Abstract
Background: Premature aging and related diseases have been documented in HIV-infected adults. Data are now emerging also regarding accelerated aging process in HIV-infected children.Methods: A narrative review was performed searching studies on PubMed published in English language in 2004-2017, using appropriate key words, including “aging”, “children”, “HIV”, “AIDS”, “immunosenescence”, “pathogenesis”, “clinical conditions”.Results: Premature immunosenescence phenotype of B and T cells in HIV-infected children is mediated through immune system activation and chronic inflammation. Ongoing inflammation processes have been documented by increased levels of pathogen-associated molecular patterns (PAMPS), increased mitochondrial damage, higher levels of pro-inflammatory cytokines, and a positive correlation between sCD14 levels and percentages of activated CD8+ cells. Other reported features of premature aging include cellular replicative senescence, linked to an accelerated telomeres shortening. Finally, acceleration of age-associated methylation pattern and other epigenetic modifications have been described in HIV-infected children. All these features may favor the clinical manifestations related to premature aging. Lipid and bone metabolism, cancers, cardiovascular, renal, and neurological systems should be carefully monitored, particularly in children with detectable viremia and/or with CD4/CD8 ratio inversion.Conclusion: Aging processes in children with HIV infection impact their quality and length of life. Further studies regarding the mechanisms involved in premature aging are needed to search for potential targets of treatment.
Highlights
To the introduction of the combined highly active antiretroviral therapy (ART), life expectancy of HIV-unexposed uninfected (HIV-)infected adults has increased dramatically, but it is currently not yet comparable to that of healthy individuals [1]
Further studies regarding the mechanisms involved in premature aging are needed to search for potential targets of treatment
ART and HIV infection coexist in children from birth, moving up immunosenescence and aging processes; these are more pronounced in children with detectable viremia, focusing attention on the need for early and long-standing control of HIV replication
Summary
To the introduction of the combined highly active antiretroviral therapy (ART), life expectancy of HIV-infected adults has increased dramatically, but it is currently not yet comparable to that of healthy individuals [1]. It is important to underline that by the end of 2013, 3.3 million children under 15 years old were living with HIV infection worldwide, and 630,000 of them had access to ART [6] These children receive antiretroviral drugs for all their lifetime and, having a longer life expectancy than in the past, must face a chronic condition. Infected children have higher HIV plasma viremia and faster disease progression compared to adults [12,13]. This slower control of viral replication may depend from the fact that the immune system is still maturing. This narrative review describes the pathogenic mechanisms of premature aging in children, possibly underlying the main related clinical features
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