Dr. Louisa Pollock MRCPCH Ph.D.
Consultant Paediatrician in Infectious Diseases
Her interest in rotavirus began with clinical work in Malawi, where preventable child deaths from diarrhoeal illness were a routine tragedy.
Her research work has included studying the effect of maternal antibody on vaccine response and other factors which may explain differences in enteric vaccine response between high and low-income countries.
She completed a Wellcome Trust Clinical Ph.D. fellowship in 2017, examining predictors of rotavirus vaccine response in Malawian infants. She is currently based at the Royal Hospital for Children in Glasgow and maintains links to Malawi.
Topic of the presentation-HBGA and Rotavirus Vaccine Failure
Several in-vitro studies have shown strain-specific binding of rotavirus VP8* to histo-blood group antigens (HBGA), complex carbohydrates found on the surface of blood and mucosal epithelial cells. Secretion of HBGA, as free oligosaccharides in saliva and other exocrine secretions, is determined by expression of the FUT2 gene. Mutations of FUT2 result in a non-functional enzyme and “non-secretor” phenotype.
A combination of FUT2 and FUT3 gene expression determines the Lewis HBGA phenotype. Epidemiological studies have shown that secretor and Lewis positive phenotypes are associated with increased risk of P and P rotavirus gastroenteritis (RVGE), and Lewis negative phenotype with increased risk of P RVGE. Both the monovalent human rotavirus vaccine Rotarix® (RV1) and pentavalent human-bovine reassortant vaccine Rotateq®, are based on attenuated P strains. HBGA-associated resistance to P vaccine virus replication could therefore diminish vaccine response.
This will talk will summarize the evidence to date supporting the hypothesis that nonsecretor/Lewis-negative phenotype leads to reduced vaccine take following vaccination with P based vaccines. The important question of whether any reduction in vaccine take leads to reduced clinical protection will also be addressed, with recent data from Malawi showing that non-secretor infants are actually at reduced risk of clinical rotavirus vaccine failure. In the context of this new data, the question of whether population differences in HBGA phenotype distribution could contribute to the rotavirus vaccine efficacy gap between high and low-income countries will be discussed.