7129779, PMID 19481037.
  14. ^ LTCI Product Information, T-Cyte Therapeutics, Inc., archived from the original on 16 August 2012, retrieved 28 July 2012
  15. ^ T-Cyte Therapeutics, Inc., T-Cyte Therapeutics, Inc., retrieved 28 July 2012
  16. ^ Beardsley, et al. "Induction of T-Cell Maturation by a Cloned Line of Thymic Epithelium (TEPI) Immunology 80: pp. 6005-6009, (Oct. 1983).
  17. ^ US patent 7196060, Beardsley, Terry R., "Method to enhance hematopoiesis", published 2005-05-19, issued 2007-03-27 
  18. ^ Levy, J; Crawford, C; Hartmann, K; Hofmann-Lehmann, R; Little, S; Sundahl, E; Thayer, V (2008), "2008 American Association of Feline Practitioners' feline retrovirus management guidelines", Journal of Feline Medicine & Surgery, 10 (3): 300–16, doi:10.1016/j.jfms.2008.03.002, PMID 18455463
  19. ^ Huang, C.; Conlee, D.; Loop, J.; Champ, D.; Gill, M.; Chu, H.J. (2004), "Efficacy and safety of a feline immunodeficiency virus vaccine", Animal Health Research Reviews, 5 (2): 295–300, doi:10.1079/AHR200487, PMID 15984343, S2CID 38671875
  20. ^ Dunham, S.P.; Bruce, J.; Mackay, S.; Golder, M.; Jarrett, O.; Neil, J.C. (2006), "Limited efficacy of an inactivated feline immunodeficiency virus vaccine", Veterinary Record, 158 (16): 561–562, doi:10.1136/vr.158.16.561, PMID 16632531, S2CID 37946050
  21. ^ Kusuhara, H.; Hohdatsu, T.; Okumura, M.; Sato, K.; Suzuki, Y.; Motokawa, K.; Gemma, T.; Watanabe, R.; et al. (2005), "Dual-subtype vaccine (Fel-O-Vax FIV) protects cats against contact challenge with heterologous subtype B FIV infected cats", Veterinary Microbiology, 108 (3–4): 155–165, doi:10.1016/j.vetmic.2005.02.014, PMID 15899558
  22. ^ Pu, R.; Coleman, J.; Coisman, J.; Sato, E.; Tanabe, T.; Arai, M.; Yamamoto, JK. (2005), "Dual-subtype FIV vaccine (Fel-O-Vax FIV) protection against a heterologous subtype B FIV isolate", Journal of Feline Medicine and Surgery, 7 (1): 65–70, doi:10.1016/j.jfms.2004.08.005, PMID 15686976, S2CID 26525327
  23. ^ Levy, J; Crawford, C; Hartmann, K; Hofmann-Lehmann, R; Little, S; Sundahl, E; Thayer, V (2008), "2008 American Association of Feline Practitioners' feline retrovirus management guidelines", Journal of Feline Medicine & Surgery, 10 (3): 300–316, doi:10.1016/j.jfms.2008.03.002, PMID 18455463
  24. ^ a b Pecon Slattery, J; O'Brien, S J (March 1998). "Patterns of Y and X chromosome DNA sequence divergence during the Felidae radiation". Genetics. 148 (3): 1245–1255. doi:10.1093/genetics/148.3.1245. ISSN 0016-6731. PMC 1460026. PMID 9539439.
  25. ^ a b Pecon-Slattery, Jill; McCracken, Carrie L; Troyer, Jennifer L; VandeWoude, Sue; Roelke, Melody; Sondgeroth, Kerry; Winterbach, Christiaan; Winterbach, Hanlie; O'Brien, Stephen J (2008). "Genomic organization, sequence divergence, and recombination of feline immunodeficiency virus from lions in the wild". BMC Genomics. 9 (1): 66. doi:10.1186/1471-2164-9-66. ISSN 1471-2164. PMC 2270836. PMID 18251995.
  26. ^ Talbott, R. L.; Sparger, E. E.; Lovelace, K. M.; Fitch, W. M.; Pedersen, N. C.; Luciw, P. A.; Elder, J. H. (1989-08-01). "Nucleotide sequence and genomic organization of feline immunodeficiency virus". Proceedings of the National Academy of Sciences. 86 (15): 5743–5747. Bibcode:1989PNAS...86.5743T. doi:10.1073/pnas.86.15.5743. ISSN 0027-8424. PMC 297706. PMID 2762293.
  27. ^ a b c Carpenter, Margaret A.; Brown, Eric W.; MacDonald, D.W.; O'Brien, Stephen J. (November 1998). "Phylogeographic Patterns of Feline Immunodeficiency Virus Genetic Diversity in the Domestic Cat". Virology. 251 (2): 234–243. doi:10.1006/viro.1998.9402. PMID 9837787.
  28. ^ a b Poeschla E, Wong-Staal F, Looney D (1998), "Efficient transduction of nondividing cells by feline immunodeficiency virus lentiviral vectors", Nature Medicine, 4 (3): 354–357, doi:10.1038/nm0398-354, PMID 9500613, S2CID 6624732
  29. ^ Harper SQ, Staber PD, Beck CR, Fineberg SK, Stein C, Ochoa D, Davidson BL (Oct 2006), "Optimization of Feline Immunodeficiency Virus Vectors for RNA Interference", J Virol, 80 (19): 9371–80, doi:10.1128/JVI.00958-06, PMC 1617215, PMID 16973543
  30. ^ Valori CF, Ning K, Wyles M, Azzouz M (Dec 2008), "Development and applications of non-HIV-based lentiviral vectors in neurological disorders", Curr Gene Ther, 8 (6): 406–18, doi:10.2174/156652308786848030, PMID 19075624
  31. ^ Carpenter, M A; Brown, E W; Culver, M; Johnson, W E; Pecon-Slattery, J; Brousset, D; O'Brien, S J (1996). "Genetic and phylogenetic divergence of feline immunodeficiency virus in the puma (Puma concolor)". Journal of Virology. 70 (10): 6682–6693. doi:10.1128/JVI.70.10.6682-6693.1996. ISSN 0022-538X. PMC 190710. PMID 8794304.
  32. ^ Hofmann-Lehmann, R; Fehr, D; Grob, M; Elgizoli, M; Packer, C; Martenson, J S; O'Brien, S J; Lutz, H (September 1996). "Prevalence of antibodies to feline parvovirus, calicivirus, herpesvirus, coronavirus, and immunodeficiency virus and of feline leukemia virus antigen and the interrelationship of these viral infections in free-ranging lions in east Africa". Clinical and Diagnostic Laboratory Immunology. 3 (5): 554–562. doi:10.1128/CDLI.3.5.554-562.1996. ISSN 1071-412X. PMC 170405. PMID 8877134.
  33. ^ Quérat, G.; Barban, V.; Sauze, N.; Vigne, R.; Payne, A.; York, D.; de Villiers, E.M.; Verwoerd, D.W. (May 1987). "Characteristics of a novel lentivirus derived from South African sheep with pulmonary adenocarcinoma (jaagsiekte)". Virology. 158 (1): 158–167. doi:10.1016/0042-6822(87)90249-2. PMID 2437695.
  34. ^ Hirsch, V (December 1995). "Phylogeny and natural history of the primate lentiviruses, SIV and HIV". Current Opinion in Genetics & Development. 5 (6): 798–806. doi:10.1016/0959-437X(95)80014-V. PMID 8745080.
  35. ^ a b c d Johnson, W. E. (2006-01-06). "The Late Miocene Radiation of Modern Felidae: A Genetic Assessment". Science. 311 (5757): 73–77. Bibcode:2006Sci...311...73J. doi:10.1126/science.1122277. ISSN 0036-8075. PMID 16400146. S2CID 41672825.
  36. ^ Eizirik, Eduardo; Kim, Jae-Heup; Menotti-Raymond, Marilyn; Crawshaw JR., Peter G.; O'Brien, Stephen J.; Johnson, Warren E. (January 2001). "Phylogeography, population history and conservation genetics of jaguars (Panthera onca, Mammalia, Felidae)". Molecular Ecology. 10 (1): 65–79. doi:10.1046/j.1365-294X.2001.01144.x. ISSN 0962-1083. PMID 11251788. S2CID 3916428.
  37. ^ a b c Carpenter, M. A.; Brown, E. W.; Culver, M.; Johnson, W. E.; Pecon-Slattery, J.; Brousset, D.; O'Brien, S. J. (October 1996). "Genetic and phylogenetic divergence of feline immunodeficiency virus in the puma (Puma concolor)". Journal of Virology. 70 (10): 6682–6693. doi:10.1128/JVI.70.10.6682-6693.1996. ISSN 0022-538X. PMC 190710. PMID 8794304.
  38. ^ Antunes, Agostinho; Troyer, Jennifer L.; Roelke, Melody E.; Pecon-Slattery, Jill; Packer, Craig; Winterbach, Christiaan; Winterbach, Hanlie; Hemson, Graham; Frank, Laurence; Stander, Philip; Siefert, Ludwig (2008-11-07). Estoup, Arnaud (ed.). "The Evolutionary Dynamics of the Lion Panthera leo Revealed by Host and Viral Population Genomics". PLOS Genetics. 4 (11): e1000251. doi:10.1371/journal.pgen.1000251. ISSN 1553-7404. PMC 2572142. PMID 18989457.
  39. ^ a b Barr, Margaret C; Zou, Lily; Long, Fan; Hoose, Wendy A; Avery, Roger J (February 1997). "Proviral Organization and Sequence Analysis of Feline Immunodeficiency Virus Isolated from a Pallas' Cat". Virology. 228 (1): 84–91. doi:10.1006/viro.1996.8358. PMID 9024812.
  40. ^ Brown, E W; Yuhki, N; Packer, C; O'Brien, S J (1994). "A lion lentivirus related to feline immunodeficiency virus: epidemiologic and phylogenetic aspects". Journal of Virology. 68 (9): 5953–5968. doi:10.1128/JVI.68.9.5953-5968.1994. ISSN 0022-538X. PMC 237001. PMID 8057472.
  41. ^ Lutz, H.; Isenbügel, E.; Lehmann, R.; Sabapara, R.H.; Wolfensberger, C. (December 1992). "Retrovirus infections in non-domestic felids: serological studies and attempts to isolate a lentivirus". Veterinary Immunology and Immunopathology. 35 (1–2): 215–224. doi:10.1016/0165-2427(92)90133-B. PMID 1337398.
  42. ^ Olmsted, R. A.; Hirsch, V. M.; Purcell, R. H.; Johnson, P. R. (1989-10-01). "Nucleotide sequence analysis of feline immunodeficiency virus: genome organization and relationship to other lentiviruses". Proceedings of the National Academy of Sciences. 86 (20): 8088–8092. Bibcode:1989PNAS...86.8088O. doi:10.1073/pnas.86.20.8088. ISSN 0027-8424. PMC 298220. PMID 2813380.
  43. ^ Fromont, E.; Pontier, D.; Sager, A.; Jouquelet, E.; Artois, M.; Léger, F.; Stahl, P.; Bourguemestre, F. (2000). "Prevalence and pathogenicity of retroviruses in wildcats in France". Veterinary Record. 146 (11): 317–319. doi:10.1136/vr.146.11.317. ISSN 2042-7670. PMID 10766116. S2CID 34803834.
  44. ^ Troyer, Jennifer L.; Pecon-Slattery, Jill; Roelke, Melody E.; Johnson, Warren; VandeWoude, Sue; Vazquez-Salat, Nuria; Brown, Meredith; Frank, Laurence; Woodroffe, Rosie; Winterbach, Christiaan; Winterbach, Hanlie (2005-07-01). "Seroprevalence and Genomic Divergence of Circulating Strains of Feline Immunodeficiency Virus among Felidae and Hyaenidae Species". Journal of Virology. 79 (13): 8282–8294. doi:10.1128/JVI.79.13.8282-8294.2005. ISSN 0022-538X. PMC 1143723. PMID 15956574.

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