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Inflammation and RONS Dysregulation by Redox Enzymes as Mechanistic Links in HIV-1–Cancer Comorbidity
Journal article   Open access   Peer reviewed

Inflammation and RONS Dysregulation by Redox Enzymes as Mechanistic Links in HIV-1–Cancer Comorbidity

Charles Gotuaco Ang, Shreya Eyunni and Irwin M. Chaiken
Pathogens (Basel), v 15(4), 423
14 Apr 2026
DOI: https://doi.org/10.3390/pathogens15040423
Featured in Collection :   Drexel's Newest Publications
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https://doi.org/10.3390/pathogens15040423View
Published, Version of Record (VoR) Open Access Discount via Drexel Libraries Read and Publish Program 2026 Open CC BY V4.0

Abstract

cancer comorbidity disulfides HIV-1 Protein Disulfide Isomerase redox reactive oxygen/nitrogen species thiols thioredoxin
Antiretroviral therapy (ART) effectively controls Human Immunodeficiency Virus Type-1 (HIV-1) infection in people with HIV-1 (PWH), preventing the progression of their infections to AIDS. However, as PWH age, they experience lifestyle- and age-related diseases, notably various types of cancer beyond those traditionally associated with AIDS, with greater incidence and mortality than their non-HIV-1-positive counterparts, despite effective arrest of HIV-1 infection by ART. Dysregulation of redox enzymes presents an underexplored linkage between HIV-1 infection and cancer comorbidity, impacting reactive oxygen/nitrogen species (RONS) management, inflammation, immune function, and mitochondrial function. Chronic HIV-1 infection increases both RONS production and RONS neutralization responses, accelerating development of a sustained RONS-rich environment that still possesses sufficient dampening to prevent outright cytotoxic effects. Such an environment promotes both tumor proliferation and resistance adaptations to chemo- and radiotherapies. This review considers the effects of chronic HIV-1 infection on redox enzyme function and links these effects to tumorigenic mechanisms as potentially shared pathways. We then examine current methods of modulating redox function, consider how these could potentially impact both HIV-1 infection and cancer progression, and lastly propose future methods of co-treatment that could be explored.

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