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Centre international de recherche sur les maladies diarrhéiques de Bangladesh (icddr,b)

O-specific polysaccharide (OSP)-specific memory B cell responses in young children, older children and adults infected with Vibrio cholerae O1 Ogawa in Bangladesh

Aktar A, Rahman MA, Afrin S, Faruk MO, Uddin T, Akter A, Sami MI, Yasmin T, Chowdhury F, Khan AI, Leung DT, LaRocque RC, Charles RC, Bhuiyan TR, Mandlik A, Bufano MK, Kováč P, Xu P, Calderwood SB, Harris JB, Qadri F, Ryan ET

Clin Vaccine Immunol. 2016 Mar 23

Abstract

Cholera caused by V. choleraeO1 confers at least 3-10 years of protection against subsequent disease irrelevant of age, despite relatively rapid fall in antibody levels in peripheral blood, suggesting memory B cell responses may play an important role in protection. The V. choleraeO1 -specific polysaccharide (OSP) component of lipopolysaccharide (LPS) is responsible for serogroup specificity, and it is unclear if young children are capable of developing memory B cell responses against OSP, a T cell-independent antigen, following cholera. To address this, we assessed OSP-specific memory B cell responses in young children (2-5 years, n= 11), older children (6-17 years, n=21), and adults (18-55 years, n=28) with cholera caused by V. choleraeO1 in Dhaka, Bangladesh. We also assessed memory B cell responses against LPS and vibriocidal responses, and plasma antibody responses against OSP, LPS, and cholera toxin B subunit (CtxB; a T cell-dependent antigen) on days 2, 7, as well as 30, 90 and 180 after convalescence. In all age cohorts, vibriocidal responses and plasma OSP, LPS, and CtxB-specific responses peaked on day 7, and fell toward baseline over the follow-up period. In comparison, we were able to detect OSP memory B cell responses in all age cohorts of patients with detectable responses over baseline for 90-180 days. Our results suggest that OSP-specific memory B cell responses can occur following cholera, even in the youngest children, and may explain in part the age-independent induction of long-term immunity following naturally acquired disease.

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