Special Issue "Ubiquitin and Ubiquitin-Like Pathways in Viral Infection"
A special issue of Viruses (ISSN 1999-4915).
Deadline for manuscript submissions: 31 December 2020.
Interests: innate immunity to virus infection and immune signaling; Type-I interferons (IFN) and other cytokines; the E3-ubiquitin ligase Tripartite Motif (TRIM) family of proteins in immunity; the role of ubiquitin in immunity and virus replication; viral evasion mechanisms; the role of the ubiquitin system in replication of viruses including Ebola, Nipah, dengue, Zika, West Nile, and Influenza; virus–host interactions and viral pathogenesis via the ubiquitin system
The Ubiquitin (Ub) system is a major conserved post-translational process critical in many cellular functions, including regulation of immunity, virus replication, and modulation of virus–host intercations. The function of ubiquitinated proteins depends on the linkage type of the polyubiquitin chain, the length of the chain, and the the presence of ubiquitin-binding domains (UBDs) on specific proteins. Ub conjugation requires an E1-activating enzyme, an E2-conjugase, and an E3-ligase, which transfers Ub to the target protein. Each of these factors can be exploited by viruses to enhance their replication. Since the Ub system is also critical for the activation of antiviral immune signaling, this raises the question regarding the importance of Ub in promoting virus replication versus its role in inducing antiviral responses. To develop antiviral strategies, we need a better understanding of which factors of the Ub system can be targeted to reduce virus replication and at the same time decrease immune pathology. Extensive research has been done on mechanisms used by viruses that promote the degradation of antiviral host factors through Ub-dependent mechanisms or inhibit innate immune signaling pathways by blocking ubiquitination of host signaling components. Previously unrecognized mechanisms include the presence of ubiquitinated viral proteins or unanchored (not-covalently attached) Ub in infectious virions, which help virus entry and replication. In this Special Issue, we will explore novel aspects of virus antagonism of the immune reponse by targeting the host ubiquitin machinery and how viruses hijack ubiquitin factors to enhance their replication, a mechanism that ultimetely can be targeted to design antiviral strategies.
Dr. Ricardo Rajsbaum
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 papers will be 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 2000 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.
- innate immunity
- Type-I interferons
- inflammatory cytokines
- Tripartite Motif (TRIM) proteins
- unanchored ubiquitin
- ubiquitin-like proteins
- virus antagonism
- ubiquitin ligases and conjugating enzymes
- virus adaptation
- cell signaling
- ubiquitin/proteasome system
The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.
Title: Viral manipulation of the ubiquitin machinery to evade detection by RIG-I-like receptors
Authors: Michaela U. Gack; et al.
Affiliation: University of Chicago