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1 ren in group 1 born to anti-HAV-negative and anti-HAV-positive mothers, respectively, and 4% of group
2               Serological response rates and anti-HAV antibody titers were compared at weeks 24 and 4
3   Although unexplained mechanistically, both anti-HAV antibody and inactivated whole-virus vaccines p
4       When examined by 5-year birth cohorts, anti-HAV prevalence increased in children born between 1
5 ith compensated liver disease had detectable anti-HAV antibody compared with 37.1% with decompensated
6 26 adults tested at 8-9 years had detectable anti-HAV.
7                        Importantly, elevated anti-HAV Ig titers were broadly observed across plasma u
8  clinical trial, PWH who tested negative for anti-HAV antibodies after receiving a standard 2-dose se
9 n 94% of all vaccinees were seropositive for anti-HAV after the complete vaccination course.
10                                  Eighty-four anti-HAV antibody-negative patients, 49 with compensated
11           Of the 391 patients, 205 (52%) had anti-HAV IgG antibodies.
12  age-adjusted prevalence of antibody to HAV (anti-HAV) was 51% in 1983 and 49% in 1993 (P=.506).
13 tion schedule generated significantly higher anti-HAV antibody titers and was more likely to elicit s
14 V RNA at baseline was associated with higher anti-HAV antibody titers after the second vaccine dose.
15                                     However, anti-HAV antibody titers were consistently higher in the
16                          Postvaccination IgG anti-HAV were determined at 1, 6, and 7 months after the
17             Recent trends show a decrease in anti-HAV antibodies in the general population, with conc
18 ining 105 children, immunization resulted in anti-HAV levels of 17-572 mIU/mL.
19 t age 6 months (50%-75%), and among maternal anti-HAV-positive children in groups 2 and 3 (67%-87%),
20 h group, infants were randomized by maternal anti-HAV status.
21  10 years regardless of presence of maternal anti-HAV.
22 r significantly by vaccine group or maternal anti-HAV status.
23  each group randomized according to maternal anti-HAV status.
24 al antibodies to hepatitis A virus (maternal anti-HAV) may lower the infant's immune response to the
25 cted hepatitis A subclinically (>8000 mIU/mL anti-HAV).
26 d into naive mice but contained neutralizing anti-HAV antibody.
27 assay, while reciprocal GMTs of neutralizing anti-HAV were 6.5 and 15.0 by an 80% radioimmunofocus in
28 int, a lower geometric mean concentration of anti-HAV was observed for each group of CLD patients com
29                                   The GMC of anti-HAV antibody at week 48 for three-dose HIV-infected
30    The geometric mean concentration (GMC) of anti-HAV antibody was determined at weeks 48 and 72.
31          The geometric mean titers (GMTs) of anti-HAV were 49.3 and 45.2 mIU/mL by immunoassay, while
32 ng elicited an average 29.7-fold increase of anti-HAV levels.
33                        We obtained levels of anti-HAV at intervals through age 15-16 years among thre
34                            The prevalence of anti-HAV-IgG, anti-HBc, anti-HBsAg, anti-HCV, anti-HEV a
35                             A broad range of anti-HAV Ig plasma titers was observed among these cente
36 10 years of age correlated with initial peak anti-HAV levels (tested at 1 month after the second dose
37 was measured by qualitative and quantitative anti-HAV antibody measurements 1 month after each vaccin
38                              Seropositivity (anti-HAV >/=20 mIU/mL) 30 years after the second vaccine
39  years, all children retained seroprotective anti-HAV levels except for only 7% and 11% of children i
40        Nonetheless, the model indicated that anti-HAV seropositivity should persist for >/=30 years a
41 ly 7% and 11% of children in group 1 born to anti-HAV-negative and anti-HAV-positive mothers, respect
42                At 10 years, children born to anti-HAV-negative mothers in group 3 had the highest geo
43 ectively, and 4% of group 3 children born to anti-HAV-negative mothers.
44 nterval, 71-133 mIU/mL) and children born to anti-HAV-positive mothers in group 1 had the lowest GMC
45 y indirect immunofluorescence analysis using anti-HAV monoclonal antibodies.
46 evalence of antibodies to hepatitis A virus (anti-HAV) and hepatitis E virus (anti-HEV) was 65.2% (95
47 re tested for antibody to hepatitis A virus (anti-HAV) by ELISA.
48 rred maternal antibody to hepatitis A virus (anti-HAV) on the duration of seropositivity after hepati
49             Antibodies to hepatitis A virus (anti-HAV) were measured in children from two separate va
50    The presenting features of 29 adults with anti-HAV IgM positive ALF enrolled in the ALFSG_between