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Purpose <p>Cytomegalovirus (CMV) infection is nearly universal among people with HIV (PWH) and contributes to chronic inflammation, immune senescence, and accelerated biological aging despite suppressive antiretroviral therapy (ART). This review summarizes recent advances in understanding the role of CMV in multimorbidity and aging in PWH, focusing on immune and tissue-based mechanisms, comorbidities, and emerging interventions.</p> Recent Findings <p>CMV reactivation drives clonal T-cell expansion, innate immune reprogramming, adipose tissue inflammation, metabolic rewiring, and durable cellular epigenetic changes that amplify risks for vascular disease, frailty, brain health disorders, diabetes mellitus, and cancer. Early interventional data indicate that letermovir can reduce inflammation and improve immune and frailty outcomes in PWH, while vaccines are advancing in clinical evaluation.</p> Summary <p>CMV is a modifiable driver of immune dysfunction and aging in PWH. Targeted antiviral, vaccine, and host-directed approaches may reduce multimorbidity and promote healthy aging, particularly in populations at greatest risk.</p>

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Cytomegalovirus in HIV: A Modifiable Driver of Inflammation, Frailty, and Aging

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年3月20日

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  • Alfonso Cabello Ubeda,
  • Kristine M. Erlandson,
  • Michael L. Freeman,
  • Scott L. Letendre,
  • Celestine N. Wanjalla,
  • John R. Koethe,
  • Michael J. Corley,
  • Peter W. Hunt,
  • Sara Gianella

摘要

Purpose

Cytomegalovirus (CMV) infection is nearly universal among people with HIV (PWH) and contributes to chronic inflammation, immune senescence, and accelerated biological aging despite suppressive antiretroviral therapy (ART). This review summarizes recent advances in understanding the role of CMV in multimorbidity and aging in PWH, focusing on immune and tissue-based mechanisms, comorbidities, and emerging interventions.

Recent Findings

CMV reactivation drives clonal T-cell expansion, innate immune reprogramming, adipose tissue inflammation, metabolic rewiring, and durable cellular epigenetic changes that amplify risks for vascular disease, frailty, brain health disorders, diabetes mellitus, and cancer. Early interventional data indicate that letermovir can reduce inflammation and improve immune and frailty outcomes in PWH, while vaccines are advancing in clinical evaluation.

Summary

CMV is a modifiable driver of immune dysfunction and aging in PWH. Targeted antiviral, vaccine, and host-directed approaches may reduce multimorbidity and promote healthy aging, particularly in populations at greatest risk.