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Journals
Viruses
Special Issues
Biologics for Emerging and Reemerging Viral Infections
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Biologics for Emerging and Reemerging Viral Infections

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Viral Immunology, Vaccines, and Antivirals".

Deadline for manuscript submissions: closed (29 February 2024) | Viewed by 3636

Special Issue Editors

Prof. Dr. Qiang (Shawn) Chen

E-Mail Website
Guest Editor
The Biodesign Institute and School of Life Sciences, Arizona State University, Tempe, Arizona 85225, USA
Interests: biologics against viral infections and cancer; flavivirus; vaccines; monoclonal antibodies
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Fengwei Bai

E-Mail Website
Guest Editor
Cell and Molecular Biology Program, University of Southern Mississippi, Hattiesburg, MS 39406, USA
Interests: flavivirus; mosquito transmitted virus; antiviral; vaccine; viral pathogenesis
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Xiaohong Zhou

E-Mail Website
Guest Editor
Institute of Tropical Medicine and School of Public Health, Southern Medical University, Guangzhou 510515, China
Interests: prevention and control of mosquito-borne arboviral diseases; flavivirus; molecular epidemiology; host-vector-pathogen interactions

Special Issue Information

Dear Colleagues,

The current COVID-19 pandemic demonstrates the devastation and destruction that viral infections can cause for human life and the world economy. Our collective response to the pandemic, however, highlights our tremendous capability in innovation, research and development, and manufacture to rapidly develop and produce biologics for the prevention, treatment, diagnosis of SARS-CoV-2. This Special Issue aims to focus on the development of novel biologics using various traditional and alternative platforms and production hosts against emerging and reemerging viral infections.

Prof. Dr. Qiang (Shawn) Chen
Prof. Dr. Fengwei Bai
Prof. Dr. Xiaohong Zhou
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. 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

  • emerging and reemerging viral infections
  • vaccine
  • monoclonal antibody
  • diagnostic biologics
  • glycoengineering
  • plant and insect cell-produced biologics
  • host-vector-pathogen interactions
  • molecular epidemiology

Published Papers (2 papers)

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Research

16 pages, 2911 KiB  
Article
Efficiency of Interferon-γ in Activating Dendritic Cells and Its Potential Synergy with Toll-like Receptor Agonists
by Yuanzhi Bian, Debra L. Walter and Chenming Zhang
Viruses 2023, 15(5), 1198; https://doi.org/10.3390/v15051198 - 19 May 2023
Cited by 4 | Viewed by 1513
Abstract
Interferon-γ (IFN-γ) is a cytokine that plays an important role in immune regulation, especially in the activation and differentiation of immune cells. Toll-like receptors (TLRs) are a family of pattern-recognition receptors that sense structural motifs related to pathogens and alert immune cells to [...] Read more.
Interferon-γ (IFN-γ) is a cytokine that plays an important role in immune regulation, especially in the activation and differentiation of immune cells. Toll-like receptors (TLRs) are a family of pattern-recognition receptors that sense structural motifs related to pathogens and alert immune cells to the invasion. Both IFN-γ and TLR agonists have been used as immunoadjuvants to augment the efficacy of cancer immunotherapies and vaccines against infectious diseases or psychoactive compounds. In this study, we aimed to explore the potential of IFN-γ and TLR agonists being applied simultaneously to boost dendritic cell activation and the subsequent antigen presentation. In brief, murine dendritic cells were treated with IFN-γ and/or the TLR agonists, polyinosinic–polycytidylic acid (poly I:C), or resiquimod (R848). Next, the dendritic cells were stained for an activation marker, a cluster of differentiation 86 (CD86), and the percentage of CD86-positive cells was measured by flow cytometry. From the cytometric analysis, IFN-γ efficiently stimulated a considerable number of the dendritic cells, while the TLR agonists by themselves could merely activate a few compared to the control. The combination of IFN-γ with poly I:C or R848 triggered a higher amount of dendritic cell activation than IFN-γ alone. For instance, 10 ng/mL IFN-γ with 100 µg/mL poly I:C achieved 59.1% cell activation, which was significantly higher than the 33.4% CD86-positive cells obtained by 10 ng/mL IFN-γ. These results suggested that IFN-γ and TLR agonists could be applied as complementary systems to promote dendritic cell activation and antigen presentation. There might be a synergy between the two classes of molecules, but further investigation is warranted to ascertain the interaction of their promotive activities. Full article
(This article belongs to the Special Issue Biologics for Emerging and Reemerging Viral Infections)
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17 pages, 3639 KiB  
Article
A Dual-Approach Strategy to Optimize the Safety and Efficacy of Anti-Zika Virus Monoclonal Antibody Therapeutics
by Haiyan Sun, Ming Yang, Huafang Lai, Biswas Neupane, Audrey Y.-H. Teh, Collin Jugler, Julian K.-C. Ma, Herta Steinkellner, Fengwei Bai and Qiang Chen
Viruses 2023, 15(5), 1156; https://doi.org/10.3390/v15051156 - 11 May 2023
Cited by 2 | Viewed by 1587
Abstract
Antibody-dependent enhancement of infection (ADE) is clinically relevant to Dengue virus (DENV) infection and poses a major risk to the application of monoclonal antibody (mAb)-based therapeutics against related flaviviruses such as the Zika virus (ZIKV). Here, we tested a two-tier approach for selecting [...] Read more.
Antibody-dependent enhancement of infection (ADE) is clinically relevant to Dengue virus (DENV) infection and poses a major risk to the application of monoclonal antibody (mAb)-based therapeutics against related flaviviruses such as the Zika virus (ZIKV). Here, we tested a two-tier approach for selecting non-cross-reactive mAbs combined with modulating Fc glycosylation as a strategy to doubly secure the elimination of ADE while preserving Fc effector functions. To this end, we selected a ZIKV-specific mAb (ZV54) and generated three ZV54 variants using Chinese hamster ovary cells and wild-type (WT) and glycoengineered ΔXF Nicotiana benthamiana plants as production hosts (ZV54CHO, ZV54WT, and ZV54ΔXF). The three ZV54 variants shared an identical polypeptide backbone, but each exhibited a distinct Fc N-glycosylation profile. All three ZV54 variants showed similar neutralization potency against ZIKV but no ADE activity for DENV infection, validating the importance of selecting the virus/serotype-specific mAbs for avoiding ADE by related flaviviruses. For ZIKV infection, however, ZV54CHO and ZV54ΔXF showed significant ADE activity while ZV54WT completely forwent ADE, suggesting that Fc glycan modulation may yield mAb glycoforms that abrogate ADE even for homologous viruses. In contrast to the current strategies for Fc mutations that abrogate all effector functions along with ADE, our approach allowed the preservation of effector functions as all ZV54 glycovariants retained antibody-dependent cellular cytotoxicity (ADCC) against the ZIKV-infected cells. Furthermore, the ADE-free ZV54WT demonstrated in vivo efficacy in a ZIKV-infection mouse model. Collectively, our study provides further support for the hypothesis that antibody–viral surface antigen and Fc-mediated host cell interactions are both prerequisites for ADE, and that a dual-approach strategy, as shown herein, contributes to the development of highly safe and efficacious anti-ZIKV mAb therapeutics. Our findings may be impactful to other ADE-prone viruses, including SARS-CoV-2. Full article
(This article belongs to the Special Issue Biologics for Emerging and Reemerging Viral Infections)
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