About this Research Topic
HIV infection leads to chronic immune activation and inflammation, which accelerates the aging of the immune system, a phenomenon known as immunosenescence. This accelerated immune aging is characterized by the depletion of naïve T cells, an increase in memory and exhausted T cells, and a higher prevalence of senescent cells. Genetic factors significantly influence the extent and progression of immunosenescence in HIV-positive individuals.
One key aspect of genetic variation involves human leukocyte antigen (HLA) genes, which are crucial for the immune system's ability to recognize and respond to pathogens. Certain HLA alleles are associated with better control of HIV infection and slower progression to AIDS. For instance, individuals with the HLA-B*57 allele tend to have lower viral loads and better immune function, which may mitigate the effects of immune aging. Conversely, other HLA alleles are linked to faster disease progression and more pronounced immune aging.
Another genetic factor is the presence of single nucleotide polymorphisms (SNPs) in genes related to immune function. NPs in genes such as C-C chemokine receptor type 5 (CCR5), interleukin-7 receptor (IL-7R), and killer-cell immunoglobulin-like receptors (KIR) can affect the susceptibility to HIV infection and the rate of immune system decline. For example, the CCR5-Δ32 mutation provides resistance to HIV infection and has been associated with slower immune aging in HIV-positive individuals.
Genetic variation significantly influences immune aging in HIV-positive individuals. Therefore, understanding these genetic factors can help in developing personalized therapeutic strategies to mitigate the effects of immunosenescence and improve the quality of life for those living with HIV. We welcome Original Research Articles, Reviews, Mini-Reviews, Systematic Reviews, Perspectives, Commentaries, Data notes, and technical notes.
Manuscripts covering pure bioinformatic analyses are not in scope of the Immunogenetics section of Frontiers in Genetics. Experimental (wet lab) validation of the in silico obtained results is a prerequisite for peer-review. Further, reports oriented towards the application of genetic analyses are not to be primarily targeted to the Immunogenetics unless they evolve in detail around the MHC (HLA) or other major immunogenetic systems and how those affect immune response and or therapy documented by real laboratory and/or clinical data, not solely bioinformatic analyses.
The topics may include but are not limited to:
• Studies on epigenetic changes, such as DNA methylation and histone modification, which provide insights into how gene expression changes with HIV infection.
• Research related to genetic and molecular biomarkers of immune senescence in HIV-positive individuals.
• Research on how genetic variations interact with environmental factors, such as antiretroviral therapy to influence immune aging in HIV-positive individuals.
• Leveraging genetic insights to identify new therapeutic targets, including gene therapy and precision medicine approaches.
One key aspect of genetic variation involves human leukocyte antigen (HLA) genes, which are crucial for the immune system's ability to recognize and respond to pathogens. Certain HLA alleles are associated with better control of HIV infection and slower progression to AIDS. For instance, individuals with the HLA-B*57 allele tend to have lower viral loads and better immune function, which may mitigate the effects of immune aging. Conversely, other HLA alleles are linked to faster disease progression and more pronounced immune aging.
Another genetic factor is the presence of single nucleotide polymorphisms (SNPs) in genes related to immune function. NPs in genes such as C-C chemokine receptor type 5 (CCR5), interleukin-7 receptor (IL-7R), and killer-cell immunoglobulin-like receptors (KIR) can affect the susceptibility to HIV infection and the rate of immune system decline. For example, the CCR5-Δ32 mutation provides resistance to HIV infection and has been associated with slower immune aging in HIV-positive individuals.
Genetic variation significantly influences immune aging in HIV-positive individuals. Therefore, understanding these genetic factors can help in developing personalized therapeutic strategies to mitigate the effects of immunosenescence and improve the quality of life for those living with HIV. We welcome Original Research Articles, Reviews, Mini-Reviews, Systematic Reviews, Perspectives, Commentaries, Data notes, and technical notes.
Manuscripts covering pure bioinformatic analyses are not in scope of the Immunogenetics section of Frontiers in Genetics. Experimental (wet lab) validation of the in silico obtained results is a prerequisite for peer-review. Further, reports oriented towards the application of genetic analyses are not to be primarily targeted to the Immunogenetics unless they evolve in detail around the MHC (HLA) or other major immunogenetic systems and how those affect immune response and or therapy documented by real laboratory and/or clinical data, not solely bioinformatic analyses.
The topics may include but are not limited to:
• Studies on epigenetic changes, such as DNA methylation and histone modification, which provide insights into how gene expression changes with HIV infection.
• Research related to genetic and molecular biomarkers of immune senescence in HIV-positive individuals.
• Research on how genetic variations interact with environmental factors, such as antiretroviral therapy to influence immune aging in HIV-positive individuals.
• Leveraging genetic insights to identify new therapeutic targets, including gene therapy and precision medicine approaches.
Keywords: HIV, Human Immunodeficiency Virus, AIDS, Genetic Variation, Immune Aging
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
