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Corrected and republished from: "VP4 Is a Determinant of Alpha-Defensin Modulation of Rotaviral Infection".
Hu, Ciara T; Diaz, Karina; Yang, Linda C; Sharma, Anjali; Greenberg, Harry B; Smith, Jason G.
Affiliation
  • Hu CT; Department of Microbiology, University of Washington School of Medicine , Seattle, Washington, USA.
  • Diaz K; Department of Microbiology, University of Washington School of Medicine , Seattle, Washington, USA.
  • Yang LC; Department of Microbiology, University of Washington School of Medicine , Seattle, Washington, USA.
  • Sharma A; Department of Microbiology, University of Washington School of Medicine , Seattle, Washington, USA.
  • Greenberg HB; Department of Medicine, Stanford School of Medicine , Stanford, California, USA.
  • Smith JG; Department of Microbiology and Immunology, Stanford School of Medicine , Stanford, California, USA.
J Virol ; 97(10): e0096223, 2023 10 31.
Article in En | MEDLINE | ID: mdl-37787534
ABSTRACT
IMPORTANCE Rotavirus is a leading cause of severe diarrhea in young children. Like other fecal-oral pathogens, rotaviruses encounter abundant, constitutively expressed defensins in the small intestine. These peptides are a vital part of the vertebrate innate immune system. By investigating the impact that defensins from multiple species have on the infectivity of different strains of rotavirus, we show that some rotaviral infections can be inhibited by defensins. We also found that rotaviruses may have evolved resistance to defensins in the intestine of their host species, and some even appropriate defensins to increase their infectivity. Because rotaviruses infect a broad range of animals and rotaviral infections are highly prevalent in children, identifying immune defenses against infection and how they vary across species and among viral genotypes is important for our understanding of the evolution, transmission, and zoonotic potential of these viruses as well as the improvement of vaccines.
Key words

Full text: 1 Collection: 01-internacional Database: MEDLINE Language: En Journal: J Virol Year: 2023 Type: Article Affiliation country: United States

Full text: 1 Collection: 01-internacional Database: MEDLINE Language: En Journal: J Virol Year: 2023 Type: Article Affiliation country: United States