maternal antibody


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maternal antibody

An antibody produced by the mother and transferred to the fetus in utero or during breastfeeding.
See also: antibody
References in periodicals archive ?
Optimal timing is between 27 and 36 weeks gestation to maximize the maternal antibody response and passive antibody transfer to the infant.
Viral transmission from mother to fetus may be increased if the maternal antibody response is of low avidity or of poor neutralizing activity.
Kittens were specific pathogen free, thus there was no maternal antibody to interfere with vaccine response.
The rationale considers several potential mechanisms, the first two relate to lowering or even eliminating maternal antibody in the fetal circulation (maternal perspective): increased catabolism of maternal antibody and decreased placental transport of maternal antibody.
In the control group, average maternal antibody levels were as high as 8 of HI antibody titer at hatch and thereafter decreased quickly.
The maximum increase has occurred at 20-30th days of the disease, but antibody increase has not happened in infants younger than 4 months of age who had high maternal antibody titers (27).
Laboratory criteria for diagnosis of CRS were: demonstration of rubella-specific IgM antibody in cord blood, or demonstration of rubella-specific IgM antibody in infant blood at 8th wk of age, or infant rubella antibody level persisting at a higher level and for a longer period than expected from passive transfer of maternal antibody (i.e., rubella titre that does not drop at the expected rate of a two-fold dilution per month) (2,3).
This variable rate of maternal antibody decline makes the timing of vaccine administration difficult.
Researchers there are targeting two opposing forces affecting neonate health: the need for effective passive transfer of maternal antibodies and the maternal antibody interference that hinders the newborn's ability to develop vaccine-based immunity to common pathogens.
A major factor protecting infants from developing disseminated herpes is the presence of maternal antibody,[15] but acyclovir may diminish antibody response to HSV.[16] As previously suggested by Brown and Baker,[17] it is theoretically possible that acyclovir could blunt the humoral immune response during pregnancy after an episode of primary genital herpes and thereby increase the risk of the neonate developing HSV infection.
Because the mean age of women at first birth in developed countries is high, we hypothesize that low nAb titers in women of childbearing age, and therefore the lack of adequate maternal antibody protection, contribute to the occurrence of PeV-A3 outbreaks in infants.

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