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Pathogens
Special Issues
Pathogen–Host Interactions: Death, Defense, and Disease
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Pathogen–Host Interactions: Death, Defense, and Disease

A special issue of Pathogens (ISSN 2076-0817). This special issue belongs to the section "Immunological Responses and Immune Defense Mechanisms".

Deadline for manuscript submissions: 20 September 2026 | Viewed by 7428

Special Issue Editors

Dr. Hongyan Guo

E-Mail Website
Guest Editor
Department of Microbiology & Immunology, Louisiana State University in Shreveport, Shreveport, LA, USA
Interests: herpesvirus; virus–host interactions; innate immunity; cell death; pathogenesis
Special Issues, Collections and Topics in MDPI journals
Dr. Heather S. Koehler

E-Mail Website
Guest Editor
Center for Reproductive Biology, Washington State University Pullman, Pullman, WA, USA
Interests: vaccinia virus; monkeypox; cell death; pathogenesis; ZRNA
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Pathogen–host interactions drive a continual evolutionary arms race that shapes infection outcomes, host survival, and pathogen persistence. This Special Issue explores the complex interplay between microbial virulence strategies and host immune defenses across molecular, cellular, and ecological contexts. We invite original research and reviews that address mechanisms of pathogen evasion (e.g., immune suppression, antigenic variation), host defense responses (e.g., innate and adaptive immunity, metabolic reprogramming), and the pathological consequences of their imbalance (chronic infection, immunopathology, or cell death). We are particularly interested in studies involving human pathogens, emerging zoonotic agents, vector-borne infections, and microbiome-mediated host responses. Submissions that integrate experimental, computational, and translational approaches are especially encouraged, with the goal of uncovering novel therapeutic strategies and evolutionary insights into the ongoing conflict between infection and immunity.

Dr. Hongyan Guo
Dr. Heather S. Koehler
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

  • host–pathogen interaction
  • immune evasion
  • virulence factors
  • antimicrobial resistance
  • zoonosis

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Published Papers (2 papers)

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Review

25 pages, 1246 KB  
Review
Mitochondrial Dysfunction in Aging, HIV, and Long COVID: Mechanisms and Therapeutic Opportunities
by María Victoria Delpino and Jorge Quarleri
Pathogens 2025, 14(10), 1045; https://doi.org/10.3390/pathogens14101045 - 16 Oct 2025
Viewed by 5246
Abstract
We hypothesize that a unified mitochondrial perspective on aging, HIV, and long COVID reveals shared pathogenic mechanisms and specific therapeutic vulnerabilities that are overlooked when these conditions are treated independently. Mitochondrial dysfunction is increasingly recognized as a common factor driving aging, HIV, and [...] Read more.
We hypothesize that a unified mitochondrial perspective on aging, HIV, and long COVID reveals shared pathogenic mechanisms and specific therapeutic vulnerabilities that are overlooked when these conditions are treated independently. Mitochondrial dysfunction is increasingly recognized as a common factor driving aging, HIV, and long COVID. Shared mechanisms—including oxidative stress, impaired mitophagy and dynamics, mtDNA damage, and metabolic reprogramming—contribute to ongoing energy failure and chronic inflammation. Recent advancements highlight new therapeutic strategies such as mitochondrial transfer, transplantation, and genome-level correction of mtDNA variants, with early preclinical and clinical studies providing proof-of-concept. This review summarizes current evidence on mitochondrial changes across aging and post-viral syndromes, examines emerging organelle-based therapies, and discusses key challenges related to safety, durability, and translation. Full article
(This article belongs to the Special Issue Pathogen–Host Interactions: Death, Defense, and Disease)
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20 pages, 2459 KB  
Review
The Immunoregulatory Mechanisms of Human Cytomegalovirus from Primary Infection to Reactivation
by Xiaodan Liu, Chang Liu and Ting Zhang
Pathogens 2025, 14(10), 998; https://doi.org/10.3390/pathogens14100998 - 2 Oct 2025
Cited by 1 | Viewed by 1880
Abstract
Human cytomegalovirus (HCMV) establishes lifelong latency following primary infection, residing within myeloid progenitor cells and monocytes. To achieve this, the virus employs multiple immune evasion strategies. It suppresses innate immune signaling by inhibiting Toll-like receptor and cGAS-STING pathways. In addition, the virus suppresses [...] Read more.
Human cytomegalovirus (HCMV) establishes lifelong latency following primary infection, residing within myeloid progenitor cells and monocytes. To achieve this, the virus employs multiple immune evasion strategies. It suppresses innate immune signaling by inhibiting Toll-like receptor and cGAS-STING pathways. In addition, the virus suppresses major histocompatibility complex (MHC)-dependent antigen presentation to evade T cell recognition. As the downregulation of MHC molecules may trigger NK cell activation, the virus compensates for this by expressing proteins such as UL40 and IL-10, which engage inhibitory NK cell receptors and block activating signals, thereby suppressing NK cell immune surveillance. Viral proteins like UL36 and UL37 block host cell apoptosis and necroptosis, allowing HCMV to persist undetected and avoid clearance. In settings of profound immunosuppression, such as after allogeneic hematopoietic stem cell transplantation (allo-HSCT) or solid organ transplantation, slow immune reconstitution creates a window for viral reactivation. Likewise, immunosenescence and chronic low-grade inflammation during aging increases the risk of reactivation. Once reactivated, HCMV triggers programmed cell death, releasing viral PAMPs (pathogen-associated molecular patterns) and host-derived DAMPs (damage-associated molecular patterns). This release fuels a potent inflammatory response, promoting further viral reactivation and exacerbating tissue damage, creating a vicious cycle. This cycle of inflammation and reactivation contributes to both transplant-related complications and the decline of antiviral immunity in the elderly. Therefore, understanding the immune regulatory mechanisms that govern the switch from latency to reactivation is critical, especially within the unique immune landscapes of transplantation and aging. Elucidating these pathways is essential for developing strategies to prevent and treat HCMV-related disease in these high-risk populations. Full article
(This article belongs to the Special Issue Pathogen–Host Interactions: Death, Defense, and Disease)
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