Progressive immune dysfunction in cats experimentally infected with feline immunodeficiency virus

Abstract

Within 6 months of infection with the Petaluma isolate of feline immunodeficiency virus, specific-pathogenfree domestic cats exhibited a decrease in the percentage and number of circulating CD4+ lymphocytes and in the CD4+/CD8+ T-cell ratio, along with a marginally significant depression of pokeweed mitogen-induced lymphocyte proliferation in vitro. There was no loss of responsiveness to concanavalin A during this stage, and the cats were capable of mounting a satisfactory antibody response to a T-dependent, synthetic polypeptide immunogen. The pokeweed mitogen response deficit became clearly demonstrable by 11 to 12 months postinfection. A decline in the lymphocyte proliferative response to concanavalin A and a diminished ability to mount an in vivo antibody response to the T-dependent immunogen evolved by 25 to 44 months postinfection. Virus infection did not affect the ability of cats to mount an antibody response to a T-independent synthetic polypeptide immunogen. These data indicate that feline immunodeficiency virus produces a slowly progressive deterioration of T-cell function but does not affect the ability of B cells to recognize and respond to a T-independent antigenic stimulus.

FIV vaccine development and its importance to veterinary and human medicine: a review

“…The hallmark of infection is depletion of CD4 peripheral T-cells and reduction of CD4/CD8 ratios (Ackley et al, 1990;Taniguchi et al, 1991;Torten et al, 1991;Hoffmann-Fezer et al, 1992). Decreased CD4 T-cell counts in infected cats have been reported in both natural and experimental infections (Ackley et al, 1990;Hoffmann-Fezer et al, 1992).…”

“…In addition, CD8 T-cells from FIV-infected cats produced soluble suppressor antiviral factors resembling the CD8-mediated antiviral factor (CAF) produced in HIV-positive individuals (Flynn et al, 1999;Choi et al, 2000). Infected cats possess strong T-helper activities (increased gamma interferon and IL-10 production), during early stages of FIV infection which gradually decrease with long-term infection Torten et al, 1991;Hoffmann-Fezer et al, 1992;Bendinelli et al, 1995;Liang et al, 2000). These T-cell dysfunctions and responses in FIV-infected cats closely mimic those of HIV-positive individuals (Rideout et al, 1992;Gebhard et al, 1999).…”

“…These T-cell dysfunctions and responses in FIV-infected cats closely mimic those of HIV-positive individuals (Rideout et al, 1992;Gebhard et al, 1999). B-cell dysfunctions involving suppressed primary antibody response (®rst time the antigen is presented to the B-cells) are less dramatic than T-cell dysfunctions (CD4 loss and CD4/CD8 inversion), and seem to be only in primary antibody responses to T-dependent antigens (Taniguchi et al, 1991;Torten et al, 1991). Virus neutralizing (VN) antibodies to FIV develop shortly after the production of anti-FIV CTL and provide additional immunity (Inoshima et al, 1996).…”

Clinical aspects of feline immunodeficiency and feline leukemia virus infection

“…Several other immunologic abnormalities can be found in FIV-infected cats. Lymphocytes may loose the ability to proliferate in response to stimulation with mitogens or antigens, and priming of lymphocytes by immunogens may be impaired (Hara et al, 1990;Hosie and Jarrett, 1990;Taniguchi et al, 1990;Barlough et al, 1991;Taniguchi et al, 1991;Torten et al, 1991;Bishop et al, 1992a,b). Lymphocyte function may be reduced by altered expression of cell surface molecules, such as CD4, major histocompatibility complex II antigens, or cytokines and cytokine receptors (Willett et al, 1991;Ohno et al, 1992;Rideout et al, 1992;Choi et al, 2000;Mizuno et al, 2003a), or through over-expression of abnormal molecules, such as receptors (Nishimura et al, 2004), leading to disrupted cytokines production or receptor function.…”

Virus–host interaction in feline immunodeficiency virus (FIV) infection

“…The immunosuppression caused by FIV infection manifests as a loss of response to viral antigens, a loss of response to mitogens, and the inability to launch a primary immune response against secondary pathogens [7]. Torten et al [36] observed that, together with the progression of the disease (25-44 months pi), the infected cats exhibited a reduction in their response to T-dependent immunogens but an adequate response to T-independent immunogens. In addition, these researchers observed a reduction in lymphocyte proliferation, which is induced by mitogens in the infected cats.…”