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Cells
Special Issues
Host–Microbial Interactions
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Host–Microbial Interactions

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: closed (30 June 2023) | Viewed by 1963

Special Issue Editors

Prof. Dr. Hung-Jen Liu

E-Mail Website
Guest Editor
Institute of Molecular Biology, National Chung Hsing University, Taichung, Taiwan
Interests: molecular virology; vaccine development; signaling transduction; biotechnology; veterinary medicine
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Muhammad Munir

E-Mail Website
Guest Editor
Division of Biomedical and Life Science, Lancaster University, Lancaster LA1 4YG, UK
Interests: zoonotic viruses; virus pathogenesis; host responses; influenza viruses; coronaviruses
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Viruses are obligatory intercellular microorganisms which exploit cellular machinery for the establishment of successful infection. On the other hands, host cells exert multi-layered defense to combat viral infections. The outcome of this virus-host interaction determines the state of health and disease. This decisive interaction spans from basic to molecular level of virus life cycle inherently rooted into the host genetics, immunity, cell biology and molecular signaling. Insights into viral modulation of cellular pathways are pre-requisite for developing novel antiviral, vaccine delivery routes and innovative modulatory and therapeutic directions.

This special issue invites reviews and research articles addressing current knowledge of the virus-host interactions, and to precipitate fruitful dialogue on aspects that shape the host cellular factors and signaling pathways important for the pathobiology of virus-induced diseases.

Prof. Dr. Hung-Jen Liu
Prof. Dr. Muhammad Munir
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 100 words) can be sent to the Editorial Office for announcement on this website.

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. Cells is an international peer-reviewed open access semimonthly 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 2700 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

  • virus–host interactions
  • signaling pathway
  • virus entry
  • life cycle

Published Papers (1 paper)

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Research

21 pages, 4681 KiB  
Article
Respiratory Syncytial Virus Matrix Protein Is Sufficient and Necessary to Remodel Host Mitochondria in Infection
by MengJie Hu, Marie A. Bogoyevitch and David A. Jans
Cells 2023, 12(9), 1311; https://doi.org/10.3390/cells12091311 - 4 May 2023
Cited by 8 | Viewed by 1716
Abstract
Although respiratory syncytial virus (RSV) is the most common cause of respiratory infection in infants, immunosuppressed adults and the elderly worldwide, there is no licensed RSV vaccine or widely applicable antiviral therapeutics We previously reported a staged redistribution of mitochondria with compromised respiratory [...] Read more.
Although respiratory syncytial virus (RSV) is the most common cause of respiratory infection in infants, immunosuppressed adults and the elderly worldwide, there is no licensed RSV vaccine or widely applicable antiviral therapeutics We previously reported a staged redistribution of mitochondria with compromised respiratory activities and increased reactive oxygen species (ROS) generation during RSV infection. Here, we show for the first time that the RSV matrix protein (M) is sufficient and necessary to induce these effects. Ectopically expressed M, but not other RSV proteins, was able to induce mitochondrial perinuclear clustering, inhibition of mitochondrial respiration, loss of mitochondrial membrane potential (Δψm), and enhanced generation of mitochondrial ROS (mtROS) in infection. Truncation and mutagenic analysis revealed that the central nucleic acid-binding domain of M is essential for the effects on host mitochondria, with arginine/lysine residues 170/172 being critically important. Recombinant RSV carrying the arginine/lysine mutations in M was unable to elicit effects on host mitochondria. Further, wild-type but not mutant RSV was found to inhibit the mRNA expression of genes encoding mitochondrial proteins, including Complex I subunits. Importantly, the RSV mutant was impaired in virus production, underlining the importance of M-dependent effects on mitochondria to RSV infection. Together, our results highlight M’s unique ability to remodel host cell mitochondria and its critical role in RSV infection, representing a novel, potential target for future anti-RSV strategies. Full article
(This article belongs to the Special Issue Host–Microbial Interactions)
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