The virus–receptor interaction in the replication of feline immunodeficiency virus (FIV)

Abstract

Graphical abstract

Central and peripheral reservoirs of feline immunodeficiency virus in cats: a review

“…These CRD2-independent isolates, which are characteristic of the later stages of FIV infection, were also shown to be less efficient for transmission and replication during acute infection when compared to CRD2-dependent isolates in experimental infection studies. These findings generated a hypothesis that CRD2-dependent FIV isolates, which are efficiently transmitted in vivo and able to achieve higher virus loads during early infection, may be analogous to CCR5-dependent HIV-1 isolates that also transmit much more efficiently during primary HIV-1 infection of humans when compared to later-emerging CXCR4-tropic variants in HIV-1 infection [49,50]. Specific CD4+ T cell subsets that may be specific targets for these CRD2-dependent FIV isolates and their role in viral pathogenesis remain to be determined.…”

“…Table 1 summarizes key studies that have identified FIV cell reservoirs and the modalities used to detect infection or susceptibility to infection. It is important to note that the leukocyte subsets that have proven most consistently infected in vivo and susceptible to infection in vitro are CD4+ T cells and monocyte/ macrophages, which are also target cell reservoirs for HIV [13,49,54,[60][61][62]. Evidence thus far is conflicting regarding productive infection of dendritic cells in vivo [29,30,54,63], although multiple studies support productive FIV infection of cultivated dendritic cells [43,63,64].…”

“…Accordingly, HIV-1 and FIV utilize similar strategies for entry of target cells by Env binding of a primary cell surface receptor, CD4 and CD134, respectively, that facilitates Env interactions with either the CCR5 (HIV-1 only) or CXCR4 (HIV-1 and FIV) chemokine coreceptors [37,49]. Furthermore, targeting CD4+ T cells through either CD4 or CD134 surface proteins results in a similar immunopathogenesis, characterized by a progressive CD4+ T cell depletion, lymphoid depletion and immune exhaustion during the chronic phases of HIV-1 and FIV infections, respectively.…”

Antiviral efficacy of nine nucleoside reverse transcriptase inhibitors against feline immunodeficiency virus in feline peripheral blood mononuclear cells

“…antagonists will prevent binding of the FIV major SU glycoprotein to this receptor and prevent infection of the target cell. In the whole cell entry process of the virus, this step lies between the initial attachment of the virus to the CD134 receptor and the fusion of the virus with the cell membrane mediated by gp41 (DE CLERCQ, 2009;WILLETT and HOSIE, 2013). The amino acid sequence of feline and human CXCR4 is highly similar (94.9% sequence identity) (WILLETT et al, 1997b) and hence CXCR4 antagonists developed against HIV could also be effective against FIV (MOHAMMADI and BIENZLE, 2012).…”

Single aromatic residue location alters nucleic acid binding and chaperone function of FIV nucleocapsid protein

“…FIV can be transmitted among various feline species. However, there is no evidence of FIV transmission to human beings, despite efficient infection of CD4+ T-cells through interactions with CD134 and CXCR4 (Willett and Hosie, 2013); this is possibly due to poor recognition of the FIV promoter (5′-LTR) in human cells (Mustafa et al, 2005). As the only non-primate lentivirus to cause an AIDS- like syndrome, FIV is an excellent animal model for human immunodeficiency virus type 1 (HIV-1) pathogenesis (Luttge and Freed, 2010) and an attractive system to develop anti-retroviral vaccines, drugs and non-pathogenic gene therapy vectors.…”