Studies on feline CD8+ T cell non-cytolytic anti-feline immunodeficiency virus (FIV) activity

Hohdatsu, Tsutomu; Miyagawa, N; Ohkubo, M; Kida, Kouji; Koyama, Hiroyuki

doi:10.1007/s007050070006

Cited by 12 publications

(8 citation statements)

References 32 publications

(33 reference statements)

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“…ϩ T cells release soluble factors and suppress the synthesis of FIV mRNA from FIV proviral DNA, thereby inhibiting the expression of FIV proteins on the surface of infected cells (10,12). Thus, CD4 ϩ cells evade damage and can live while suppressing FIV replication.…”

Section: Discussionmentioning

confidence: 99%

Ability of CD8⁺ T Cell Anti‐Feline Immunodeficiency Virus Activity Correlated with Peripheral CD4⁺ T Cell Counts and Plasma Viremia

Hohdatsu

Yamazaki

Yamada

et al. 2003

Microbiology and Immunology

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In the host defense mechanism against feline immunodeficiency virus (FIV) infection, CD8+ T cells specifically attack virus‐infected cells and suppress the replication of the virus in a non‐cytolytic manner by secreting soluble factors. In this study, we measured CD8+ T cell anti‐FIV activity in 30 FIV‐infected cats. We investigated its relationship with the number of peripheral blood lymphocytes, particularly the CD4+ T cell and CD8+ T cell counts, and the relationship between anti‐FIV activity and the number of T cells of CD8α+βlo and CD8α+β− phenotypes. A clearly significant correlation was observed between anti‐FIV activity and the number of CD4+ T cells. A weaker anti‐FIV activity was associated with a greater decrease in the number of CD4+ T cells. However, there was no significant correlation between anti‐FIV activity and the number of B or CD8+ T cells. Compared with SPF cats, FIV‐infected cats had significantly higher CD8α+βlo T cell and CD8α+β− T cell counts, but, no significant correlation was observed between these cell counts and anti‐FIV activity. This anti‐FIV activity significantly correlated with plasma viremia, which was detected in cats with a weak anti‐FIV activity. These results suggest that the anti‐FIV activity of CD8+ T cells plays an important role in plasma viremia and the maintenance of CD4+ T cells in the body. It is unlikely that CD8α+βlo or CD8α+β− T cells appearing after FIV infection represent a phenotype of CD8+ cells with anti‐FIV activity.

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Section: Discussionmentioning

confidence: 99%

Ability of CD8⁺ T Cell Anti‐Feline Immunodeficiency Virus Activity Correlated with Peripheral CD4⁺ T Cell Counts and Plasma Viremia

Hohdatsu

Yamazaki

Yamada

et al. 2003

Microbiology and Immunology

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“…Detection of non-cytolytic antiviral activity can be assayed in vitro by depletion of the CD8+ population from the sample and correlates temporally with the reduction in virus burden during the acute phase of infection [26,81,96,98]. Noncytolytic activity can be detected as early as 1 week following infection, is seen prior to detection of cytolytic activity, and can be detected in multiple lymphoid tissues [81].…”

Section: Cd8 Effector Activitymentioning

confidence: 98%

Transmission and Immunopathogenesis of FIV in Cats as a Model for HIV

Burkhard

Dean²

2003

CHR

119

139

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The feline immunodeficiency virus (FIV) model provides a system to study lentivirus transmission, virus kinetics, pathogenesis, host responses, and immune dysfunction in a natural, out-bred host, under controlled conditions with specific-pathogen-free animals. The diversity of primary FIV strains can be exploited to mirror the range of disease manifestations associated with HIV infection. FIV is infectious via intravenous, intraperitoneal, intradermal, or subcutaneous injection as well as by atraumatic instillation onto the oral, vaginal, or rectal mucosa. Together, these features allow investigators to model specific aspects of HIV infection in a highly relevant and relatively inexpensive animal model. Well-developed areas of the FIV model include: (1) transmission of cell-associated as well as cell-free virus; (2) mucosal infectivity and immunopathogenesis; (3) vertical transmission; (4) acquired immunodeficiency including defects of the innate immune system; (5) thymic dysfunction; (6) neurotropism and neuropathogenesis; (7) host-virus interactions and the role of specific gene products; (8) efficacy of antiviral therapy; and (9) efficacy and immune correlates of experimental vaccines. This review will encompass areas specific to transmission and immunopathogenesis.

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“…These CD8+T cells are thought to play an important role in the control of systemic and brain infection Gebhard et al 1999;Hohdatsu et al 2000;Hohdatsu et al 2002). Eventually, a severe immunodeficiency develops with accompanying opportunistic infections (English et al 1994).…”

Section: Fiv: a Lentivirus Similar To Hivmentioning

confidence: 99%

Feline Immunodeficiency Virus Neuropathogenesis: From Cats to Calcium

Meeker

2006

Jrnl Neuroimmune Pharm

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Invasion of human immunodeficiency virus (HIV) into the central and peripheral nervous system produces a wide range of neurological symptoms, which continue to persist even with adequate therapeutic suppression of the systemic viremia. The development of therapies designed to prevent the neurological complications of HIV require a detailed understanding of the mechanisms of virus penetration into the nervous system, infection, and subsequent neuropathogenesis. These processes, however, are difficult to study in humans. The identification of animal lentiviruses similar to HIV has provided useful models of HIV infection that have greatly facilitated these efforts. This review summarizes contributions made from in vitro and in vivo studies on the infectious and pathological interactions of feline immunodeficiency virus (FIV) with the nervous system. In vivo studies on FIV have provided insights into the natural progression of CNS disease as well as the contribution of various risk factors. In vitro studies have contributed to our understanding of immune cell trafficking, CNS infection and neuropathogenesis. Together, these studies have made unique contributions to our understanding of (1) lentiviral interactions at the blood-cerebrospinal fluid (CSF) barrier within the choroid plexus, (2) early FIV invasion and pathogenesis in the brain, and (3) lentiviral effects on intracellular calcium deregulation and neuronal dysfunction. The ability to combine in vitro and in vivo studies on FIV offers enormous potential to explore neuropathogenic mechanisms and generate information necessary for the development of effective therapeutic interventions.

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Studies on feline CD8+ T cell non-cytolytic anti-feline immunodeficiency virus (FIV) activity

Cited by 12 publications

References 32 publications

Ability of CD8⁺ T Cell Anti‐Feline Immunodeficiency Virus Activity Correlated with Peripheral CD4⁺ T Cell Counts and Plasma Viremia

Ability of CD8⁺ T Cell Anti‐Feline Immunodeficiency Virus Activity Correlated with Peripheral CD4⁺ T Cell Counts and Plasma Viremia

Transmission and Immunopathogenesis of FIV in Cats as a Model for HIV

Feline Immunodeficiency Virus Neuropathogenesis: From Cats to Calcium

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Studies on feline CD8+ T cell non-cytolytic anti-feline immunodeficiency virus (FIV) activity

Cited by 12 publications

References 32 publications

Ability of CD8+ T Cell Anti‐Feline Immunodeficiency Virus Activity Correlated with Peripheral CD4+ T Cell Counts and Plasma Viremia

Ability of CD8+ T Cell Anti‐Feline Immunodeficiency Virus Activity Correlated with Peripheral CD4+ T Cell Counts and Plasma Viremia

Transmission and Immunopathogenesis of FIV in Cats as a Model for HIV

Feline Immunodeficiency Virus Neuropathogenesis: From Cats to Calcium

Contact Info

Product

Resources

About

Ability of CD8⁺ T Cell Anti‐Feline Immunodeficiency Virus Activity Correlated with Peripheral CD4⁺ T Cell Counts and Plasma Viremia

Ability of CD8⁺ T Cell Anti‐Feline Immunodeficiency Virus Activity Correlated with Peripheral CD4⁺ T Cell Counts and Plasma Viremia