B-cell-independent lymphoid tissue infection by a B-cell-tropic rhadinovirus

被引:4
作者
Chao, Brittany [1 ]
Frederico, Bruno [1 ]
Stevenson, Philip G. [1 ,2 ,3 ]
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.
引用
收藏
页码:2788 / 2793
页数:6
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