Abstract Title
Characterization of intestinal mucosal immunity in Nicaraguan children with sapovirus acute gastroenteritis
Presenter
Sylvia Becker-Dreps, University of North Carolina at Chapel Hill
Co-Author(s)
Filemon Bucardo (a,b), Lisa Lindesmith (c), Sean Diehl (d), Yaoska Reyes (c), Fredman Gonzalez (e), Benjamin McElvany (d), Jan Vinjé (f) , Ralph Baric (c), Sylvia Becker-Dreps (b,c).
a Department of Microbiology and Immunology, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC; b Department of Family Medicine, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC; c Department of Epidemiology, Gillings School of Global Public Health, University of North Carolina at Chapel Hill, Chapel Hill, NC; d Department of Microbiology and Molecular Genetics, The University of Vermont Larner College of Medicine, Vaccine Testing Center, Burlington, BT. e Independent researcher; f Division of Viral Diseases, Centers for Disease Control and Prevention, Atlanta, GA
Abstract Category
Vaccines and immunity
Abstract
INTRODUCTION. Mucosal IgA antibodies are the first line of defense against enteric viruses. Characterizing stool antibodies against sapovirus can reveal immune responses proximal to the site of infection and potentially identify a correlate of protection.
METHODS. We developed in-house ELISAs to identify intestinal sapovirus sIgA responses in children followed weekly for sapovirus acute gastroenteritis (SAGE) during the first 2 years of life. Stool samples collected from children (n = 51) pre- and post-SAGE were tested for sIgA against GI.1 and GV.1 virus-like particles. Specific and total IgA was measured in clarified fecal samples treated with protease inhibitors. Total and specific Geometric Mean Titers (GMTs) were estimated using an IgA colostrum standard and reported in ng of specific IgA/100µg total IgA.
Result. Twenty-six (51%) and 19 (37%) of the 51 children showed an increase of ≥50% in GI.1 and GV.1 IgA concentrations post-infection, respectively. In these children, the GMT pre- and post-infection for GI.1 was 9.2 (95% CI 6.0-14.1) and 51.7 (95% CI 35.9-74.3), respectively. A similar trend was observed for GV.1 (pre: 14.78 (95% CI 8.3-26.3) and post: 67.7 (95% CI 35.4-129.5)). The increase in IgA concentration after SaV infection does not correlate between GI.1 and GV.1 (r = 0.13 (95%CI -0.15 to 0.39), R2 = 0.01743).
Conclusion. Following natural infection, at least 50% of the children had a significant increase in the sapovirus GI.1 IgA concentration in the intestine. The lack of correlation between the increase of GI.1 and GV.1 IgA concentration post infection suggests a genogroup-specific response.
METHODS. We developed in-house ELISAs to identify intestinal sapovirus sIgA responses in children followed weekly for sapovirus acute gastroenteritis (SAGE) during the first 2 years of life. Stool samples collected from children (n = 51) pre- and post-SAGE were tested for sIgA against GI.1 and GV.1 virus-like particles. Specific and total IgA was measured in clarified fecal samples treated with protease inhibitors. Total and specific Geometric Mean Titers (GMTs) were estimated using an IgA colostrum standard and reported in ng of specific IgA/100µg total IgA.
Result. Twenty-six (51%) and 19 (37%) of the 51 children showed an increase of ≥50% in GI.1 and GV.1 IgA concentrations post-infection, respectively. In these children, the GMT pre- and post-infection for GI.1 was 9.2 (95% CI 6.0-14.1) and 51.7 (95% CI 35.9-74.3), respectively. A similar trend was observed for GV.1 (pre: 14.78 (95% CI 8.3-26.3) and post: 67.7 (95% CI 35.4-129.5)). The increase in IgA concentration after SaV infection does not correlate between GI.1 and GV.1 (r = 0.13 (95%CI -0.15 to 0.39), R2 = 0.01743).
Conclusion. Following natural infection, at least 50% of the children had a significant increase in the sapovirus GI.1 IgA concentration in the intestine. The lack of correlation between the increase of GI.1 and GV.1 IgA concentration post infection suggests a genogroup-specific response.