HIV-2 infection and chemokine receptors usage - clues to reduced virulence of HIV-2.
Human immunodeficiency virus type 1 (HIV-1) and type 2 (HIV-2) are the causative agents of Acquired Immunodeficiency Syndrome (AIDS). Without therapeutic intervention, HIV-1 or HIV-2 infections in humans are characterized by a gradual and irreversible immunologic failure that ultimately leads to the onset of a severe immunodeficiency that constitutes the hallmark of AIDS. In the last two decades AIDS has evolved into a global epidemic affecting millions of persons worldwide. Although sharing several identical properties, HIV-1 and HIV-2 have shown some important differences in vivo. In fact, a significant amount of epidemiologic, clinical and virologic data suggest that HIV-2 is in general less virulent than HIV-1. This reduced virulence is revealed by the longer asymptomatic period and the smaller transmission rate that characteristically are observed in HIV-2 infection. In this context, studies using HIV-2 as a model of a naturally less pathogenic infection could bring important new insights to HIV pathogenesis opening to new strategies to vaccines or therapeutic design. The reasons underlying the reduced pathogenicity of HIV-2 are still essentially unknown and surely are the outcome of a combination of distinct factors. In this review we will discuss the importance and the possible implications in HIV-2 pathogenesis, particularly during the asymptomatic period, of a less fitted interaction between viral envelope glycoproteins and cellular receptors that have been described in the way HIV-2 and HIV-1 use these receptors.
Azevedo-Pereira
José Miguel
JM
Unidade dos Retrovirus e Infecções Associadas, Centro de Patogénese Molecular, Faculdade de Farmácia, Universidade de Lisboa, Portugal. Miguel.Pereira@ff.ul.pt
Santos-Costa
Quirina
Q
Moniz-Pereira
José
J
D015658:HIV Infections / Q000453:epidemiology / Q000821:virology*; D015498:HIV-2 / Q000378:metabolism / Q000472:pathogenicity*; D006801:Humans; D019713:Receptors, CCR5 / Q000378:metabolism*; D019718:Receptors, CXCR4 / Q000378:metabolism*; D014774:Virulence
D019713:Receptors, CCR5; D019718:Receptors, CXCR4