T cell subpopulations mediating inhibition of feline immunodeficiency virus replication in mucosally infected cats

Downmodulation of CD3ε expression in CD8α + β − T cells of feline immunodeficiency virus-infected cats

“…Previously, we found that feline CD (fCD)8a + b 2 and fCD8a + b low cells increased in number in the peripheral blood of FIV-infected cats (Shimojima et al, 1998a). These subsets were reported to play roles in the suppression of FIV replication (Bucci et al, 1998;Flynn et al, 2002;Gebhard et al, 1999;Shimojima et al, 2004). The induction of similar subpopulations was also confirmed in human diseases, such as HIV infection (Schmitz et al, 1998).…”

FIV as a Model for HIV: An Overview

“…212,334,374,[376][377][378][379] A similar expansion of an CD8a + b low T-cell subset has also been observed in HIV-1 infection. 380,381 Furthermore, this cell population has been shown to express markers associated with lymphocyte activation and adhesion and to exhibit antiviral activity 311,376,379 comparable to a noncytolytic CD8 antiviral activity previously described for HIV-1 infection. 382,383 FIV-induced immunodeficiency is characterized by other defects that are similar to those described for HIV-1 infection and include reduced proliferative T-cell responses to mitogens, dysregulation of cytokine networks, and humoral immune response deficits.…”

“…Detection of virus in semen of infected cats has been observed 303,304 and experimental infection by artificial insemination has also been reported. 305,306 Numerous experimental studies have shown the feasibility of infection by the vaginal route [16][17][18][21][22][23][307][308][309][310][311] and demonstrated the utility Lymphoid follicular hyperplasia Same as FIV (early) and CD8a+blow T-cell subset expansion, followed by lymphoid depletion, CD4 T-cell depletion, cytokine dysregulation, and AIDS of this feline animal model for examination of mucosal transmission and viral pathogenesis. Although these observations and experimental studies suggest the possibility of sexual transmission of FIV, definitive observations of natural transmission by this route so far have not been reported.…”

“…364,414 In vitro syncytia formation of FIV-infected cells has been well documented and is due to viral envelope fusion with cellular membranes and associated with specific cell types and FIV strains. 224,238,245,248,311,[415][416][417] Programmed cell death or apoptosis has been hypothesized as one of several important mechanisms involved in FIV/HIV-1 immunopathogenesis based on observations of apoptotic cells in virus-infected cell cultures [418][419][420][421] and in PBMC [422][423][424][425] and lymphoid and thymic tissues 22,425,426 isolated from FIV-infected cats. Recent reports have shown that binding of cell surface chemokine and virus receptor CXCR4 by FIV TM may trigger apoptosis.…”

“…376,499 However, these studies also show conflicting data on the issue of a restriction of antiviral activity to the CD8a + b low subset with some data suggesting that both CD8a + b low and CD8a + bsubsets are capable of noncytolytic antiviral activity. 311,379,492,[499][500][501][502] A lack of agreement is also apparent among studies regarding correlations between CD8 T-cell noncytolytic antiviral activity and either CD4 T-cell counts, clinical disease in vivo, distribution patterns of this cell subset in blood and lymphoid tissues, or persistent expansion of the CD8a + b low subset throughout the course of virus infection. 212,308,376,379,503 More recent reports indicate that CD8 antiviral activity production could be enhanced or induced in vitro by exposure to either virus-infected cells or to cells expressing an irrelevant antigen, but is not induced by mitogen activation.…”