Abstract
Feline immunodeficiency virus (FIV) is a lentivirus associated with an AIDS-like syndrome in the domestic cat. The hallmark of the infection is a gradual depletion of CD4+helper T lymphocytes. The FIV enter cells by sequential interaction between its envelope glycoprotein (ENV) and the primary receptors, CD 134, and subsequently with the co-receptor the chemokine recepotrs CXCR4. The expression of those receptors is restricted to activated cells. The FIV possesses a broad tropism for CD4+lymphocytes, CD8+lymphocytes, B lymphocytes and monocyte-derived macrophages. CD4+ cell has the greatest provirus burden during the acute phase of infection but during the chronic phase, asymptomatic stage, B cells bears the major FIV provirus. This change could be the result of the different way that the ENV interacts with its receptors. This review is a brief overview of the interaction between FIV and its receptors. The molecular mechanisms of this relation and the viral cell tropism with disease progression not only did are important to development of vaccine approaches and therapeutic interventions but also to the understanding of pathogenesis of lentiviruses. DOI: http://dx.doi.org/10.17525/vrr.v15i1.39
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