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1 is based on false-positive tests for primary Epstein-Barr virus infection.
2 geal carcinoma resulted in identification of Epstein-Barr virus infection.
3 ation is distinct from MHC associations with Epstein-Barr virus infection.
4 lymphoproliferative disease associated with Epstein-Barr virus infection.
5 nteresting results regarding the dynamics of Epstein-Barr virus infection.
6 ort of individuals with acute through latent Epstein-Barr virus infection.
7 protein that is induced in B lymphocytes by Epstein-Barr virus infection.
8 more rarely T cells, associated with clonal Epstein-Barr virus infection.
9 sfunction associated with chronic, low-grade Epstein-Barr virus infection.
10 hly expressed in spleen and upregulated upon Epstein-Barr-virus infection.
11 ty to control B-cell proliferation caused by Epstein-Barr virus infections.
12 g intensity of immunosuppression, control of Epstein-Barr virus infection among transplant recipients
15 he incidence of PTLD include allograft type, Epstein-Barr virus infection, and immunosuppression.
16 nt with, but do not in themselves establish, Epstein-Barr virus infection as an etiologic factor in l
18 -into-F1 model has two major similarities to Epstein-Barr virus infection: CD4 T-cell-driven polyclon
20 e of AIDS-related PCNSL, which is related to Epstein-Barr virus infections, has fallen with the insti
24 in peripheral blood lymphocytes established Epstein-Barr virus infection in the peripheral blood of
27 yndrome, characterized by fatal responses to Epstein-Barr virus infection, is caused by mutations aff
28 ovide insight into the pathogenesis of fatal Epstein-Barr virus infection, lymphomas, Hodgkins diseas
29 order characterized by abnormal responses to Epstein-Barr virus infection, lymphoproliferative syndro
32 ever, as fascin expression may be induced by Epstein-Barr virus infection of B cells, the possibility
33 cell-like gene expression program, and that Epstein-Barr virus infection of HRS cells has a minor tr
35 s, such as the incidence of acute rejection, Epstein-Barr virus infection, sepsis, biliary and vascul
36 cells from a Burkitt's lymphoma with latent Epstein-Barr virus infection showed dramatic proliferati
37 , the dominant CD4+ T cell antigen of latent Epstein-Barr virus infection, slowly accumulated in cyto
38 n risk factors include vitamin D deficiency, Epstein-Barr virus infection, smoking, HLA genes, and mi
39 eloped many episodes of PTLD associated with Epstein-Barr virus infection that were resistant to seve
40 Recently, an individual with chronic active Epstein-Barr virus infection was found to have mutations
44 , H-ras, K-ras, N-ras, and p53 genes and for Epstein-Barr virus infection, which are commonly involve
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