Key result
Nicotinamide suppressed Hepatitis A Virus replication partly by inhibiting AP-1 activity and HAV IRES-mediated translation.
Why the study?
Does nicotinamide inhibit HAV replication in preclinical models?
Does nicotinamide inhibit HAV replication in preclinical models?
Nicotinamide inhibits Hepatitis A virus replication by suppressing AP-1 activity and IRES-mediated translation, suggesting potential utility for acute HAV infection.
Answers are grounded in this paper and cite their sources.
Nicotinamide shows anti-HAV activity in preclinical models; leaves open clinical efficacy in acute infection.
Drug screening methods targeting HAV IRES-mediated translation with reporter assays are attractive and useful for drug repurposing. Nicotinamide (vitamin B3, niacin) has been shown to effectively inhibit HAV replication. Transcription complex activator protein 1 (AP-1) plays an important role in the transcriptional regulation of cellular immunity or viral replication. The results of this study provide evidence that AP-1 is involved in HAV replication and plays a role in the HAV life cycle. In addition, nicotinamide was shown to suppress HAV replication partly by inhibiting AP-1 activity and HAV IRES-mediated translation. Nicotinamide may be useful for the control of acute HAV infection by inhibiting cellular AP-1 activity during HAV infection processes.
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Sasaki et al. (2023) studied Hepatitis A Virus (HAV) infection. Nicotinamide was evaluated on HAV replication and AP-1 activity. Nicotinamide suppressed Hepatitis A Virus replication partly by inhibiting AP-1 activity and HAV IRES-mediated translation.
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