12/5/2023 0 Comments Feline hiv transmission![]() Also like other lentiviruses, FIV uses a tRNA lys primer-binding site to prime first strand synthesis by reverse transcriptase (RT). The integrated provirus is bordered by long terminal repeats (LTRs) and possesses gag, pol, and env genes, common elements of all retroviruses. The length of the FIV genome is around 9400 nucleotides, approximating that of HIV and other lentiviruses. As with human AIDS, FIV-infected cats ultimately succumb to opportunistic infections.įIV and HIV share many features in their genomes, but also have important differences that influence the utility of comparative studies ( 27– 29). Neurological manifestations are often evident ( 12 22– 25), noted by delays auditory evoked and visual evoked potential changes ( 22, 23) and marked alterations in sleep patterns in experimentally infected animals ( 26). Lymphoid tissue alterations are similar to those noted with primate lentivirus infections, including thymic depletion, lymphoid hyperplasia, plasmacytosis, and terminal lymphoid depletion ( 2, 8– 10, 13, 19, 21). The terminal phase is marked by further decline in the antiviral response, with resultant increase in plasma viral load and onset of clinical symptoms of immunodeficiency. As with HIV-infected people, FIV-infected cats vary in the response to infection, with some animals remaining phenotypically normal throughout the course of the infection, while others suffer from assorted maladies including oral lesions, febrile episodes, bouts of diarrhea, and dehydration. The rate of progression of the disease can dependant on the genotype of the infecting FIV and is also likely influenced by undefined genetic determinants of the particular cat. As with HIV infections in man, this latent phase can be quite protracted in the cat, lasting from several months to several years. The acute phase is followed by what is often referred to as an “asymptomatic”, or Latent phase denoted by relative quiescence of the infection in the face of strong antiviral immune responses, with lower viral titers and minimal clinical symptoms. However, most infected cats exhibit an increase in CD8 + T cells along with a strong humoral antibody response which allows them to weather this initial phase of the infection ( 19, 20). During this time, CD4 + T cells decline as well as neutrophils and a percentage of cats will not recover and require humane euthanasia in experimental infections. The course of the disease is also similar in cats and man, with a relatively short acute phase measure in weeks and denoted by increasing viral loads, febrile episodes, weight loss, lymphadenopathy, and neutropenia. Although CD4 + cell decline is a hallmark of FIV infection, FIV has a broader lymphocyte tropism than CD4 + T cells, with infection also evident in at least a subset of CD8 + T cells and B cells in vitro and in vivo ( 16– 18). FIV RNA has also been demonstrated in association with follicular dendritic cells (FDC) ( 13– 15). ![]() In vivo tissue tropism studies ( 11, 12) have demonstrated viral RNA in T cells, macrophages, and CNS cells. FIV is tropic for T cells ( 1– 6) macrophages ( 7– 10), and central nervous system cells (CNS ( 11, 12)). Like HIV, FIV can be transmitted via mucosal exposure, blood transfer, and vertically via prenatal and postnatal routes. ![]() FIV causes an AIDS-like syndrome in the domestic cat, with many similarities to HIV-induced AIDS in man ( 1 Table 1). ![]()
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