IMMUNE AGING IN THE YOUNG: CONSEQUENCES OF HIV-INDUCED SENESCENCE IN CHILDREN

Emmanuel Ifeanyi Obeagu; Chukwuma J. Okafor

doi:10.22270/ujpr.v11i1.1491

Emmanuel Ifeanyi Obeagu Department of Biomedical and Laboratory Science, Africa University, Mutare, Zimbabwe.
Chukwuma J. Okafor Department of Pathology and Biochemistry, State University of Zanzibar, Tanzania.

10.22270/ujpr.v11i1.1491

Keywords:

Chronic inflammation, HIV, immune senescence, pediatric immunology, T-cell exhaustion

Abstract

The immune systems of children that are still developing are particularly susceptible to being affected by long-lasting infections like HIV. Children infected perinatally show indications of immune aging or immune senescence significantly sooner than their uninfected counterparts, even with the prompt start of combination antiretroviral therapy (cART). This rapid aging process is marked by persistent immune activation, thymic impairment, disrupted hematopoiesis, and the premature buildup of senescent and weary immune cells. These changes jeopardize immune function during a vital period of growth and development. At the heart of HIV-related senescence in children is the ongoing condition of systemic inflammation and immune imbalance, despite the presence of viral suppression. Thymic involution diminishes the production of naïve T-cells, whereas telomere shortening and increased levels of senescence markers like p16^INK4a and PD-1 indicate cellular tiredness. These immunological changes have significant clinical consequences, including heightened vulnerability to infections, insufficient vaccine efficacy, and premature development of non-AIDS-related comorbidities like cardiovascular and neurocognitive issues.