Host–Microbial Interactions

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

Deadline for manuscript submissions: closed (30 June 2023) | Viewed by 2644

Special Issue Editors


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Guest Editor
Institute of Molecular Biology, National Chung Hsing University, Taichung, Taiwan
Interests: molecular virology; vaccine development; signaling transduction; biotechnology; veterinary medicine
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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

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Keywords

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

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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 2325
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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