ライフサイエンスコーパス: Epstein-Barr virus infection

1 sfunction associated with chronic, low-grade Epstein-Barr virus infection.

2 geal carcinoma resulted in identification of Epstein-Barr virus infection.

3 lymphoproliferative disease associated with Epstein-Barr virus infection.

4 is based on false-positive tests for primary 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 ation is distinct from MHC associations with Epstein-Barr virus infection.

8 protein that is induced in B lymphocytes by Epstein-Barr virus infection.

9 more rarely T cells, associated with clonal 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

13 e sought evidence for an association between Epstein-Barr virus infection and lupus.

14 ponsible for the association between delayed Epstein-Barr virus infection and multiple sclerosis risk

15 deficiency with increased susceptibility to Epstein-Barr virus infection and N-linked glycosylation

16 renewed attention include vitamin D status, Epstein-Barr virus infection and smoking.

17 vironmental risk factors, including smoking, Epstein-Barr Virus infection, and childhood obesity.

18 he incidence of PTLD include allograft type, Epstein-Barr virus infection, and immunosuppression.

19 Epstein-Barr virus infection, and perhaps almost exclusi

20 nt with, but do not in themselves establish, Epstein-Barr virus infection as an etiologic factor in l

21 Chronic active Epstein-Barr virus infection (CAEBV) is a rare disease i

22 -into-F1 model has two major similarities to Epstein-Barr virus infection: CD4 T-cell-driven polyclon

23 indings and, if so, elucidation of why early Epstein-Barr virus infection does not usually trigger th

24 Epstein-Barr virus infection has a role in the pathogene

25 Epstein-Barr virus infection has been epidemiologically

26 e of AIDS-related PCNSL, which is related to Epstein-Barr virus infections, has fallen with the insti

27 uses on the roles of c-myc dysregulation and Epstein-Barr virus infection in Burkitt's lymphoma.

28 n situ hybridization revealed no evidence of Epstein-Barr virus infection in examined tissues.

29 yngeal mucosal space, associated with latent Epstein-Barr virus infection in most cases.

30 in peripheral blood lymphocytes established Epstein-Barr virus infection in the peripheral blood of

31 Epstein-Barr virus infection in vitro immortalizes prima

32 Although Epstein-Barr virus infection is a known risk factor, oth

33 If the hypothesis that delayed Epstein-Barr virus infection is necessary for the develo

34 IMPORTANCE Epstein-Barr virus infection is predominantly latent in

35 necessitated by the fact that age at primary Epstein-Barr virus infection is unknown for practically

36 yndrome, characterized by fatal responses to Epstein-Barr virus infection, is caused by mutations aff

37 In this study, we demonstrate that Epstein-Barr virus infection leads to a reduction in cer

38 ovide insight into the pathogenesis of fatal Epstein-Barr virus infection, lymphomas, Hodgkins diseas

39 order characterized by abnormal responses to Epstein-Barr virus infection, lymphoproliferative syndro

40 We conclude that Epstein-Barr virus infection manifesting as IM in adoles

41 Epstein-Barr virus infection occurred in 6 of 19 childre

42 ever, as fascin expression may be induced by Epstein-Barr virus infection of B cells, the possibility

43 cell-like gene expression program, and that Epstein-Barr virus infection of HRS cells has a minor tr

44 SAP mutation, and not Epstein-Barr virus infection per se, may be critical for

45 During B-cell activation and Epstein-Barr virus infection, redirection of splicing fr

46 tion, and perhaps almost exclusively delayed Epstein-Barr virus infection, seems to be a prerequisite

47 s, such as the incidence of acute rejection, Epstein-Barr virus infection, sepsis, biliary and vascul

48 cells from a Burkitt's lymphoma with latent Epstein-Barr virus infection showed dramatic proliferati

49 , the dominant CD4+ T cell antigen of latent Epstein-Barr virus infection, slowly accumulated in cyto

50 n risk factors include vitamin D deficiency, Epstein-Barr virus infection, smoking, HLA genes, and mi

51 Genomic lesions, Epstein-Barr virus infection, soluble factors, and tumor

52 eloped many episodes of PTLD associated with Epstein-Barr virus infection that were resistant to seve

53 Recently, an individual with chronic active Epstein-Barr virus infection was found to have mutations

54 Comparatively, the incidence of Epstein-Barr virus infection was similar in both groups

55 e bcl-1, bcl-2, or ras genes and evidence of Epstein-Barr virus infection were not observed.

56 cases of BK virus infection, and one case of Epstein-Barr virus infection were observed.

57 , H-ras, K-ras, N-ras, and p53 genes and for Epstein-Barr virus infection, which are commonly involve

58 Despite strong evidence linking Epstein-Barr virus infection with human lupus, the exact

59 s by occasionally preventing delayed primary Epstein-Barr virus infection, with its associated high r