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Enoxacin shows a broad-spectrum antiviral activity against diverse viruses by enhancing antiviral RNAi in insects

ABSTRACT: Enoxacin shows a broad-spectrum antiviral activity against diverse viruses by enhancing antiviral RNAi in insects

PROVIDER: PRJNA781957 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16987534.fastq.gz	Fastqsanger.gz
	SRR16987535.fastq.gz	Fastqsanger.gz

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Enoxacin shows a broad-spectrum antiviral activity against diverse viruses by enhancing antiviral RNAi in insects

Project description:RNA interference (RNAi) functions as the major host antiviral defense in insects, while less is understood about how to utilize antiviral RNAi in controlling viral infection in insects. Enoxacin belongs to the family of synthetic antibacterial compounds based on a fluoroquinolone skeleton that has been previously found to enhance RNAi in mammalian cells. In this study, we showed that enoxacin efficiently inhibited viral replication of Drosophila C virus (DCV) and Cricket paralysis virus (CrPV) in cultured Drosophila cells. Enoxacin promoted the loading of Dicer-2-processed virus-derived siRNA into the RNA-induced silencing complex, thereby enhancing antiviral RNAi response in infected cells. Moreover, enoxacin treatment elicited an RNAi-dependent in vivo protective efficacy against DCV or CrPV challenge in adult fruit flies. In addition, enoxacin also inhibited replication of flaviviruses, including Dengue virus and Zika virus, in Aedes mosquito cells in an RNAi-dependent manner. Together, our findings demonstrated that enoxacin can enhance RNAi in insects, and enhancing RNAi by enoxacin is an effective antiviral strategy against diverse viruses in insects, which may be exploited as a broad-spectrum antiviral agent to control vector transmission of arboviruses or viral diseases in insect farming.

2021-11-22 | GSE189204 | GEO

Enoxacin Shows Broad-Spectrum Antiviral Activity against Diverse Viruses by Enhancing Antiviral RNA Interference in Insects.

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A reversible broad-spectrum antiviral targets the human V-ATPase VO domain

Project description:Increasing threats of viral disease underscore the urgent need for broad-spectrum antiviral drugs (BSADs). Host proteins utilized by human pathogenic viruses are key BSAD targets. The vacuolar-type H⁺-ATPase (V-ATPase) has been identified as a proviral factor for most pH-dependent enveloped viruses classified as pandemic threats. We report here the discovery of cladoniamide A (CA)—a V-ATPase inhibitor with single-digit nanomolar antiviral activity and a high selectivity index (SI: 103-104) against human enveloped viruses [e.g., SARS-CoV-2 variants, influenza A viruses (H1N1, H5N1), respiratory syncytial virus, dengue serotypes 1–4, and Zika virus]. Transcriptome profiling, pH estimation assays, and V-ATPase bioassays indicate that CA interferes with V-ATPase-dependent acidification of the host endolysosomal network thus preventing viral entry. Using pseudoviruses derived from five pathogenic virus families, we confirmed that CA is a BSAD acting as an entry inhibitor. CryoEM revealed that CA inhibits the V-ATPase rotary motor by occupying unique binding sites in the membrane-embedded Vo motor. Importantly, intranasal CA treatment in mice infected with influenza A H1N1 significantly reduced viral load in the lung by four log orders. Together, these findings pave the way for developing next-generation BSADs targeted at unique druggable pockets that enable the reversible pharmacological modulation of the human V-ATPase.

2026-02-11 | GSE313871 | GEO

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