Enterovirus 71 (EV-A71) is a major causative pathogen of hand, foot, and mouth disease (HFMD) epidemics. No antiviral therapies are currently available for treating EV-A71 infections. Here, we selected five reported enterovirus inhibitors (suramin, itraconazole [ITZ], GW5074, rupintrivir, and favipiravir) with different mechanisms of action to test their abilities to inhibit EV-A71 replication alone and in combination. All selected compounds have anti-EV-A71 activities in cell culture. The combination of rupintrivir and ITZ or favipiravir was synergistic, while the combination of rupintrivir and suramin was additive. The combination of suramin and favipiravir exerted a strong synergistic antiviral effect. The observed synergy was not due to cytotoxicity, as there was no significant increase in cytotoxicity when compounds were used in combinations at the tested doses. To investigate the potential inhibitory mechanism of favipiravir against enterovirus, two favipiravir-resistant EV-A71 variants were independently selected, and both of them carried an S121N mutation in the finger subdomain of the 3D polymerase. Reverse engineering of this 3D S121N mutation into an infectious clone of EV-A71 confirmed the resistant phenotype. Moreover, viruses resistant to ITZ or favipiravir remained susceptible to other inhibitors. Most notably, combined with ITZ, rupintrivir prevented the development of ITZ-resistant variants. Taken together, these results provide a rational basis for the design of combination regimens for use in the treatment of EV-A71 infections.
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http://dx.doi.org/10.1128/AAC.01073-16 | DOI Listing |
Cell Host Microbe
December 2024
Cancer Center, The First Hospital of Jilin University, Changchun, Jilin 130021, China; Institute of Virology and AIDS Research, The First Hospital of Jilin University, Changchun, Jilin 130021, China; Institute of Translational Medicine, Key Laboratory of Organ Regeneration and Transplantation of Ministry of Education, The First Hospital of Jilin University, Changchun, Jilin 130021, China. Electronic address:
Enterovirus D68 (EV-D68) is a leading non-polio enterovirus that causes severe respiratory diseases and poliomyelitis-like illness in children. Viral entry represents a potential multifaceted target for antiviral intervention; however, there are no approved inhibitors to block EV-D68. Here, we identify the functionally undescribed membrane protein major facilitator superfamily-domain-containing protein 6 (MFSD6) as an EV-D68 entry factor amenable to therapeutic intervention.
View Article and Find Full Text PDFJ Virol
January 2025
Department of Infectious Diseases, Center of Infectious Diseases and Pathogen Biology, Institute of Virology and AIDS Research, Key Laboratory of Organ Regeneration and Transplantation of The Ministry of Education, The First Hospital of Jilin University, Changchun, Jilin, China.
Unlabelled: Platelet factor 4 (PF4) has been shown to regulate several viral infections. Our previous study demonstrated that PF4 inhibits the entry of enterovirus A 71 (EV71) and coxsackievirus A16 (CA16), which cause hand, foot, and mouth disease (HFMD). In this study, we report that PF4 also inhibits the circulating HFMD pathogen coxsackievirus A6 (CA6) and the re-emerging enterovirus D68 (EVD68).
View Article and Find Full Text PDFACS Infect Dis
January 2025
Aix-Marseille Université, CNRS, ICR UMR_7273, LPCR, Faculté de Pharmacie, Marseille 13385, France.
Enterovirus (EV) is a genus that includes a large diversity of viruses spread around the world. They are the main cause of numerous diseases with seasonal clusters, like hand-foot-mouth disease (HFMD). A vaccine is marketed in China for the prevention of HFMD caused by EV-A71.
View Article and Find Full Text PDFImmun Inflamm Dis
November 2024
Department of Cardiology, The First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Background: Viral myocarditis (VMC) plays a significant role in heart failure, and there is currently a shortage of available targeted treatments. Macrophage phenotype and function are closely associated with the beta-2 adrenergic receptor (β2-AR).
Method: This research employed a BALB/c mouse model of VMC generated using Coxsackievirus B3 (CVB3), and the β2-AR agonist formoterol was administered as treatment.
Viruses
October 2024
Department of Biochemistry and Molecular Biology, The Pennsylvania State University, University Park, PA 16802, USA.
Virus spread at the single-cell level is largely uncharacterized. We have designed and constructed a microfluidic device in which each nanowell contains a single, infected cell (donor) and a single, uninfected cell (recipient). Using a GFP-expressing poliovirus as our model, we observed both lytic and non-lytic spread.
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