Host factors influencing susceptibility to HIV infection and AIDS progression

Abstract

Transmission of HIV first results in an acute infection, followed by an apparently asymptomatic period that averages ten years. In the absence of antiretroviral treatment, most patients progress into a generalized immune dysfunction that culminates in death. The length of the asymptomatic period varies, and in rare cases infected individuals never progress to AIDS. Other individuals whose behavioral traits put them at high-risk of HIV transmission, surprisingly appear resistant and never succumb to infection. These unique cases highlight the fact that susceptibility to HIV infection and progression to disease are complex traits modulated by environmental and genetic factors. Recent evidence has indicated that natural variations in host genes can influence the outcome of HIV infection and its transmission. In this review we summarize the available literature on the roles of cellular factors and their genetic variation in modulating HIV infection and disease progression.

Innate, Adaptive and Intrinsic Immunity in Human Immunodeficiency Virus Infection

“…Defensins are small natural endogenous cysteine rich cationic peptides with high anti-HIV1 activity (Lama and Planelles, 2007). Mammalian defensins are classified into alpha-, beta-and theta defensins according to structural characteristics (Rodrıguez-Garcıa et al, 2010).…”

“…In human's α-defensins and β-defensins are shown to produce anti HIV1 activity (Rodrıguez-Garcıa et al, 2010). There are 6 varieties of α-defensins or Human Neutrophil Peptides (HNP), of which HNP 1-3 are primarily produced by neutrophils (Lama and Planelles, 2007). α-defensins are known to block HIV-1 entry at several steps.…”

“…α-defensins are known to block HIV-1 entry at several steps. Apart from membrane disruption of HIV1 by binding to glycoproteins and down regulating the expression CD4 α-defensins 1-3 display multiple immune stimulatory activities such as chemo attraction of naive T cells and immature dendritic cells and induction of cytokine and chemokine production (Rodrıguez-Garcıa et al, 2010;Lama and Planelles, 2007).…”

“…There are six known β-defensins in humans mainly in epithelial cells, β-defensins have a similar mechanism of action to α-defensins 1-3 and are known to viral entry of both X4-and R5-tropic HIV-1 strains (Lama and Planelles, 2007). β-defensins 2 and 3 are also associated with down-modulation of CXCR4, but not CCR5, receptors on T cells (Lama and Planelles, 2007).…”

Non-POU Domain-Containing Octamer-Binding Protein Negatively Regulates HIV-1 Infection in CD4+T Cells

“…There are numerous host factors that may interact directly or indirectly with viral components during HIV-1 replication. 39,40 Many of these interactions occur at early stages of replication resulting in abortive substrates, modification or degradation of viral cDNA, or induction of an innate immune response. As NonO was identified interacting with the HIV-1 PIC, we initially hypothesized that NonO would exert a predominant effect at integration.…”