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Enterovirus A71 (EV-A71) has caused hand, foot, and mouth disease with an increased prevalence of neurological complications and acute mortality, threatening young children around the globe. By provoking mucosal immunity, intranasal vaccination has been suggested to prevent EV-A71 infection. However, antigens delivered via the nasal route usually fail to induce a protective memory response.

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Platelet factor 4-derived C15 peptide broadly inhibits enteroviruses by disrupting viral attachment.

J 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).

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Unlabelled: Enterovirus A71 (EV-A71) is a common small RNA virus that is highly neuroinvasive. Emerging evidence indicates that the complement fragment C5a and its receptor C5aR1 are important drivers of neuroinflammation. However, the potential role of the C5a-C5aR1 axis in EV-A71 encephalitis remains largely elusive.

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Deep mutation, insertion and deletion scanning across the Enterovirus A proteome reveals constraints shaping viral evolution.

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Quantitative Virology and Evolution Unit, Laboratory of Viral Diseases, NIH-NIAID Division of Intramural Research, Bethesda, MD, USA.

Article Synopsis
  • Insertions and deletions (InDels) are key factors in how viruses, especially RNA viruses, evolve and develop new traits, influencing their interactions with hosts.
  • This study examines the mutational tolerance of the Enterovirus A71 proteome by performing extensive tests on around 45,000 InDels, 6,000 deletions, and 41,000 amino acid substitutions.
  • Findings indicate that most InDels are harmful to the virus, with only a few specific sites tolerated, which are linked to crucial functions like host recognition and immune response.
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Neutrophil-derived IL-10 increases CVB3-induced acute pancreatitis pathology via suppressing CD8T cell activation while increasing macrophage STAT3-IL-6 cascade.

Cytokine

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Institutes of Biology and Medical Sciences, Soochow University, Jiangsu Key Labotrary of Infection and Immunity, Suzhou 215123, China. Electronic address:

Acute pancreatitis (AP) is a lethal inflammatory disease of the pancreas. Its pathogenesis remains obscure and specific treatments are lacking. An increase in Interleukin-10 (IL-10) in the early stage of AP patients is closely related to AP severity.

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