作者: R L Broome , P T Vo , R L Ward , H F Clark , H B Greenberg
DOI: 10.1128/JVI.67.5.2448-2455.1993
关键词:
摘要: Simian rotavirus (RRV) and murine (EDIM-RW) differ dramatically in the oral inoculum required to cause diarrheal disease neonatal mouse pups their ability spread uninoculated littermates. A genetic approach was used explore molecular basis of these differences. Reassortant viruses were produced vivo by coinfecting infant mice with RRV EDIM-RW. isolated plaque purification progeny virus obtained from pup intestines on MA104 cells. The plaque-purified reassortants evaluated for 50% diarrhea dose (DD50) parental strain had a DD50 10(5) PFU per animal, while EDIM-RW less than 1 animal. never spreads inoculated littermates causes disease. Twenty-three tested. Of great interest D1/5 C3/2, which derived genes 4 7 (encoding VP4 VP7) RRV. These similar or identical that efficiently pups. We conclude major outer capsid proteins VP7 are not primarily responsible virulence host range restriction model using homologous rotavirus.