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Viruses
Special Issues
Viral Replication Inhibitors
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Viral Replication Inhibitors

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

Deadline for manuscript submissions: 30 November 2024 | Viewed by 1097

Special Issue Editors

Dr. Danielle Poulin Porter

E-Mail Website
Guest Editor
Gilead Sciences, 333 Lakeside Drive, Foster City, CA 94404, USA
Interests: virology; microbiology; molecular biology; biotechnology
Dr. Meghan Vermillion

E-Mail Website
Guest Editor
Gilead Sciences, 333 Lakeside Drive, Foster City, CA 94404, USA
Interests: models of infectious disease; respiratory physiology; mucosal immunology; reproductive biology

Special Issue Information

Dear Colleagues,

Many of the most effective antiviral agents currently approved for the treatment of human viral infections, including those caused by human immunodeficiency virus (HIV), hepatitis C virus (HCV), hepatitis B virus (HBV), hepatitis delta virus (HDV), herpesviruses, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), Ebola virus and influenza virus, act by successfully disrupting essential steps of the viral replication cycle. Viral replication inhibitors frequently target viral enzymes required for replication such as polymerases, proteases, integrases and reverse transcriptases. Other critical stages of the virus life cycle, such as viral attachment and entry, are also potential targets for inhibition. While tremendous progress has been made in the past several decades in developing viral replication inhibitors for clinical use, there are still many significant human viral diseases for which no treatment is currently available, including infections caused by measles virus, respiratory syncytial virus (RSV), rhinovirus, poliovirus, norovirus, yellow fever virus and dengue virus.

We are pleased to invite you to contribute a manuscript to this Special Issue of Viruses on viral replication inhibitors. Here, we aim to address recent advances in the development and application of replication inhibitors of human pathogenic viruses. We welcome the submission of original research, reviews, and mini-reviews covering, but not limited to, the following topics: mechanism of action (MOA) studies, viral drug resistance, novel inhibitors, expanded applications of existing inhibitors, animal efficacy data, clinical data and case studies.

We look forward to receiving your contributions.

Dr. Danielle Poulin Porter
Dr. Meghan Vermillion
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

  • antiviral drugs
  • integrase inhibitors
  • mechanism of action
  • reverse transcriptase inhibitors
  • protease inhibitors
  • polymerase inhibitors
  • entry inhibitors
  • viral infectious disease
  • small-molecule inhibitors
  • antibodies
  • viral resistance

Published Papers (1 paper)

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Research

14 pages, 2298 KiB  
Article
No Remdesivir Resistance Observed in the Phase 3 Severe and Moderate COVID-19 SIMPLE Trials
by Charlotte Hedskog, Christoph D. Spinner, Ulrike Protzer, Dieter Hoffmann, Chunkyu Ko, Robert L. Gottlieb, Medhat Askar, Meta Roestenberg, Jutte J. C. de Vries, Ellen C. Carbo, Ross Martin, Jiani Li, Dong Han, Lauren Rodriguez, Aiyappa Parvangada, Jason K. Perry, Ricard Ferrer, Andrés Antón, Cristina Andrés, Vanessa Casares, Huldrych F. Günthard, Michael Huber, Grace A. McComsey, Navid Sadri, Judith A. Aberg, Harm van Bakel and Danielle P. Porteradd Show full author list remove Hide full author list
Viruses 2024, 16(4), 546; https://doi.org/10.3390/v16040546 - 31 Mar 2024
Viewed by 873
Abstract
Remdesivir (RDV) is a broad-spectrum nucleotide analog prodrug approved for the treatment of COVID-19 in hospitalized and non-hospitalized patients with clinical benefit demonstrated in multiple Phase 3 trials. Here we present SARS-CoV-2 resistance analyses from the Phase 3 SIMPLE clinical studies evaluating RDV [...] Read more.
Remdesivir (RDV) is a broad-spectrum nucleotide analog prodrug approved for the treatment of COVID-19 in hospitalized and non-hospitalized patients with clinical benefit demonstrated in multiple Phase 3 trials. Here we present SARS-CoV-2 resistance analyses from the Phase 3 SIMPLE clinical studies evaluating RDV in hospitalized participants with severe or moderate COVID-19 disease. The severe and moderate studies enrolled participants with radiologic evidence of pneumonia and a room-air oxygen saturation of ≤94% or >94%, respectively. Virology sample collection was optional in the study protocols. Sequencing and related viral load data were obtained retrospectively from participants at a subset of study sites with local sequencing capabilities (10 of 183 sites) at timepoints with detectable viral load. Among participants with both baseline and post-baseline sequencing data treated with RDV, emergent Nsp12 substitutions were observed in 4 of 19 (21%) participants in the severe study and none of the 2 participants in the moderate study. The following 5 substitutions emerged: T76I, A526V, A554V, E665K, and C697F. The substitutions T76I, A526V, A554V, and C697F had an EC50 fold change of ≤1.5 relative to the wildtype reference using a SARS-CoV-2 subgenomic replicon system, indicating no significant change in the susceptibility to RDV. The phenotyping of E665K could not be determined due to a lack of replication. These data reveal no evidence of relevant resistance emergence and further confirm the established efficacy profile of RDV with a high resistance barrier in COVID-19 patients. Full article
(This article belongs to the Special Issue Viral Replication Inhibitors)
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