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Histo-blood group antigens and rotavirus vaccine shedding in Nicaraguan infants
Natl Autonomous Univ Nicaragua, Nicaragua.
Natl Autonomous Univ Nicaragua, Nicaragua.
Linköping University, Department of Clinical and Experimental Medicine, Division of Hematopoiesis and Developmental Biology. Linköping University, Faculty of Medicine and Health Sciences.
Natl Autonomous Univ Nicaragua, Nicaragua.
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2019 (English)In: Scientific Reports, ISSN 2045-2322, E-ISSN 2045-2322, Vol. 9, article id 10764Article in journal (Refereed) Published
Abstract [en]

ABO, Lewis and secretor histo-blood group antigens (HBGA) are susceptibility factors for rotavirus in a P-genotype dependent manner and can influence IgA seroconversion rates following rotavirus vaccination. To investigate the association between HBGA phenotypes and rotavirus vaccine shedding fecal samples (n = 304) from a total of 141 infants vaccinated with Rotarix (n = 71) and RotaTeq (n = 70) were prospectively sampled in three time frames (= 3, 4-7 and = 8 days) after first vaccination dose. Rotavirus was detected with qPCR and genotypes determined by G/P multiplex PCR and/or sequencing. HBGAs were determined by hemagglutination and saliva based ELISA. Low shedding rates were observed, with slightly more children vaccinated with RotaTeq (19%) than Rotarix (11%) shedding rotavirus at = 4 days post vaccination (DPV). At = 4 DPV no infant of Lewis A (n = 6) or nonsecretor (n = 9) phenotype in the Rotarix cohort shed rotavirus; the same observation was made for Lewis A infants (n = 7) in the RotaTeq cohort. Putative in-vivo gene reassortment among RotaTeq strains occurred, yielding mainly G1P[8] strains. The bovine derived P[5] genotype included in RotaTeq was able to replicate and be shed at long time frames (amp;gt;13 DPV). The results of this study are consistent with that HBGA phenotype influences vaccine strain shedding as similarly observed for natural infections. Due to the low overall shedding rates observed, additional studies are however warranted.

Place, publisher, year, edition, pages
NATURE PUBLISHING GROUP , 2019. Vol. 9, article id 10764
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Infectious Medicine
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URN: urn:nbn:se:liu:diva-159575DOI: 10.1038/s41598-019-47166-9ISI: 000476874600062PubMedID: 31341254OAI: oai:DiVA.org:liu-159575DiVA, id: diva2:1342415
Note

Funding Agencies|Swedish Research Council [348-2013-6587, 2011-3469-90642-57, 2014-320301]

Available from: 2019-08-13 Created: 2019-08-13 Last updated: 2019-08-13

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