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Unlabelled: APOBEC3 proteins (A3s) play an important role in host innate immunity against viruses and DNA mutations in cancer. A3s-induced mutations in both viral and human DNA genomes vary significantly from non-lethal mutations in viruses to localized hypermutations, such as kataegis in cancer. How A3s are regulated remains largely unknown.

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Background: Direct acting antivirals (DAAs) have demonstrated remarkable efficacy, in achieving hepatitis C viral (HCV) elimination rates higher than 90%. One particular concern associated with treatment failure is the emergence of resistance associated substitutions (RASs) in the genome. The occurrence of RASs highlights the adaptability and resilience of the HCV.

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With the advent of a variety of vaccines against viral infections, there are multiple viruses that can be prevented via vaccination. However, breakthrough infections or uncovered strains can still cause vaccine-preventable viral infections (VPVIs). Therefore, timely diagnosis, treatment, and surveillance of these viruses is critical to patient care and public health.

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The Development of a One-Step PCR Assay for Rapid Detection of an Attenuated Vaccine Strain of Duck Hepatitis Virus Type 3 in Korea.

Vet Sci

December 2024

Department of Avian Diseases, College of Veterinary Medicine and Center for Avian Disease, Jeonbuk National University, Iksan 54596, Republic of Korea.

Duck hepatitis A virus type 3 (DHAV-3) is a viral pathogen that causes acute, high-mortality hepatitis in ducklings, and vaccination with attenuated live vaccines is currently the main preventive measure against it. However, differentiating infected from vaccinated animals (DIVA) is crucial for clinical diagnosis and effective disease control. This study aimed to develop a rapid mismatch amplification mutation assay PCR (MAMA-PCR) diagnostic method to simultaneously detect and differentiate between wild-type and vaccine strains.

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The outcomes of retreatment patients infected with hepatitis C virus genotype 3, cirrhosis, with velpatasvir may be affected by treatment failure with velpatasvir. The efficacy of SOF+GLE/PIB+RIB 16-24 weeks of treatment has been shown. The presence of NS5A resistance-associated substitution mutations, including Y93H, and the number and regimens of the past failed therapy do not influence the likelihood of achieving sustained virological response.

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