ライフサイエンスコーパス: virus antibody

1 munoassay (EIA) for the presence of vaccinia virus antibody.

2 eir serum samples were tested for anti-Nipah virus antibody.

3 and antigen-selected human IgG1lambda rabies virus antibody.

4 ncephalopathy by testing for John Cunningham virus antibodies.

5 fore the diagnosis were positive for anti-JC virus antibodies.

6 us immune complexes formed with human dengue virus antibodies.

7 ed in the absence of antibody to hepatitis C virus antibodies.

8 on of screening donor plasma for hepatitis C virus antibodies.

9 tively, had seroprotective levels of measles virus antibodies; 100.0% and 99.6%, respectively, showed

10 ingdom blood donor screening for hepatitis C virus antibody:18 of 39 (46%) and those treated after th

11 29 tested were seropositive for hepatitis C virus antibody (31%); in total, 22 cases were seropositi

12 emonstrate a 50 to 60% prevalence of anti-JC virus antibodies, a low false-negative rate, and an asso

13 etect anti-p17 (HIV, human immune deficiency virus) antibodies (Ab) in phosphate buffered solutions (

14 al vaccine should target conserved influenza virus antibody and T cell epitopes that do not vary from

15 YLD virus does not cross-react with vaccinia virus antibodies, and it replicates efficiently in human

16 e for measles virus, mumps virus, or rubella virus antibodies, and there were no significant differen

17 epatitis B surface antigen, anti-hepatitis C virus antibody, and diabetes mellitus) (hazard ratio = 3

18 histochemical assays using a mouse anti-Zika virus antibody, and RT-PCR assays targeting the NS5 and

19 nsequence of the complex interaction between virus, antibody, and target cell.

20 Gs), and our studies on their recognition by viruses, antibodies, and glycan-binding proteins (GBPs),

21 munoassays (EIA-2 and EIA-3) for hepatitis C virus antibody (anti-HCV) are the most practical screeni

22 dy formation, and false-negative hepatitis C virus antibody (anti-HCV) tests have been reported in in

23 If the occurrence of hepatitis E virus antibody (anti-HEV) in regions where the disease i

24 ctive mechanism underlying this example of a virus-antibody arms race, illustrate the functional sign

25 This work has revealed that a virus-antibody "arms race" occurs in which a HIV-1 trans

26 uses and B cells evolve together, creating a virus-antibody "arms race." Analysis of samples from an

27 ical false-negative rate of a 2-step anti-JC virus antibody assay.

28 The measles virus antibody avidity indexes were high for all childre

29 ypocomplementemia and a positive hepatitis C virus antibody but negative hepatitis C virus PCR.

30 r of these (7.1%) were positive for vaccinia virus antibody by EIA.

31 However, not every virus-antibody combination results in complete neutraliz

32 mined the three-dimensional structure of the virus-antibody complex.

33 Two of these were virus-antibody complexes having contrasting transcriptio

34 Among the 4 serotypes of dengue virus, antibody-dependent enhancement is thought to enha

35 ge expressing broadly neutralizing influenza virus antibodies derived from a subject immunized with t

36 nd plasma samples were collected for anti-JC virus antibody detection using an analytically validated

37 We investigated whether Zika virus antibodies enhance dengue virus replication, by ex

38 isolate B cells whose genes encode influenza virus antibodies from a patient vaccinated for avian inf

39 Patients who were positive for anti-JC virus antibodies, had taken immunosuppressants before th

40 We showed that Zika virus antibodies have the ability to enhance dengue viru

41 ize infants with maternally acquired measles virus antibodies in whom the current parenterally admini

42 m the NHANES sampling frame have hepatitis C virus antibody, including 500,000 incarcerated people, 2

43 We create two spatial models of virus-antibody interaction and show that for realistic p

44 We use a mathematical model of virus-antibody interaction to elucidate the conditions u

45 -4 to determine how gB-NT contributes to the virus-antibody interaction.

46 Structural studies of virus-antibody interactions can offer insights into mech

47 c studies showed that these mutations affect virus-antibody interactions during postbinding steps of

48 f two highly efficacious anti-H5N1 influenza virus antibodies into a bispecific FcDART molecule, whic

49 Adjustment for Epstein-Barr virus antibody levels and C-reactive protein levels had

50 edule was associated with protective measles virus antibody levels at 24 months of age in nearly all

51 months of age, 75% had nonprotective measles virus antibody levels.

52 hat like other heterosubtypic anti-influenza virus antibodies, MAb 3.1 contacts a hydrophobic groove

53 Reports suggest that anti-dengue virus antibody may enhance Zika virus replication.

54 i-human immunoglobulin G Fab fragment to the virus-antibody mixture prior to infection.

55 moreover, SM E041 was simian T-cell leukemia virus antibody negative.

56 pared their diagnostic efficacies by using B virus antibody-negative (n = 40) and -positive (n = 75)

57 In contrast to genetically inactivated virus, antibody-neutralized virus did not induce diarrhe

58 000, were routinely screened for hepatitis C virus antibody on admission.

59 between 9 and 24 months of age for influenza virus antibodies, performed HI tests for the positive se

60 Many JC virus antibody-positive relapsing-remitting multiple scl

61 atients switching from natalizumab due to JC virus antibody positivity at 3 Swedish multiple sclerosi

62 tients who switch from natalizumab due to JC virus antibody positivity.

63 TIFY-1 will confirm the stability of anti-JC virus antibody prevalence over time.

64 At baseline (n = 1,096), overall anti-JC virus antibody prevalence was 56.0% (95% confidence inte

65 age and male gender with increasing anti-JC virus antibody prevalence.

66 e or negative status with respect to anti-JC virus antibodies, prior or no prior use of immunosuppres

67 ors: positive status with respect to anti-JC virus antibodies, prior use of immunosuppressants, and i

68 Positive status with respect to anti-JC virus antibodies, prior use of immunosuppressants, and i

69 rbent assay-determined specific Epstein-Barr virus antibody profiles had a sensitivity and specificit

70 We tested the measles virus antibody response at 4.5, 9, 18, and 24 months of

71 placed to target the same DLN, the influenza virus antibody response is enhanced.

72 ffect on the ability to mount anti-influenza virus antibody responses.

73 ith vaccination, recovery of vaccine-related virus, antibody responses, and immunohistochemical assay

74 t myelin destruction in the presence of anti-virus antibodies results from a combination of complemen

75 w tools for risk stratification including JC-virus antibody status, prior immunosuppression, and leng

76 During infection with non-enveloped viruses, antibodies stimulate immunity from inside cells

77 zation is highly effective against cell-free virus, antibodies targeting different sites of envelope

78 amples consecutively submitted for West Nile virus antibody testing during 2 days of the 2003 West Ni

79 Blood samples were available for anti-JC virus antibody testing from 5896 patients with multiple

80 The measles virus antibody titer, however, is a potency requirement

81 63 resulted in a decrease in average measles virus antibody titers among plasma donors, which is refl

82 combination with M8 increased anti-influenza virus antibody titers and protected animals from lethal

83 To mitigate the decline in measles virus antibody titers in IVIGs and to ensure consistent

84 Neutralizing measles virus antibody titers were above the threshold for prote

85 ated with increased pulmonary anti-influenza virus antibody titers, and this was dependent upon the p

86 ed subjects developed protective anti-rabies virus antibody titers.

87 s been demonstrated to regulate neutralizing virus antibody titers.

88 fants had a similar transplacental influenza virus antibody transfer ratio, lower titers, and a lower

89 JC virus antibodies were found in 5 of 13 patients.

90 .3%) (P > 0.05), while hepatitis A, B, and C virus antibodies were more prevalent in the high-risk gr

91 f an inverse association of varicella-zoster virus antibodies with adult onset glioma.

92 g the patients who were negative for anti-JC virus antibodies, with the incidence estimated to be 0.0