期刊
JOURNAL OF VIROLOGY
卷 77, 期 22, 页码 12352-12356出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.77.22.12352-12356.2003
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资金
- NIAID NIH HHS [R01 AI016687, T32 AI007471, R01-AI 16687, T32-AI 07471] Funding Source: Medline
- NIDDK NIH HHS [P30 DK056338, DK56338] Funding Source: Medline
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI016687, T32AI007471] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [P30DK056338] Funding Source: NIH RePORTER
We used the neonatal mouse model of rotavirus infection and virus strains SA11-clone 4 (SA11-04) and Rhesus rotavirus (RRV) to examine the mechanism of the extraintestinal spread of viruses following oral inoculation. The spread-competent viruses, RRV and reassortant R7, demonstrated a temporal progression from the intestine, to the terminal ileum, to the mesenteric lymph nodes (MLN), and to the peripheral tissues. SA11-04 was not found outside the intestine. Reassortant virus S7, which was unable to reach the liver in previous studies (E. C. Mossel and R. F. Ramig, J. Virol. 76:6502-6509, 2002), was recovered from 60% of the MLN, suggesting that there are multiple determinants for the spread of virus from the intestine to the MLN. Phenotypic segregation analysis identified RRV genome segment 6 (VP6) as a secondary determinant of the spread of virus to the MLN (P = 0.02) in reassortant viruses containing segment 7 from the spread-incompetent parent. These data suggest that in the orally infected neonatal mouse, the extraintestinal spread of rotavirus occurs via a lymphatic pathway, and the spread phenotype is primarily determined by NSP3 and can be modified by VP6.
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