Determinant genetic factors of resistance to HIV infection and control of AIDS progression: Implications about pathogenesis and therapeutic strategies for HIV eradication - Genetic factors in HIV infection

In this review, we describe and discuss the genetic factors that, up to som e point, determine resistance to the infection and control the progression of the disease in HN-infected individuals. Genetic factors may account for non-progression or slow progression of the disease in some of so called lon g-term non progressors HIV-infected individuals. In general, this group sho ws no symptoms for more than 10 years, while their circulating T CD4+ cells levels remain stable and they usually have a low virus load. Even though n on-progression and rapid progression phenomenon are still not fully underst ood, there probability exists that some class I and class II MHC alleles ar e associated with a greater or smaller risk to develop AIDS. Class I HLA-B* 35 and C omega*04 alleles are the ones commonly associated with the rapid t ransition of the infection into AIDS. In contrast, heterozygosity for class I HLA alleles and, particularly, the absence of HLA-B*35 and C omega*04 ma y contribute to non-progression, Studies which set forward other HLA allele s as possibly faking part of the pathogenic mechanism of non-progression ar e also described; although, relevant methodological problems can be noticed . Furthermore, this review explains and discusses allelic variations for so me of the components of the chemokine receptors family, particularly the ge nes which codify for CCR6 and CCR2 and other genetic factors such as the SD F1-3'. A variant of the alpha SDF1 chemokine gene that have been associated with AIDS' slow progression or non- progression in HN-infected individuals . As a whole, the factors described in this review are those that influence the natural history of the dis-ease due to HN and give an example of what genetic or multigenetic influence can have over the pattern of evolution of HN infection. Finally, we mention the possible implications that the ident ification of the genetic markers has in the pathogenesis of HN disease and in the development of the new therapeutic strategies to control or eliminat e HN.