Evidence map›Paper›PMID 42075743›Full record

ReviewPathogens (Basel, Switzerland)2026

HIV and Cancer: Insights into Viral-Mediated Oncogenesis and Immunosuppression.

Angioletta Lasagna, Giacomo Pozza, Maddalena Matone, Cinzia Fasola, Lorenzo Ruggieri, Nicla La Verde, Paolo Pedrazzoli, Davide Dalu

Abstract readReview
In one paragraph

Review in Pathogens (Basel, Switzerland), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Angioletta LasagnaDepartment of Oncology, Comprehensive Cancer Center, Fondazione IRCCS Policlinico San Matteo, 27100 Pavia, Italy.ORCID 0000-0002-9611-1164
Giacomo PozzaDepartment of Infectious Diseases, Luigi Sacco Hospital, ASST Fatebenefratelli Sacco, 20100 Milan, Italy.ORCID 0009-0001-1498-3250
Maddalena MatoneDepartment of Infectious Diseases, Luigi Sacco Hospital, ASST Fatebenefratelli Sacco, 20100 Milan, Italy.ORCID 0009-0002-2317-6984
Cinzia FasolaDepartment of Infectious Diseases, Luigi Sacco Hospital, ASST Fatebenefratelli Sacco, 20100 Milan, Italy.
Lorenzo RuggieriInfectious Disease Oncology Unit, Department of Oncology, Luigi Sacco Hospital, ASST Fatebenefratelli Sacco, 20100 Milan, Italy.ORCID 0000-0002-9972-2761
Nicla La VerdeInfectious Disease Oncology Unit, Department of Oncology, Luigi Sacco Hospital, ASST Fatebenefratelli Sacco, 20100 Milan, Italy.ORCID 0000-0002-2884-1632
Paolo PedrazzoliDepartment of Oncology, Comprehensive Cancer Center, Fondazione IRCCS Policlinico San Matteo, 27100 Pavia, Italy.ORCID 0000-0002-9419-7160
Davide DaluInfectious Disease Oncology Unit, Department of Oncology, Luigi Sacco Hospital, ASST Fatebenefratelli Sacco, 20100 Milan, Italy.ORCID 0000-0002-8017-2149

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPeople living with HIV (PLWH) have a substantially increased risk of both AIDS-defining cancers (ADCs) and non-AIDS-defining cancers (NADCs), which remain a major cause of morbidity despite effective antiretroviral therapy (ART); this review aims to integrate current epidemiological, molecular, and clinical evidence on HIV-associated oncogenesis.

methodsA structured literature search was conducted in PubMed (2000-2026) using predefined keywords, including "HIV", "cancer", "oncogenesis", and "immune dysregulation", with inclusion of original studies, systematic reviews, and meta-analyses meeting predefined quality criteria.

resultsAvailable evidence indicates that HIV contributes to cancer development through both direct and indirect mechanisms: viral proteins such as Tat, Nef, and Vpr disrupt apoptosis, DNA repair, and cell cycle regulation, while chronic immune activation, persistent inflammation, and immunosuppression impair tumor immune surveillance and facilitate oncogenic viral co-infections, including Epstein-Barr virus, human papillomavirus, and human herpesvirus 8. Emerging pathways, such as epigenetic alterations, microRNA dysregulation, metabolic reprogramming, and the contribution of HIV reservoirs to pro-tumorigenic microenvironments, further modulate cancer risk.

conclusionsHIV may function as a cofactor that enhances the effects of oncogenic viruses by promoting viral persistence and immune dysregulation; while biologically plausible, direct evidence linking HIV to amplification of tumorigenesis in humans remains limited.

Indexed as

CarcinogenesisHIV InfectionsNeoplasmsHumansImmune ToleranceHHV-8immune cell exhaustionimmunosenescenceoncogenic virus

Identifiers

PMID42075743
PMCPMC13118630

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.