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Biomedicines
Special Issues
Host–Pathogen Interactions, Immune Modulation, and Translational Therapeutics
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Host–Pathogen Interactions, Immune Modulation, and Translational Therapeutics

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Microbiology in Human Health and Disease".

Deadline for manuscript submissions: 31 January 2027 | Viewed by 118

Editor

Dr. Gaopeng Hou

E-Mail Website
Guest Editor
Institute of Modern Biology, Nanjing University, Nanjing, China
Interests: enteric virus infection; mucosal immunology; virus-host interaction; innate immunity; vaccine development

Special Issue Information

Dear Colleagues,

Host-pathogen interactions and immune regulation are central to understanding infectious diseases, inflammatory disorders, vaccine responses, and therapeutic efficacy. Recent advances in virology, immunology, molecular medicine, and drug development have revealed new mechanisms by which pathogens evade host defense, alter tissue tropism, and shape disease outcomes, while also creating opportunities for rational vaccine design and precision therapeutics.

This Special Issue aims to highlight recent progress in host-pathogen interactions, immune modulation, vaccine innovation, and translational therapeutic development. We welcome original research articles, reviews, and perspectives addressing enteric virus infection, viral pathogenesis, virus–host interactions, innate and adaptive immunity, mucosal immunity, antiviral defense, immune evasion, host range restriction, and novel vaccine strategies. We also encourage submissions on emerging therapeutic platforms, including antibody-drug conjugates, immune checkpoint inhibitors, nucleic acid therapeutics, immune adjuvants, gene-editing technologies, and related drug-development approaches.

By bringing together studies from infection biology, immunology, pharmacology, and translational medicine, this Special Issue seeks to promote interdisciplinary discussion and provide new insights into disease mechanisms, immune intervention, and therapeutic innovation.

Dr. Gaopeng Hou
Guest Editor

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-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines 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 2600 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

  • host-pathogen interaction
  • immune modulation
  • enteric virus infection
  • vaccine development
  • translational therapeutics

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Published Papers (1 paper)

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Review

23 pages, 1512 KB  
Review
Beyond Acute Infection: A Conceptual Framework Linking Zoonotic Bacterial Pathogens to Pulmonary Fibrosis and Lung Carcinogenesis
by Ju Hee Lee, Nam Yee Kim, Chang-Min Choi and Minjeong Yeon
Biomedicines 2026, 14(8), 1776; https://doi.org/10.3390/biomedicines14081776 - 6 Aug 2026
Abstract
Zoonotic bacterial pathogens are transmitted through various routes and are traditionally associated with acute febrile illnesses that may include pulmonary complications. However, in some survivors, the disease extends beyond the acute phase, leading to the remodeling of pulmonary architecture and driving progressive fibrosis. [...] Read more.
Zoonotic bacterial pathogens are transmitted through various routes and are traditionally associated with acute febrile illnesses that may include pulmonary complications. However, in some survivors, the disease extends beyond the acute phase, leading to the remodeling of pulmonary architecture and driving progressive fibrosis. Although no direct cases have been reported, these pathogens may plausibly predispose injured lungs to carcinogenesis, similar to the well-recognized phenomenon of tuberculosis-associated scar cancer. As such long-term sequelae remain largely overlooked in current clinical practice, their potential contribution to fibrotic and malignant lung disease represents a critical and underexplored knowledge gap. This review proposes a unified mechanistic framework linking acute pathogen-mediated alveolar damage to chronic pulmonary fibrosis and subsequent lung carcinogenesis. We delineate four convergent biological pillars driving this continuum: (1) pathogen persistence establishing chronic Interleukin-1β (IL-1β)/Tumor necrosis factor-α (TNF-α)-mediated inflammation; (2) sustained TGF-β signaling and mechanotransduction driving progressive extracellular matrix remodeling; (3) unresolved reactive oxygen species (ROS) generation causing profound oxidative DNA damage; and (4) aberrant epithelial–mesenchymal transition (EMT) that perpetuates fibrosis and generates pre-malignant cell populations. Together, these sequelae alter lung biomechanics, suppress local immune surveillance, and create a mutagenic environment that is highly conductive to malignant transformation. Although direct epidemiological data remain emerging, the significant mechanistic overlap with idiopathic pulmonary fibrosis (IPF) presents a compelling rationale for shared oncogenic risk. We advocate for a paradigm shift in clinical practice, emphasizing the potential value of long-term surveillance for survivors of severe pulmonary infections. By integrating infectious diseases, pulmonology, and oncology, this framework highlights a neglected cause of fibrotic lung disease and establishes a foundation for future translational research. Full article
(This article belongs to the Special Issue Host–Pathogen Interactions, Immune Modulation, and Translational Therapeutics)
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