ライフサイエンスコーパス: enteroviral

1 The enteroviral 2A proteinase (2A(pro)) is essential for rep

2 Subsequently, the spectrum of antirhino/enteroviral activity of the more interesting analogues w

3 lipid microenvironment is essential for both enteroviral and flaviviral RNA replication; PI4KIIIbeta

4 It is desirable to localize enteroviral antigens so as to establish a link between t

5 r biology have improved our understanding of enteroviral biology and of potential alternative pathoge

6 The presence of enteroviral capsid protein 1 (VP1) and the expression of

7 Protease 2A has a significant role in enteroviral cardiomyopathy and alone is sufficient to in

8 However, the direct effect of protease 2A in enteroviral cardiomyopathy is less clear because other v

9 To determine whether low-level enteroviral gene expression similar to that observed wit

10 naturally occurring genomic alteration to an enteroviral genome associated with long-term viral persi

11 ls a novel mode of viral transmission, where enteroviral genomes are transmitted from cell-to-cell en

12 demonstrates that restricted replication of enteroviral genomes in myocytes in a pattern similar to

13 a demonstrate that restricted replication of enteroviral genomes in the heart can induce dilated card

14 gammaglobulinemia were examined to determine enteroviral genotypic variability.

15 Adult human enteroviral heart disease is often associated with the d

16 red cells decreased the cytopathic effect of enteroviral infection and the release of virus from the

17 Enteroviral infection can cause an acquired form of dila

18 suggest a molecular mechanism through which enteroviral infection contributes to the pathogenesis of

19 istent with the possibility that a low-grade enteroviral infection in the pancreatic islets contribut

20 Both enteroviral infection of the heart and mutations in the

21 e cleavage of initiation factor eIF5B during enteroviral infection, along with the viral internal rib

22 Many cases are attributable to enteroviral infection, and in particular to coxsackievir

23 may have a blunted innate immune response to enteroviral infection, leading to reduced viral clearanc

24 stance to the acute cardiac injury caused by enteroviral infection.

25 ype 1 diabetes have suggested a link between enteroviral infections and the development of this disea

26 etic autoimmunity to determine whether acute enteroviral infections can promote progression from auto

27 Enteroviral infections of the heart are among the most c

28 ailable antiviral for the treatment of rhino/enteroviral infections, a series of vinylacetylene benzi

29 al sequelae might be expected after neonatal enteroviral infections, yet antiviral treatment initiate

30 ular methods for the detection and typing of enteroviral infections.

31 nervous system, particularly for herpes and enteroviral infections.

32 interactions between HLA class II genes and enteroviral infections.

33 The assay detected all enteroviral isolates tested with no cross-reactivity to

34 oles for the endocytic machinery in both the enteroviral life cycle and host cell cholesterol homeost

35 s of two representative sequence variants of enteroviral loop B RNA.

36 ystrophin is critical for viral propagation, enteroviral-mediated cytopathic effects, and the develop

37 ssay should prove useful in the diagnosis of enteroviral meningitis versus bacterial meningitis, ther

38 The overall prevalence of enteroviral meningitis was 26.04%.

39 Clinical truth for enteroviral meningitis was defined as clinical evidence

40 ed as the new gold standard for diagnosis of enteroviral meningitis, and their use can improve the ma

41 d a high degree of accuracy for diagnosis of enteroviral meningitis.

42 rease the costs for caring for children with enteroviral meningitis.

43 (95% CI, 94.6 to 100%) for the diagnosis of enteroviral meningitis.

44 T-PCR results were used to classify cases of enteroviral meningitis.

45 ly useful treatments, such as pleconaril for enteroviral meningoencephalitis are under clinical evalu

46 d cardiomyopathy seen in humans with chronic enteroviral myocarditis.

47 We screened TLR3 in patients diagnosed with enteroviral myocarditis/cardiomyopathy and identified a

48 Although enteroviral nucleic acids have been detected in selected

49 Here, we demonstrate that clusters of enteroviral particles are packaged within phosphatidylse

50 Enteroviral persistence has been implicated in the patho

51 d Pro(357), which is absolutely conserved in enteroviral polymerases, was found to be critical for pr

52 Upon CV infection, enteroviral protease 2A cleaves a small number of host p

53 We previously demonstrated that the enteroviral protease 2A cleaves dystrophin; therefore, w

54 We previously demonstrated that enteroviral protease 2A directly cleaves the cytoskeleta

55 ophin is the first cellular substrate of the enteroviral protease 2A that was identified using by a b

56 h inducible cardiac-restricted expression of enteroviral protease 2A was generated.

57 and which has been shown previously to bind enteroviral protein 3A and to be required for viral RNA

58 The two enteroviral proteinases, 2A proteinase (2A(pro)) and 3C

59 Enteroviral proteins were radiolabeled with [35S]methion

60 te cholesterol as a critical determinant for enteroviral replication and outline roles for the endocy

61 zyme immunoassay (DEIA) kit for detection of enteroviral reverse transcription-PCR (RT-PCR) products

62 Enteroviral ribonucleic acids have been identified in he

63 We detected enteroviral RNA and cultured infectious virus from a ser

64 ated CSF protein levels and the detection of enteroviral RNA by reverse transcription (RT)-PCR.

65 se is often associated with the detection of enteroviral RNA in cardiac muscle tissue in the absence

66 inhibition interferes with this process; and enteroviral RNA polymerases specifically bind PI4P.

67 Enteroviral RNA was detected in 6 of 11 myocarditis samp

68 opose that such studies use assays to detect enteroviral RNA, in addition to IgM serology.

69 reproducibly quantify down to 510 copies of enteroviral RNA/ml of cerebrospinal fluid.

70 presence of West Nile virus during the 2002 enteroviral season contributed to a change in these corr

71 ) samples submitted during the 2007 and 2008 enteroviral seasons were included in a study to determin

72 Enteroviral sequences were detected in seven patients an

73 prototype strains belonging to 20 different enteroviral serotypes.

74 mong children < or =7 years of age, elevated enteroviral titers were more frequent in those with juve

75 onset date, and young patients have elevated enteroviral titers, as do young geographic controls.

76 ion for the development of new nonpoliovirus enteroviral vectors.

77 A consensus enteroviral VPg protein had the same distinctive high pK