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B-cell-independent lymphoid tissue infection by a B-cell-tropic rhadinovirus
被引:4
作者:

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Frederico, Bruno
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机构:
Univ Cambridge, Dept Pathol, Div Virol, Cambridge CB2 1QP, England Univ Cambridge, Dept Pathol, Div Virol, Cambridge CB2 1QP, England

Stevenson, Philip G.
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机构:
Univ Cambridge, Dept Pathol, Div Virol, Cambridge CB2 1QP, England
Royal Childrens Hosp, Sir Albert Sakzewski Virus Res Ctr, Clin Med Virol Ctr, Sch Chem & Mol Biosci, Brisbane, Qld, Australia
Univ Queensland, Brisbane, Qld, Australia Univ Cambridge, Dept Pathol, Div Virol, Cambridge CB2 1QP, England
机构:
[1] Univ Cambridge, Dept Pathol, Div Virol, Cambridge CB2 1QP, England
[2] Royal Childrens Hosp, Sir Albert Sakzewski Virus Res Ctr, Clin Med Virol Ctr, Sch Chem & Mol Biosci, Brisbane, Qld, Australia
[3] Univ Queensland, Brisbane, Qld, Australia
基金:
英国医学研究理事会;
澳大利亚研究理事会;
关键词:
EPSTEIN-BARR-VIRUS;
MURINE GAMMAHERPESVIRUS 68;
IN-VIVO;
SUBCAPSULAR SINUS;
NODE;
PATHOGENESIS;
MACROPHAGES;
ESTABLISHES;
TRANSPORT;
ANTIGEN;
D O I:
10.1099/vir.0.000188
中图分类号:
Q81 [生物工程学(生物技术)];
Q93 [微生物学];
学科分类号:
071005 ;
0836 ;
090102 ;
100705 ;
摘要:
Lymphocytes provide gammaherpesviruses with a self-renewing substrate for persistent infection and with transport to mucosal sites for host exit. Their role in the initial colonization of new hosts is less clear. Murid herpesvirus 4 (MuHV-4), an experimentally accessible, B-cell-tropic rhadinovirus (gamma-2 herpesvirus), persistently infects both innmunocompetent and B-cell-deficient mice. A lack of B-cells did not compromise MuHV-4 entry into lymphoid tissue, which involved myeloid cell infection. However, it impaired infection amplification and MuHV-4 exit from lymphoid tissue, which involved myeloid to B-cell transfer.
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页码:2788 / 2793
页数:6
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