The pathogenesis of Epstein-Barr virus persistent infection

被引:165
作者
Thorley-Lawson, David A. [1 ]
Hawkins, Jared B. [1 ]
Tracy, Sean I. [1 ]
Shapiro, Michael [1 ]
机构
[1] Tufts Univ, Sch Med, Dept Pathol, Boston, MA 02111 USA
关键词
MEMORY B-CELLS; IN-VIVO; GERMINAL CENTER; EBV PERSISTENCE; DIFFERENTIATION; IDENTIFICATION; LYMPHOMAS; MONONUCLEOSIS; COMPARTMENT; RESPONSES;
D O I
10.1016/j.coviro.2013.04.005
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Epstein-Barr virus (EBV) maintains a lifelong infection. According to the germinal center model (GCM), latently infected B cells transit the germinal center (GC) to become resting memory cells. Here, the virus resides quiescently occasionally reactivating to infect new B cells, completing the cycle of infection. The GCM remains the only model that explains EBV biology and the pathogenesis of lymphoma. Recent work suggests modifications to the model notably that the virus contributes only modestly to the GC process and predictions from mathematical models that quiescence within memory B cells shapes the overall structure of viral infection but is not essential for persistence. Rather, it is the cycle of infection which allows viral persistence at the very low levels observed.
引用
收藏
页码:227 / 232
页数:6
相关论文
共 46 条
  • [1] The expression pattern of Epstein-Barr virus latent genes in vivo is dependent upon the differentiation stage of the infected B cell
    Babcock, GJ
    Hochberg, D
    Thorley-Lawson, DA
    [J]. IMMUNITY, 2000, 13 (04) : 497 - 506
  • [2] EBV persistence in memory B cells in vivo
    Babcock, GJ
    Decker, LL
    Volk, M
    Thorley-Lawson, DA
    [J]. IMMUNITY, 1998, 9 (03) : 395 - 404
  • [3] Epstein-Barr virus LMP2A drives B cell development and survival in the absence of normal B cell receptor signals
    Caldwell, RG
    Wilson, JB
    Anderson, SJ
    Longnecker, R
    [J]. IMMUNITY, 1998, 9 (03) : 405 - 411
  • [4] B cell receptor signal strength determines B cell fate
    Casola, S
    Otipoby, KL
    Alimzhanov, M
    Humme, S
    Uyttersprot, N
    Kutok, JL
    Carroll, MC
    Rajewsky, K
    [J]. NATURE IMMUNOLOGY, 2004, 5 (03) : 317 - 327
  • [5] Simulating Epstein-Barr virus infection with C-ImmSim
    Castiglione, Filippo
    Duca, Karen
    Jarrah, Abdul
    Laubenbacher, Reinhard
    Hochberg, Donna
    Thorley-Lawson, David
    [J]. BIOINFORMATICS, 2007, 23 (11) : 1371 - 1377
  • [6] Epstein-Barr virus persistence in the absence of conventional memory B cells:: IgM+IgD+CD27+ B cells harbor the virus in X-linked lymphoproliferative disease patients
    Chaganti, Sridhar
    Ma, Cindy S.
    Bell, Andrew I.
    Croom-Carter, Debbie
    Hislop, Andrew D.
    Tangye, Stuart G.
    Rickinson, Alan B.
    [J]. BLOOD, 2008, 112 (03) : 672 - 679
  • [7] Epstein-Barr virus colonization of tonsillar and peripheral blood B-cell subsets in primary infection and persistence
    Chaganti, Sridhar
    Heath, Emily M.
    Bergler, Wolfgang
    Kuo, Michael
    Buettner, Maike
    Niedobitek, Gerald
    Rickinson, Alan B.
    Bell, Andrew I.
    [J]. BLOOD, 2009, 113 (25) : 6372 - 6381
  • [8] A model of host response to a multi-stage pathogen
    Delgado-Eckert, Edgar
    Shapiro, Michael
    [J]. JOURNAL OF MATHEMATICAL BIOLOGY, 2011, 63 (02) : 201 - 227
  • [9] A virtual look at Epstein-Barr virus infection: Biological interpretations
    Duca, Karen A.
    Shapiro, Michael
    Delgado-Eckert, Edgar
    Hadinoto, Vey
    Jarrah, Abdul S.
    Laubenbacher, Reinhard
    Lee, Kichol
    Luzuriaga, Katherine
    Polys, Nicholas F.
    Thorley-Lawson, David A.
    [J]. PLOS PATHOGENS, 2007, 3 (10) : 1388 - 1400
  • [10] Latent membrane protein 1 of Epstein-Barr virus mimics a constitutively active receptor molecule
    Gires, O
    ZimberStrobl, U
    Gonnella, R
    Ueffing, M
    Marschall, G
    Zeidler, R
    Pich, D
    Hammerschmidt, W
    [J]. EMBO JOURNAL, 1997, 16 (20) : 6131 - 6140