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• W1534854496 abstract "The natural history and pathogenic processes of human immunodeficiency virus type 1 (HIV1) infection are complex and variable, and depend on many viral and host factors and their interactions (Pantaleo et al., 1997). Individuals are not equal susceptible to the infection and have differences in their viral set points, rates of decline of CD4+ T cells, levels of viremia, emergence of citotoxic T lymphocyte (CTL) escape mutants, and development of opportunistic infections resulting in varying incubation periods of the virus (Kaur & Mehra, 2009). HIV-1 infected individuals present different rates of disease progression; while a majority of individual progress to acquired immunodeficiency syndrome (AIDS) after the infection, most of them can be turned aviremic even the absence of antiretroviral therapy (ARV) up to ten years and are called typical progressors. Most importantly, ~5% to 10% of persistently infected individuals show no signs of disease progression for over 12 years and remain asymptomatic and aviremic and are classified as long term nonprogressors (LTNPs). On the other hand, rapid progressors are individuals that rapidly progress to AIDS within four years after primary HIV-1 infection and some individuals have been known to progress to AIDS and death within a year after primary infection (Fauci et al., 1996; Rosenberg & Fauci, 1991). Genetic factors may be one of the host factors responsible for the susceptibility to infection and disease progression. However, no single gene or polymorphism is likely to be responsible for these effects. Brass et al. (2008) have reported that HIV-1 uses at least 250 host-derived dependency factors for gaining entry into target cells and completing its life cycle. Hence, multiple genetic factors are expected to be involved in susceptibility, disease pathogenesis, and progression following HIV-1 infection. Some of these genes that have been established with HIV/AIDS conclusively involve are: (1) genes influencing viral entry by altering the expression on cell surface the levels of chemokine receptors and their ligands as well cytokines (Seisdedos & Parmentier, 2006; Reiche et al., 2007); (2) genes involved in anti-HIV immune response including the antiviral Apolipoprotein B mRNA-editing enzyme, catalytic polypeptide-like 3G (APOBEC3G) gene family on chromosome 22q13 (An et al., 2009); the virus restriction factor Tripartite Interaction Motif 5  (TRIM5) on" @default.
• W1534854496 created "2016-06-24" @default.
• W1534854496 creator A5007114657 @default.
• W1534854496 creator A5033499609 @default.
• W1534854496 creator A5038684200 @default.
• W1534854496 date "2011-10-26" @default.
• W1534854496 modified "2023-09-25" @default.
• W1534854496 title "The Role of Genetic Polymorphisms in the Chemokine and their Receptors and Cytokines in the Human Immunodeficiency Virus Type 1 (HIV-1) Infection" @default.
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