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Journal of Translational Medicine

, 9:S8

First Online: 27 January 2011DOI: 10.1186-1479-5876-9-S1-S8

Cite this article as: Mariani, S.A., Vicenzi, E. & Poli, G. J Transl Med 2011 9Suppl 1: S8. doi:10.1186-1479-5876-9-S1-S8

Abstract

Susceptibility to infection by the human immunodeficiency virus type-1 HIV-1, both in vitro and in vivo, requires the interaction between its envelope Env glycoprotein gp120 Env and the primary receptor R, CD4, and Co-R, either CCR5 or CXCR4, members of the chemokine receptor family. CCR5-dependent R5 viruses are responsible for both inter-individual transmission and for sustaining the viral pandemics, while CXCR4-using viruses, usually dualtropic R5X4, emerge in ca. 50% of individuals only in the late, immunologically suppressed stage of disease. The hypothesis that such a major biological asymmetry is explained exclusively by the availability of cells expressing CCR5 or CXCR4 is challenged by several evidences. In this regard, binding of the HIV-1 gp120 Env to the entry R complex, i.e. CD4 and a chemokine R, leads to two major events: virion-cell membrane fusion and a cascade of cell signaling. While the fusion-entry process has been well defined, the role of R-Co-R signaling in the HIV-1 life cycle has been less characterized. Indeed, depending on the cellular model studied, the capacity of HIV-1 to trigger a flow of events favoring either its own latency or replication remains a debated issue. In this article, we will review the major findings related to the role of HIV R-Co-R signaling in the steps following viral entry and leading to viral spreading in CD4 T lymphocytes.

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Autor: Samanta A Mariani - Elisa Vicenzi - Guido Poli

Fuente: https://link.springer.com/







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