Review|Volume 10, Issue 11|pp 3610—3625

Accelerated aging in perinatally HIV-infected children: clinical manifestations and pathogenetic mechanisms

Elena Chiappini¹, Martina Bianconi¹, Annalisa Dalzini², Maria Raffaella Petrara², Luisa Galli¹, Carlo Giaquinto³, Anita De Rossi^2,⁴

¹Infectious Disease Unit, Meyer Children’s Hospital, Department of Science Health, University of Florence, Florence, Italy
²Section of Oncology and Immunology, Department of Surgery, Oncology and Gastroenterology, Unit of viral Oncology and AIDS Reference Center, University of Padova, Padova, Italy
³Department of Mother and Child Health, University of Padova, Padova, Italy
⁴Istituto Oncologico Veneto IOV-IRCCS, Padova, Italy

Received: June 11, 2018Accepted: October 27, 2018Published: November 11, 2018

https://doi.org/10.18632/aging.101622

Copyright: © 2018 Chiappini et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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.