In vivo lymphocyte tropism of feline immunodeficiency virus

English, Robert V.; Johnson, Calvin M.; Gebhard, David F.; Tompkins, Mary B.

doi:10.1128/jvi.67.9.5175-5186.1993

Cited by 182 publications

(89 citation statements)

References 33 publications

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“…CD134 -the primary receptor for FIV -is a T-cell activation marker and a co-stimulatory molecule and its expression is strictly confined to CD4 + T-cells [106]. With CD4 + T-cells constituting the major target for FIV early in infection [107,108], expansion of this subpopulation (through, e.g. vaccination) would provide the virus with an ideal opportunity for its replication [109].…”

Section: Fiv Vaccine Candidatesmentioning

confidence: 99%

Vaccine-induced enhancement of viral infections

Huisman

Martina

Rimmelzwaan

et al. 2009

Vaccine

163

134

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Examples of vaccine-induced enhancement of susceptibility to virus infection or of aberrant viral pathogenesis have been documented for infections by members of different virus families. Several mechanisms, many of which still are poorly understood, are at the basis of this phenomenon. Vaccine development for lentivirus infections in general, and for HIV/AIDS in particular, has been little successful. Certain experimental lentiviral vaccines even proved to be counterproductive: they rendered vaccinated subjects more susceptible to infection rather than protecting them. For vaccine-induced enhanced susceptibility to infection with certain viruses like feline coronavirus, Dengue virus, and feline immunodeficiency virus, it has been shown that antibody-dependent enhancement (ADE) plays an important role. Other mechanisms may, either in the absence of or in combination with ADE, be involved. Consequently, vaccine-induced enhancement has been a major stumble block in the development of certain flavi-, corona-, paramyxo-, and lentivirus vaccines. Also recent failures in the development of a vaccine against HIV may at least in part be attributed to induction of enhanced susceptibility to infection. There may well be a delicate balance between the induction of protective immunity on the one hand and the induction of enhanced susceptibility on the other. The present paper reviews the currently known mechanisms of vaccine-induced enhancement of susceptibility to virus infection or of aberrant viral pathogenesis.

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Section: Fiv Vaccine Candidatesmentioning

confidence: 99%

Vaccine-induced enhancement of viral infections

Huisman

Martina

Rimmelzwaan

et al. 2009

Vaccine

163

134

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“…This stage is also characterised by rapidly increasing viral loads, weight loss, lymphoadenopathy and neutropoenia. The initial burst of viraemia is associated with infection of CD4+ and CD8+ T lymphocytes [76,77] and a marked decline of CD4+ lymphocytes in circulation. At this stage virus is found throughout the lymphoid tissues, replicating in thymus, regional lymph nodes and mucosa-associated lymphoid tissues [77,78].…”

Section: Diseasementioning

confidence: 99%

Important mammalian veterinary viral immunodiseases and their control

Patel¹,

Heldens

Bakonyi

et al. 2012

Vaccine

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This paper offers an overview of important veterinary viral diseases of mammals stemming from aberrant immune response. Diseases reviewed comprise those due to lentiviruses of equine infectious anaemia, visna/maedi and caprine arthritis encephalitis and feline immunodeficiency. Diseases caused by viruses of feline infectious peritonitis, feline leukaemia, canine distemper and aquatic counterparts, Aleutian disease and malignant catarrhal fever. We also consider prospects of immunoprophylaxis for the diseases and briefly other control measures. It should be realised that the outlook for effective vaccines for many of the diseases is remote. This paper describes the current status of vaccine research and the difficulties encountered during their development.

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“…Feline immunodeficiency virus (FIV) is a lentivirus of domestic cats found associated with an AIDS-like syndrome in infected animals. As with HIV in humans, the cat virus primarily infects T-cells of the CD4 lineage (Ackley et al, 1990;Novotney et al, 1990;Brown et al, 1991;Torten et al, 1991;Willett et al, 1991;Hoffmann-Fezer et al, 1992), but also infects CD8 T-cells, monocytes/macrophages, and a subset of IgG-bearing B cells in vivo (Brunner and Pedersen, 1989;Brown et al, 1991;English et al, 1993;Dean et al, 1996) and in vitro (Brunner and Pedersen, 1989). Additionally, certain FIVs will productively infect some continuous feline cell lines, such as Crandell feline kidney cells (CrFK) and a glial cell line derived from cat brain, G355-5 (Phillips et al, 1990;Waters et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

FIV infection of IL-2-dependent and -independent feline lymphocyte lines: Host cells range distinctions and specific cytokine upregulation

Lerner¹,

Grant²,

Parseval³

et al. 1998

Veterinary Immunology and Immunopathology

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We have analyzed the ability of three molecular clones of feline immunodeficiency virus (FIV) and an ex vivo variant to infect nine distinct specific-pathogen-free feline cell lines in tissue culture. The purpose of these studies was to elucidate mechanisms by which host cells regulate the level of virus infection and expression and to assess host cell cytokine responses to virus infection. Cells used for the analyzes included four IL-2-dependent continuous T-cell lines (104-C1, 104-C7, MCH5-4 and DB FeTs) which arose from long-term passage, followed by limiting dilution cloning of peripheral blood mononuclear cells (PBMCs); two IL-2-independent T-cell lines (104-C1DL and MCH5-4DL) which originated from two of the IL-2-dependent lines, 104-C1 and MCH5-4; respectively; Crandell feline kidney cells (CrFK); G355-5 brain-derived glial cells; and the T-cell lymphoma line, 3201. Cells were infected with FIV-PPR, FIV-34TF10, FIV 34TF10orf2rep, and a variant arising from FIV-PPR during ex vivo passage on 104-C1DL cells, termed FIV-PPRglial. Infection of the IL-2-dependent T-cell line, 104-C1, by FIV-PPR resulted in the specific and distinct upregulation of cytokine expression. In particular, these cells doubled their expression of the pleiotropic cytokines, interleukin-4 and interleukin-12 after FIV infection. Interferon-gamma production also increased after infection with FIV whereas, TNFalpha expression remained constant. Also, a marked upregulation of MHC class II expression was noted post infection of MCH5-4 and 104-C1 cells with FIV-PPR. Similar results were obtained after infection with FIV-34TF10orf2rep, indicating that the upregulation of cytokine expression is not an isolate-specific phenomenon. Changes in cytokine and class II expression are similar to various reports for the in vivo cytokine alterations in FIV, SIV and HIV infections. The ex vivo infection of these cell lines offers amanipulable system to examine the mechanism(s) by which lentiviruses alter cytokine expression.

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In vivo lymphocyte tropism of feline immunodeficiency virus

Cited by 182 publications

References 33 publications

Vaccine-induced enhancement of viral infections

Vaccine-induced enhancement of viral infections

Important mammalian veterinary viral immunodiseases and their control

FIV infection of IL-2-dependent and -independent feline lymphocyte lines: Host cells range distinctions and specific cytokine upregulation

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