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Currently, there are approximately 38.4 million individuals living with the Human Immunodeficiency Virus (HIV), of which 36.7 million adults, 1.7 million children (<15 years old), with 54% of cases being females. Since the start of the HIV epidemic, an estimated 84.2 million individuals have been infected with the virus. Tragically, this global health crisis has resulted in the loss of approximately 40 million lives. In 2021 the World Health Organization (WHO) estimated 1.5 million new infections (1). In the early stages of HIV infection, several important events occur within CD4+ T cells, which are a primary target of the virus. CD4+ T cell depletion: HIV infects and destroys CD4+ T cells during the replication process. If left untreated, HIV is the virus kills infected cells directly and indirectly through immune responses that cause cell death. This progressive loss of CD4+ T cells weakens the immune system over time even following antiretroviral treatment (cART) in HIV infected individuals (2). HIV-infected individuals often experience imbalances in CD4+ T cell levels and function. While cART is highly effective in suppressing viral replication and restoring immune function, it may not completely normalize CD4+ T cell counts or fully restore immune balance in all individuals. Some HIV reservoirs, such as latently infected CD4+ T cells or tissues with lower drug penetration, may continue to harbor the virus, and chronic immune activation and inflammation associated with HIV infection can lead to immune exhaustion, where immune cells, including CD4+ T cells, become functionally impaired and less responsive. Despite extensive research, the mechanisms underlying CD4+ T cell loss and dysfunction in HIV infection are not fully understood (3). This edited topic is aimed at shedding lights on the effects of HIV infection on CD4+ T cells, considering their complexity in terms of heterogeneity and tissue distribution (4-7).
Currently, there are approximately 38.4 million individuals living with the Human Immunodeficiency Virus (HIV), of which 36.7 million adults, 1.7 million children (<15 years old), with 54% of cases being females. Since the start of the HIV epidemic, an estimated 84.2 million individuals have been infected with the virus. Tragically, this global health crisis has resulted in the loss of approximately 40 million lives. In 2021 the World Health Organization (WHO) estimated 1.5 million new infections (1). In the early stages of HIV infection, several important events occur within CD4+ T cells, which are a primary target of the virus. CD4+ T cell depletion: HIV infects and destroys CD4+ T cells during the replication process. If left untreated, HIV is the virus kills infected cells directly and indirectly through immune responses that cause cell death. This progressive loss of CD4+ T cells weakens the immune system over time even following antiretroviral treatment (cART) in HIV infected individuals (2). HIV-infected individuals often experience imbalances in CD4+ T cell levels and function. While cART is highly effective in suppressing viral replication and restoring immune function, it may not completely normalize CD4+ T cell counts or fully restore immune balance in all individuals. Some HIV reservoirs, such as latently infected CD4+ T cells or tissues with lower drug penetration, may continue to harbor the virus, and chronic immune activation and inflammation associated with HIV infection can lead to immune exhaustion, where immune cells, including CD4+ T cells, become functionally impaired and less responsive. Despite extensive research, the mechanisms underlying CD4+ T cell loss and dysfunction in HIV infection are not fully understood (3). This edited topic is aimed at shedding lights on the effects of HIV infection on CD4+ T cells, considering their complexity in terms of heterogeneity and tissue distribution (4-7).
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