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Viruses
Special Issues
Cellular Restriction Factors against Viral Infection
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Cellular Restriction Factors against Viral Infection

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "General Virology".

Deadline for manuscript submissions: 30 April 2024 | Viewed by 4536

Special Issue Editor

Dr. Stephen Barr

E-Mail Website
Guest Editor
Department of Microbiology and Immunology, Western University, London, ON, Canada
Interests: cellular restriction factors; antiviral proteins; HIV; Ebola; SARS-CoV-2; innate immunity; retroviral integration; HERC5; ISG15; viral antagonists; virus–host interactions
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cellular restriction factors are often upregulated by Type I interferons (IFNs) in an attempt by the host to rapidly and directly restrict viral replication and spread. The evolutionary origin of many restriction factors highlights their importance as a first line of defence against viruses. At the same time, the ability of viruses to counteract cellular restriction factors is critical for their survival and as we have observed recently, is an important characteristic of viruses of pandemic potential such as SARS-CoV-2. Thus, viral antagonists of host restriction factors show promise as potential targets for antiviral therapies.

In this Special Issue, we welcome submissions of original research, short communications and reviews which will contribute to an improved understanding of aspects related to the ‘protagonist–antagonistic’ relationship between viruses and host restriction factors.

Dr. Stephen Barr
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 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. Viruses 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

  • cellular restriction factors
  • antiviral proteins
  • viral antagonists
  • intrinsic immunity
  • interferon response
  • innate immunity
  • evolution of restriction factors
  • evolution of viral antagonists
  • viral antagonists as druggable targets

Published Papers (1 paper)

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Research

19 pages, 4482 KiB  
Article
Involvement of a Rarely Used Splicing SD2b Site in the Regulation of HIV-1 vif mRNA Production as Revealed by a Growth-Adaptive Mutation
by Takaaki Koma, Naoya Doi, Bao Quoc Le, Tomoyuki Kondo, Mitsuki Ishizue, Chiaki Tokaji, Chizuko Tsukada, Akio Adachi and Masako Nomaguchi
Viruses 2023, 15(12), 2424; https://doi.org/10.3390/v15122424 - 14 Dec 2023
Viewed by 4017
Abstract
We have previously reported an HIV-1 mutant designated NL-Y226tac that expresses Vif at an ultra-low level, being replication-defective in high-APOBEC3G cells, such as H9. It carries a synonymous mutation within the splicing SA1 site relative to its parental clone. In order to determine [...] Read more.
We have previously reported an HIV-1 mutant designated NL-Y226tac that expresses Vif at an ultra-low level, being replication-defective in high-APOBEC3G cells, such as H9. It carries a synonymous mutation within the splicing SA1 site relative to its parental clone. In order to determine whether a certain mutant(s) emerges during multi-infection cycles, we maintained H9 cells infected with a relatively low or high input of NL-Y226tac for extended time periods. Unexpectedly, we reproducibly identified a g5061a mutation in the SD2b site in the two independent long-term culture experiments that partially increases Vif expression and replication ability. Importantly, the adaptive mutation g5061a was demonstrated to enhance vif mRNA production by activation of the SA1 site mediated through increasing usage of a rarely used SD2b site. In the long-term culture initiated by a high virus input, we additionally found a Y226Fttc mutation at the original Y226tac site in SA1 that fully restores Vif expression and replication ability. As expected, the adaptive mutation Y226Fttc enhances vif mRNA production through increasing the splicing site usage of SA1. Our results here revealed the importance of the SD2b nucleotide sequence in producing vif mRNA involved in the HIV-1 adaptation and of mutual antagonism between Vif and APOBEC3 proteins in HIV-1 adaptation/evolution and survival. Full article
(This article belongs to the Special Issue Cellular Restriction Factors against Viral Infection)
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