All 7 infants were subsequently re-tested and were negative for anti-VCA IgG, indicating maternal origin for these antibodies at 6 months. At month 12, 49 out of 115 FCGR1A infants (42.6?%) were IgG anti-VCA positive. proportion of EBV seroconversion to 88.7?% (102/115 infants).?EBV seroconversion was significantly associated with a low maternal educational status but had no impact on infant growth or vulnerability to infections. Reduced HBsAb levels and accelerated waning of antibodies were associated with early EBV seroconversion. Conclusions We found a heterogeneous timing of acquisition of EBV with the majority of infants born from HIV?+?mothers acquiring contamination after 6 months. Anti-HBs levels were lower and appeared to wane faster in infants acquiring EBV contamination. test for quantitative variables. The Wilcoxon test was used to detect longitudinal differences. Spearmans correlation coefficient was used to evaluate correlations between quantitative variables. A linear regression analysis was performed to evaluate the determinants of EBV acquisition at Month 12, controlling for potential confounding factors (maternal age, viral load, CD4?+?cell count, WHO stage, educational levels). Differences were considered statistically significant when P??350/mm3). During pregnancy, women received a median of 10 weeks (IQR: 7.0C13.0) of ART. At the time of delivery, most of the women had viremia levels below 1000 HIV-RNA copies/ml. Socioeconomic status was determined by educational status (64.3?%: no school or primary; 35.7?% secondary), occupation status (unemployed: 60.9?%), and presence or absence of electricity at home (no electricity: 78.3?%). Most infants (97.4?%) were born by vaginal delivery. The median weight within 15 days from delivery was 3.2 Kg (IQR: 2.78C3.50). The male/female ratio was 54/61 (48/52?%). Anti-VCA IgG longitudinal study A total of 52 infants were tested for anti-VCA IgG at 6 months. 45/52 (86.5?%) were negative to the IgG anti-VCA IgG test, and 7 infants were EBV positive. All 7 infants were subsequently re-tested and were unfavorable for anti-VCA IgG, indicating maternal origin for these antibodies at 6 months. At month 12, 49 out of 115 infants (42.6?%) were IgG anti-VCA positive. Fifty-three of the remaining 66 seronegative infants (80.3?%), developed an immune response against EBV in the following 12 months, as Peretinoin showed by the presence of IgG anti-VCA. Overall, at month 24 most infants (102/115, 88.7?%) had antibodies against EBV, and only 13 (11.3?%) were EBV-negative. Maternal and infant factors influencing EBV contamination acquisitionIn the first 12 months, EBV contamination acquisition in infants was not associated with maternal Peretinoin HIV parameters (WHO stage, p?=?0.423, viral load, p?=?0.779 CD4?+?cell count, p?=?0.655), nor with the duration (p?=?1.000) or the type of regimen (p?=?0.850) of antiretroviral treatment (Table?1), while it was significantly associated with lower socioeconomic conditions: 77.6?% of the mothers of infants who Peretinoin acquired EBV had poor educational level (vs. 54.5?% of the infants not EBV-infected at 12 months p?=?0.018). In a linear regression analysis, adjusted for potentially confounding maternal variables (age, viro-immunological parameters, and ART duration), poor educational levels remained a significant determinant of EBV acquisition (p?=?0.011). Table 1 Analysis of potential maternal factors influencing EBV contamination in infants during the first 12 months of life and infants characteristics antiretroviral therapy, stavudine, nevirapine, since malaria is considered a strong predictor of early EBV primary contamination [6, 31]. Conclusions In conclusion, here we confirm that EBV acquisition in Malawian HEU infants occurs mostly during the first two years of life, and we suggest that the onset of infection can be delayed after 6 months of age, in the presence of improved immunological conditions of their HIV?+?ART-treated mothers. EBV acquisition does not seem to have an impact on childrens growth nor to increase their vulnerability to infections but.
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