Special Issue "The Host Interferon Response against RNA and DNA Viruses"
Deadline for manuscript submissions: 15 November 2021.
Interests: RNA viruses, alphaviruses, flaviviruses, virus-host interactions, innate immune responses, interferon, interferon-stimulated genes, broad-spectrum antiviral host factors
Interests: Human T cell development；T cell receptor (TCR) alpha/beta cells； TCR gamma/delta cells; plasmacytoid (lymphoid -derived) dendritic cells; myeloid derived dendritic cells; Natural Killer (NK) cells; NK-T cells and regulatory T cells; HIV
The type I (α/β) interferon (IFN) response is the first and most critical line of host defense against viruses. Upon viral invasion, the host cell recognizes pathogen-associated molecular patterns (PAMPs), such as viral double-stranded RNA or DNA, and activates transcription factors IFN regulatory factors 3 or 7 (IRF3/7), leading to the production of type I IFN. Secreted IFN binds to the cell surface receptor on the infected or neighboring cells and activates the Janus kinase (JAK)-signal transducer and activator of transcription (STAT) signaling pathway, inducing expression of an array of IFN-stimulated genes (ISGs) that establish the antiviral state.
Many ISGs with antiviral activity have been identified and shown to inhibit different stages of the viral life cycle, such as endosomal fusion, translation, and release. However, they are just the tip of the iceberg. For some ISGs, it is not clear what the exact mechanisms underlying their inhibitory effects are. As we combat emerging viruses like SARS-CoV-2, a better understanding of the mechanism of broadly active ISGs is urgently needed. In addition, the antiviral role of a plethora of ISGs is yet to be uncovered. Moreover, viruses that are not sensitive to the antiviral action of well-characterized ISGs might have evolved strategies to evade or antagonize the IFN response. Characterizing the function of ISGs will illuminate viral processes targeted by innate immunity, cellular pathways usurped for antiviral activity, and uncover novel viral evasion strategies. This knowledge will allow us to develop new therapies that either mimic ISG action or reinforce the weak points of the IFN system.
This Special Issue is intended to provide an up-to-date view of the contribution of IFN and ISGs to immune control of viral infections. The emphasis is on the antiviral role and mechanism of ISGs that have been or are yet to be identified and evasions strategies employed by RNA and DNA viruses to evade these ISGs.
Dr. Melody Li
Dr. Christel Uittenbogaart
Dr. Ting-Ting Wu
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. 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 1800 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.
- Antiviral proteins
- antiviral ISGs
- virus-host interactions
- viral evasion of IFN