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Understanding the process of replication and transcription of SARS-CoV-2 is essential for antiviral strategy development. The replicase polyprotein is indispensable for viral replication. However, whether all nsps derived from the replicase polyprotein of SARS-CoV-2 are indispensable is not fully understood. In this study, we utilized the SARS-CoV-2 replicon as the system to investigate the role of each nsp in viral replication. We found that except for nsp16, all the nsp deletions drastically impair the replication of the replicon, and nsp14 could recover the replication deficiency caused by its deletion in the viral replicon. Due to the unsuccessful expressions of nsp1, nsp3, and nsp16, we could not draw a conclusion about their -rescue functions. Our study provided a new angle to understand the role of each nsp in viral replication and transcription, helping the evaluation of nsps as the target for antiviral drug development.
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http://dx.doi.org/10.3389/fmicb.2022.907422 | DOI Listing |
J Virol
September 2025
Genome Regulation and Cell Signaling, Ellen and Ronald Caplan Cancer Center, The Wistar Institute, Philadelphia, Pennsylvania, USA.
Unlabelled: Adenoviruses are double-stranded DNA viruses widely used as platforms for vaccines, oncolytics, and gene delivery. However, tools for studying adenoviral gene expression in real time during infection remain limited. Here, we describe a set of fluorescent and bioluminescent reporter viruses built using the modular AdenoBuilder reverse genetics system and informed by high-resolution maps of Ad5 transcription.
View Article and Find Full Text PDFJ Virol
September 2025
Department of Microbiology and Immunology, Center for Pathogen Research, University of Maryland School of Medicine, Baltimore, Maryland, USA.
Unlabelled: There is a need for the development of broad-spectrum antiviral compounds that can act as first-line therapeutic countermeasures to emerging viral infections. Host-directed approaches present a promising avenue of development and carry the benefit of mitigating risks of viral escape mutants. We have previously found the SKI (super killer) complex to be a broad-spectrum, host-target with our lead compound ("UMB18") showing activity against influenza A virus, coronaviruses, and filoviruses.
View Article and Find Full Text PDFJ Virol
September 2025
Université catholique de Louvain, de Duve Institute, Brussels, Belgium.
Unrelated pathogens, including viruses and bacteria, use a common short linear motif (SLiM) to interact with cellular kinases of the RSK (p90 S6 ribosomal kinase) family. Such a "DDVF" (D/E-D/E-V-F) SLiM occurs in the leader (L) protein encoded by picornaviruses of the genus , including Theiler's murine encephalomyelitis virus (TMEV), Boone cardiovirus (BCV), and Encephalomyocarditis virus (EMCV). The L-RSK complex is targeted to the nuclear pore, where RSK triggers FG-nucleoporins hyperphosphorylation, thereby causing nucleocytoplasmic trafficking disruption.
View Article and Find Full Text PDFJ Virol
September 2025
Department of Hepatology, Center of Infectious Diseases and Pathogen Biology, Institute of Translational Medicine, The First Hospital of Jilin University, Changchun, Jilin, China.
Unlabelled: Cholesterol 25-hydroxylase (CH25H), an interferon-stimulated gene (ISG), has been implicated in broad-spectrum antiviral immunity. Here, we identify CH25H as a potent suppressor of hepatitis B virus (HBV) replication that significantly outperforms IFN-α in reducing HBV DNA, pregenomic RNA (pgRNA), HBsAg, and HBeAg, without inducing cytotoxicity. However, CH25H is weakly expressed in hepatocytes and only modestly induced by type I interferon.
View Article and Find Full Text PDFMed Int (Lond)
August 2025
Department of Epidemiology, School of Public Health, Zhengzhou University, Zhengzhou, Henan 450001, P.R. China.
Punicalagin, a polyphenolic compound extracted from pomegranate peel, has received increasing attention in recent years due to its antibacterial and antiviral properties. Punicalagin is capable of inhibiting bacterial growth at sub-inhibitory concentrations by affecting cell membrane formation, disrupting membrane integrity, altering cell permeability, affecting efflux pumps, interfering with quorum sensing and influencing virulence factors. Additionally, punicalagin inhibits viruses by modulating enzyme activity, interacting with viral surface proteins, affecting gene expression, blocking viral attachment, disrupting virus receptor interaction and inhibiting viral replication.
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