Inserm U552, Recherche antivirale, Hôpital Bichat-Claude-Bernard, 46, rue Henri-Huchard, 75018 Paris, Université Paris 7, Denis-Diderot
HIV-1 tropism is essentially defined on the basis of the chemokine receptor used for the cell-entry process, although other parameters play a role in defining the spectrum of potential target cells. Irrespective of the route of transmission, viruses that use CCR5 appear to be favored during transmission and/or early amplification in the new host. Several parameters of different nature (cellular, viral and immune) may participate to this phenomenon. CCR5-using viruses persist throughout infection, they diversify and evolve in the new host under the immune selective pressure and by competition. In a percentage of patients, viral variants able to use CXCR4 may emerge late in infection. Virus entry via CXCR4 allows to infect different cell types and tissues, and it is associated with faster disease progression. Factors potentially implicated in the delayed emergence of CXCR4-using variants and the consequences of the tropism switch are described.