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10.1016/j.coviro.2013.04.005 http://scihub22266oqcxt.onion/10.1016/j.coviro.2013.04.005 C3789532!3789532!23683686     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Curr+Opin+Virol 2013 ; 3 (3): 227-32 Nephropedia Template TP {{tp|p=23683686|t=2013. The Pathogenesis of Epstein-Barr Virus Persistent Infection |pdf=|usr=}}{{23683686}} gab.com Text The Pathogenesis of Epstein-Barr Virus Persistent Infection JO: Curr Opin Virol http://www.kidney.de/pget.php?&tw=1&pmid=23683686 #FOAvip 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. Twit Text FOAVip The Pathogenesis of Epstein-Barr Virus Persistent Infection ????Curr Opin Virol http://www.kidney.de/pget.php?&tw=1&pmid=23683686 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=23683686 #FOAvip English Wikipedia <ref>{{Cite pmid|23683686}}</ref> The Pathogenesis of Epstein-Barr Virus Persistent Infection #MMPMID23683686 Thorley-Lawson DA; Hawkins JB; Tracy SI; Shapiro M Curr Opin Virol 2013[Jun]; 3 (3): 227-32 PMID23683686show ga 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. äThe Pathogenesis of Epstein-Barr Virus Persistent Infection (epmc).pdf DeepDyve Pubget Overpricing