FIV as a Model for HIV: An Overview

Sparger, Ellen E.

doi:10.1007/0-387-25741-1_7

Cited by 30 publications

(53 citation statements)

References 607 publications

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“…Furthermore, despite there being similarities in the pathogenesis of FIV and HIV-1, there are a number of fundamental differences that limit the utility of the cat–FIV system as an animal model. For example, FIV lacks certain accessory genes that are present in HIV-1, but contains ORFs for other basal retroviral proteins that are absent from primate lentiviruses 193 . Furthermore, although FIV uses CXC-chemokine receptor 4 (CXCR4) as a co-receptor, it uses CD134 rather than CD4 as a primary receptor 194 .…”

Section: Small-animal Modelsmentioning

confidence: 99%

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Animal models for HIV/AIDS research

2012

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The AIDS pandemic continues to present us with unique scientific and public health challenges. Although the development of effective antiretroviral therapy has been a major triumph, the emergence of drug resistance requires active management of treatment regimens and the continued development of new antiretroviral drugs. Moreover, despite nearly 30 years of intensive investigation, we still lack the basic scientific knowledge necessary to produce a safe and effective vaccine against HIV-1. Animal models offer obvious advantages in the study of HIV/AIDS, allowing for a more invasive investigation of the disease and for preclinical testing of drugs and vaccines. Advances in humanized mouse models, non-human primate immunogenetics and recombinant challenge viruses have greatly increased the number and sophistication of available mouse and simian models. Understanding the advantages and limitations of each of these models is essential for the design of animal studies to guide the development of vaccines and antiretroviral therapies for the prevention and treatment of HIV-1 infection.

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Section: Small-animal Modelsmentioning

confidence: 99%

“…So, unlike HIV-1, which infects only CD4 + T cells and macrophages, FIV can also infect B cells and CD8 + T cells 195 . The chronic phase of FIV infection is also unpredictable and can be as long as a decade 193 , rendering certain applications of this model impractical. Thus, this model is currently not widely used.…”

Section: Small-animal Modelsmentioning

confidence: 99%

Animal models for HIV/AIDS research

2012

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“…FIV is similar to HIV in genome structure and immunopathogenesis [31,32], and has been utilized as the only naturally-occurring animal model of immunodeficiency for HIV-infection in people [33]. Acute FIV infection results in flu-like symptoms including peripheral lymphadenopathy, neutropenia, and pyrexia [34-36]. During terminal stages of infection, animals exhibit feline acquired immunodeficiency syndrome (FAIDS), which includes opportunistic infections, lymphomas, wasting, and death [37].…”

Section: Reviewmentioning

confidence: 99%

“…Importantly, the orf-A protein has not been shown to have significant transcriptional transactivating activity like HIV tat [42], and FIV is not known to encode any such transcriptional transactivator. In addition to genomic differences, the cellular tropism of FIV is generally thought to be broader than that of HIV as it includes all major subsets of mononuclear leukocytes [34]. However, both FIV and HIV have been shown to infect CD8+ T cells and B cells in addition to the CD4+ T cells and monocytes/macrophages, which are the primary permissive cell types in vivo [43-49].…”

Section: Reviewmentioning

confidence: 99%

Feline immunodeficiency virus latency

2013

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Despite highly effective anti-retroviral therapy, HIV is thought to persist in patients within long-lived cellular reservoirs in the form of a transcriptionally inactive (latent) integrated provirus. Lentiviral latency has therefore come to the forefront of the discussion on the possibility of a cure for HIV infection in humans. Animal models of lentiviral latency provide an essential tool to study mechanisms of latency and therapeutic manipulation. Of the three animal models that have been described, the feline immunodeficiency virus (FIV)-infected cat is the most recent and least characterized. However, several aspects of this model make it attractive for latency research, and it may be complementary to other model systems. This article reviews what is known about FIV latency and chronic FIV infection and how it compares with that of other lentiviruses. It thereby offers a framework for the usefulness of this model in future research aimed at lentiviral eradication.

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“…As is true for all lentiviruses, infection is life-long due to irreversible integration of the provirus into genomes of leukocytes including lymphocytes and macrophages, and may be associated with progressive dysfunction of the immune system. [1] Classically, there are three sequential clinical phases of FIV-infection in cats including the acute, asymptomatic, and terminal acquired immunodeficiency phase. In the acute phase there is infection of multiple leukocyte subsets, prolific viral replication and dissemination to many tissue sites including brain, intestinal tract, and primary and secondary lymphoid organs such as the bone marrow, spleen, and lymph nodes.…”

Section: Introductionmentioning

confidence: 99%

Peripheral and central immune cell reservoirs in tissues from asymptomatic cats chronically infected with feline immunodeficiency virus

et al. 2017

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Feline immunodeficiency virus (FIV) infection in cats results in life-long viral persistence and progressive immunopathology. We have previously described a cohort of experimentally infected cats demonstrating a progressive decline of peripheral blood CD4+ T-cell over six years in the face of apparent peripheral viral latency. More recently we reported findings from this same cohort that revealed popliteal lymph node tissue as sites for ongoing viral replication suggesting that tissue reservoirs are important in FIV immunopathogenesis during the late asymptomatic phase of infection. Results reported herein characterize important tissue reservoirs of active viral replication during the late asymptomatic phase by examining biopsied specimens of spleen, mesenteric lymph node (MLN), and intestine from FIV-infected and uninfected control cats. Peripheral blood collected coincident with harvest of tissues demonstrated severe CD4+ T-cell depletion, undetectable plasma viral gag RNA and rarely detectable peripheral blood mononuclear cell (PBMC)-associated viral RNA (vRNA) by real-time PCR. However, vRNA was detectable in all three tissue sites from three of four FIV-infected cats despite the absence of detectable vRNA in plasma. A novel in situ hybridization assay identified B cell lymphoid follicular domains as microanatomical foci of ongoing FIV replication. Additionally, we demonstrated that CD4+ leukocyte depletion in tissues, and CD4+ and CD21+ leukocytes as important cellular reservoirs of ongoing replication. These findings revealed that tissue reservoirs support foci of ongoing viral replication, in spite of highly restricted viral replication in blood. Lentiviral eradication strategies will need address tissue viral reservoirs.

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FIV as a Model for HIV: An Overview

Cited by 30 publications

References 607 publications

Animal models for HIV/AIDS research

Animal models for HIV/AIDS research

Feline immunodeficiency virus latency

Peripheral and central immune cell reservoirs in tissues from asymptomatic cats chronically infected with feline immunodeficiency virus

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