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Pathogens
Special Issues
Viral Infections, Chronic Inflammation and Carcinogenesis
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Viral Infections, Chronic Inflammation and Carcinogenesis

A special issue of Pathogens (ISSN 2076-0817). This special issue belongs to the section "Viral Pathogens".

Deadline for manuscript submissions: 30 September 2026 | Viewed by 577

Special Issue Editors

Dr. Angioletta Lasagna

E-Mail
Guest Editor
S.C. Oncologia Medica, Fondazione IRCCS Policlinico San Matteo, 27100 Pavia, Italy
Interests: cancer; vaccines; immunotherapy; viral infection; microbiome
Special Issues, Collections and Topics in MDPI journals
Dr. Davide Dalu

E-Mail Website
Guest Editor
Infectious Disease Oncology, Department of Oncology, Luigi Sacco University Hospital, 20157 Milan, Italy
Interests: cancer; HIV; oncogenic viruses; gender minority; vaccination

Special Issue Information

Dear Colleagues,

Viral infections account for 20% of human cancers. The seven currently recognized human oncogenic viruses are HBV, HCV, HPV, HTLV-1, EBV, KSHV/HHV-8, and Merkel cell polyomavirus (MCPyV). Although HIV is not an oncogenic virus by definition because it does not directly cause cancer, it can increase the risk of developing many types of cancer (AIDS-related cancers). In general, viruses are able to target (directly or indirectly) major cellular pathways and cause the development of cancer. Viral infection can lead to uncontrolled cell proliferation and transformation by interfering with cellular regulatory proteins, inactivating tumor suppressor genes, evading host immune responses, inducing persistent inflammatory reactions, causing epigenetic changes, stimulating angiogenesis, and activating telomerase. Some commonly known examples of virus-induced cancers are cervical squamous cell carcinoma, head and neck squamous cell carcinoma, hepatocellular carcinoma, Kaposi’s sarcoma, and Burkitt’s lymphoma. Studies on the role of viruses as a cause of cancer has led to the development of vaccines that can protect against oncogenic viral infections. Research areas of interest include (but are not limited to) the following topics:

  • Host cell responses: cellular and molecular mechanisms;
  • Hit-and-run theory;
  • Virus-host interaction;
  • Host immunity and viral evasion mechanisms;
  • Viral oncogenesis.

All types of articles will be considered for publication, including short reports, full research articles, and reviews.

Dr. Angioletta Lasagna
Dr. Davide Dalu
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Pathogens is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • oncogenic virus
  • HPV
  • AIDS-related cancers
  • HCV
  • HBV
  • hit-and-run theory
  • vaccination

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Published Papers (2 papers)

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Research

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16 pages, 2755 KB  
Article
HBV-Induced Pyruvate Increases Lactylation of Pyruvate Kinase M2 (PKM2) at K206 to Promote Liver Fibrosis
by Wenxian Wen, Qin Du, Shuhan Li, Youmin Yang, Xianding Wang, Shasha Li, Yujia Li, Shilin Li, Chunhui Yang, He Xie, Xiaoqiong Duan and Limin Chen
Pathogens 2026, 15(4), 431; https://doi.org/10.3390/pathogens15040431 (registering DOI) - 16 Apr 2026
Abstract
We previously demonstrated that HBV promotes liver fibrosis through the enhanced production of pyruvate. Pyruvate kinase M2 (PKM2), a key enzyme in pyruvate metabolism, plays an important role in liver fibrogenesis. Recently, lactylation of PKM2 has been identified, which contributes to stabilize its [...] Read more.
We previously demonstrated that HBV promotes liver fibrosis through the enhanced production of pyruvate. Pyruvate kinase M2 (PKM2), a key enzyme in pyruvate metabolism, plays an important role in liver fibrogenesis. Recently, lactylation of PKM2 has been identified, which contributes to stabilize its catalytically active tetrameric conformation. Therefore, we hypothesize that PKM2 lactylation is involved in the regulation of HBV-induced liver fibrosis. In this study, we found that sera lactate levels were increased in CHB patients and HBV-Tg mice. Moreover, the lysine lactylation levels of proteins in liver tissues were significantly increased in the HBV-Tg mice. In LX2 cells, we found that pyruvate treatment significantly increased the profibrotic gene expression and lactylation level of PKM2, which promoted its tetramer-to-dimer transition, inhibited its pyruvate kinase activity, and facilitated its nuclear distribution. Through immunoprecipitation, we identified that pyruvate induced PKM2 lactylation at the K206 site. PKM2 knockdown or K206 mutation reduced PKM2 lactylation and abrogated the induction of profibrotic gene expression by pyruvate. Collectively, our findings indicate that HBV infection stimulated pyruvate production, which increased PKM2 lactylation at K206 to promote the expression of profibrogenic genes in HSCs, leading to liver fibrogenesis. Full article
(This article belongs to the Special Issue Viral Infections, Chronic Inflammation and Carcinogenesis)
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Review

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13 pages, 273 KB  
Review
HIV and Cancer: Insights into Viral-Mediated Oncogenesis and Immunosuppression
by Angioletta Lasagna, Giacomo Pozza, Maddalena Matone, Cinzia Fasola, Lorenzo Ruggieri, Nicla La Verde, Paolo Pedrazzoli and Davide Dalu
Pathogens 2026, 15(4), 416; https://doi.org/10.3390/pathogens15040416 - 12 Apr 2026
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Abstract
Background: People 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 [...] Read more.
Background: People 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. Methods: A 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. Results: Available 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. Conclusions: HIV 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. Full article
(This article belongs to the Special Issue Viral Infections, Chronic Inflammation and Carcinogenesis)
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