Feature Papers in Viral Pathogens

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

Deadline for manuscript submissions: 10 December 2026 | Viewed by 1142

Editor


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Guest Editor
Veterinary & Biomedical Sciences Department, College of Veterinary Medicine, University of Minnesota, Twin Cities, MN 55108, USA
Interests: virus-host interactions; arenaviruses; influenza virus; viral immune evasion; innate immunity; vaccines

Special Issue Information

Dear Colleagues,

Viruses infect all forms of life, including humans, animals, plants, bacteria, and archaea. Viral infections in humans can cause mild to severe and sometimes fatal diseases, such as the common cold, flu, chickenpox, cold sores, rabies, Ebola, HIV/AIDS, SARS, and certain cancers. They have also been the cause of pandemics with significant death tolls on a global scale, such as the 1918 Spanish flu and COVID-19. Animals often serve as natural reservoirs (hosts) or intermediate hosts for viruses that cross species barriers to infect humans (viral zoonoses); therefore, viral infections in animals such as livestock, companion animals, and fish have major impacts on animal and human health, economics, food safety, and ecology. Plant viruses are responsible for more than half of emerging infectious diseases in plants and cause significant economic losses in crop yields worldwide. Bacteriophages, a common and diverse group of viruses infecting bacteria and the most abundant biological entity in aquatic environments, have been explored as novel therapeutics. The discovery and research of viral pathogens are essential for developing diagnostics and methods for preventing and treating various viral diseases.

The Special Issue “Feature Papers in Viral Pathogens” welcomes the contribution of original research and review papers covering all aspects of viral pathogens and host–virus interactions. We look forward to receiving your contributions.

Prof. Dr. Yuying Liang
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. 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 2400 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

  • viral biology (virology)
  • viral diagnostics
  • viral discovery
  • viral evolution
  • viral epidemiology
  • viral infection models
  • viral virulence
  • viral pathogenesis
  • viral oncogenesis
  • viral transmission
  • viral genomics/transcriptomics/proteomics/bioinformatics
  • virus–host interactions
  • immune responses to viruses
  • vaccines
  • antivirals
  • antiviral therapeutics
  • emerging viruses
  • oncogenic viruses

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Published Papers (1 paper)

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Research

19 pages, 2842 KB  
Article
ATG7 Limits Basal Antiviral Gene Expression and Moderately Promotes VSV Replication in Mammalian Non-Immune Cells
by Xiaohan Tong, Ruixue Wang, Yaxin Liu, Malia B. Potts, Shondra M. Pruett-Miller, Michael A. Whitt, Weikuan Gu and Kui Li
Pathogens 2026, 15(4), 404; https://doi.org/10.3390/pathogens15040404 - 8 Apr 2026
Cited by 1 | Viewed by 832
Abstract
The autophagy regulator ATG7 helps maintain cellular homeostasis and has been suggested to modulate aspects of antiviral immune responses. In Drosophila, ATG7-dependent autophagy contributes to host resistance to vesicular stomatitis virus (VSV), a negative-strand RNA virus of family Rhabdoviridae that is widely used [...] Read more.
The autophagy regulator ATG7 helps maintain cellular homeostasis and has been suggested to modulate aspects of antiviral immune responses. In Drosophila, ATG7-dependent autophagy contributes to host resistance to vesicular stomatitis virus (VSV), a negative-strand RNA virus of family Rhabdoviridae that is widely used for studying viral biology and developing vaccines and virotherapy. However, the role of ATG7 in mammalian cells, especially non-immune cell types, remains unclear. Herein, we systematically examined the impact of ATG7 on VSV infection using CRISPR-edited cell lines derived from murine embryonic fibroblast (MEF), HeLa, and Huh7.5 cells, in relation to its effect on the expression of antiviral interferon-stimulated genes (ISGs). We found that ATG7 deficiency blocked basal as well as VSV-induced LC3B lipidation, concomitant with moderate reductions in progeny virus yields, while the reconstitution of ATG7 reversed the phenotypes. Mechanistically, ATG7 did not affect viral entry but rather was associated with moderate upregulation of VSV RNA replication. Intriguingly, ATG7 inhibited baseline ISG expression, and this correlated with its pro-VSV effect in all three cell types, while its suppression of innate immune responses elicited post-VSV infection did not. Altogether, these data provide new insights into the role of ATG7 in regulating VSV replication and innate immunity and have implications for developing VSV-based prophylaxis/therapeutics. Full article
(This article belongs to the Special Issue Feature Papers in Viral Pathogens)
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