Rotavirus P[8] Infections in Persons with Secretor and Nonsecretor Phenotypes, Tunisia

Ayouni, Siwar; Sdiri-Loulizi, Khira; Rougemont, Alexis de; Estienney, Marie; Ambert-Balay, Katia; Aho, Serge; Hamami, S.; Aouni, Mahjoub; Neji-Guédiche, Mohamed; Pothier, Pierre; Belliot, Gaël

doi:10.3201/eid2111.141901

Cited by 42 publications

(38 citation statements)

References 15 publications

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“…Increasing evidence supports linkages between HBGA phenotypes and RV epidemiology, indicating that HBGAs play an important role in determining interspecies transmission and disease burden of RVs. For example, whereas P [6] and P [19] RVs in the P[II] genogroup only recognize H type 1 antigen in the absence of the Lewis fucose, P [4] and P [8] RVs require the Lewis b (Le b ) modified H type 1 antigens [19,25], supporting the observation that Leindividuals may have increased risk of P [6] RV infection whereas nonsecretors and Leindividuals may be resistant to P [4] and P [8] RV infections that require the Lewis and secretor fucose for host infection [26][27][28]. The P [9], P [14], and P [25] genotypes in the P[III] genogroup recognize type A HBGAs [9], which explains that P [14] infection in both humans and animals may due to type A HBGAs that are shared between human and animal species [9,18,29].…”

Section: Introductionmentioning

confidence: 87%

“…The discovery that P [4], P [6], and P [8] human RVs recognize the secretor epitopes of human HBGAs appears to correlated with the predominance of these genotypes in causing the vast majority (>95%) of human infections worldwide. Epidemiological and biochemical studies suggest that non-secretors and Leindividuals may be resistant to P [4] and P [8] infections [27,28,56,57]. Nonsecretors are also possible to be susceptible to infection with prevalent human RVs as other epidemiological study demonstrated no significant correlation was found between secretor status and the susceptibility to P [6] RV infections [26].…”

Section: Our Data Also Provide Clues About the Evolution Of P[ii] Rvsmentioning

confidence: 96%

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Molecular basis of P[6] and P[8] major human rotavirus VP8* domain interactions with histo-blood group antigens

Yang

Tan

et al. 2019

Preprint

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Initial cell attachment of rotavirus (RV) to specific cell surface glycans, which is the essential first step in RV infection, is mediated by the VP8* domain of the spike protein VP4. Recently, human histo-blood group antigens (HBGAs) have been identified as ligands or receptors for human RV strains. RV strains in the P[4] and P[8] genotypes of the P[II] genogroup share common recognition of the Lewis b and H type 1 antigens, while P[6], which is one of the other genotypes in P[II], only recognizes the H type 1 antigen. The molecular basis of receptor recognition by the major human P[8] RVs remains unknown due to lack of experimental structural information. Here, we used nuclear magnetic resonance (NMR) titration experiments and NMRderived high ambiguity driven docking (HADDOCK) methods to elucidate the molecular basis for P[8] VP8* recognition of the Le b and type 1 HBGAs and for P[6] recognition of H type 1 HBGAs. Unlike P[6] VP8* that recognizes H type 1 HGBAs in a binding surface composed of an α-helix and a β-sheet, referred as "βα binding domain", the P[8] VP8* binds the type 1 HBGAs requiring the presence of the Lewis epitope in a previously undescribed pocket formed by two β-sheets, referred as "β binding domain". The observation that P[6] and P[8] VP8* domains recognize different glycan structures at distinct binding sites supports the hypothesis that RV evolution is driven, at least in part, by selective pressure driven adaptation to HBGA structural diversity of their natural hosts living in the world. Recognition of the role that HBGAs play in driving RV evolution is essential to understanding RV diversity, host ranges, disease burden and zoonosis and to developing strategies to improve vaccines against RV infections.

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Section: Introductionmentioning

confidence: 87%

Section: Our Data Also Provide Clues About the Evolution Of P[ii] Rvsmentioning

confidence: 96%

Molecular basis of P[6] and P[8] major human rotavirus VP8* domain interactions with histo-blood group antigens

Yang

Tan

et al. 2019

Preprint

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Section: Genetic Risk Factorsmentioning

confidence: 99%

“…In Burkina Faso, no Lewis-negative secretors (expressing H type 1 antigen) were infected with P[8] strains, despite making up 25% of the study population [78], suggesting that the infectivity of P[8] strains may be dependent on both secretor and Lewis status. However, population-specific differences may exist; for example, P[8] infections were detected in both secretors and nonsecretors during a study in Tunisia [79].In addition to being among the globally dominant rotavirus genotypes, P[8] strains are a component of Rotarix and RotaTeq. It is therefore plausible that genotype-specific HBGA binding patterns may contribute to geographic differences in vaccine efficacy.…”

mentioning

confidence: 99%

Causes of Impaired Oral Vaccine Efficacy in Developing Countries

et al. 2017

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Oral vaccines are less immunogenic when given to infants in low-income compared with high-income countries, limiting their potential public health impact. Here, we review factors that might contribute to this phenomenon, including transplacental antibodies, breastfeeding, histo blood group antigens, enteric pathogens, malnutrition, microbiota dysbiosis and environmental enteropathy. We highlight several clear risk factors for vaccine failure, such as the inhibitory effect of enteroviruses on oral poliovirus vaccine. We also highlight the ambiguous and at times contradictory nature of the available evidence, which undoubtedly reflects the complex and interconnected nature of the factors involved. Mechanisms responsible for diminished immunogenicity may be specific to each oral vaccine. Interventions aiming to improve vaccine performance may need to reflect the diversity of these mechanisms. Enteric pathogens are a substantial threat to public health. This threat takes many forms, from the toxin-producing bacteria (e.g., Vibrio cholerae) and flagellated protozoa (e.g., Giardia lamblia) that colonize the mucosal surface of the small intestine to the enteroviruses that are capable of spreading via the bloodstream to the CNS, causing acute flaccid paralysis (e.g., poliovirus). Each year, enteric pathogens cause hundreds of millions of cases of diarrhea and approximately 800,000 deaths, the vast majority of which occur among children in low-income countries [1]. The most common causes of childhood diarrheal morbidity include rotavirus, Cryptosporidium, enterotoxigenic Escherichia coli and Shigella [2].Vaccines against enteric pathogens are important tools for mitigating this disease burden. Oral vaccines offer several distinct benefits compared with parenteral vaccines. They can be produced in large quantities at relatively low cost, are easy to administer and have the capacity to induce local immunity in the intestinal mucosa, thereby protecting vaccinated individuals against subsequent infection and -by blocking onward transmission -enhancing herd immunity [3,4]. Currently licensed oral vaccines include live-attenuated poliovirus vaccines containing one, two or three serotypes, live-attenuated rotavirus vaccines (Rotarix R , RotaTeq R , Lanzhou lamb rotavirus vaccine [China only] and Rotavac R [India only]), live-attenuated cholera vaccine (CVD 103-HgR or Vaxchora TM ), inactivated cholera vaccines (Dukoral R and Shanchol R ) and live-attenuated typhoid vaccine (Ty21a). Other oral vaccines are in development, including those against Shigella, enterotoxigenic E. coli, Campylobacter and Clostridium difficile, as well as several novel rotavirus vaccine candidates (including the human neonatal vaccine RV3-BB [5] and an oral bovine pentavalent vaccine [6]).Yet oral vaccines have an Achilles' heel -their immunogenicity and efficacy is impaired in low-income countries that experience the greatest burden of enteric disease (Box 1). For example, Rotarix has a 1-year protective efficacy against severe rotavirus-associated gas...

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“…For instance, loss of FUT2 function leads to virtually no infection with P [8] strains in countries like Vietnam 19 and the USA, 20 but not in Tunisia where among 32 children infected, P [8] was present in both secretor and non-secretors that are positive for Lewis antigen. 21 Also, in Pakistan, a study comprising 181 infants that were seronegative before immunization with three courses of a G1P [8] vaccine strain indicated that 19% (10/ 54) of responders were non-secretors whereas secretors were 51% (20/39) type O and 30% (26/88) were types A, B or AB. 22 In addition, 18 P [6] infections (from a total of 27) were seen in predominantly Lewis-negative children (a frequent phenotype in African populations), while 27 Lewis-negative individuals were resistant to P [8] infection (0 in a total of 27 children).…”

Section: Rotavirus Disease Biology and Impactmentioning

confidence: 99%

Rotavirus vaccine efficacy: current status and areas for improvement

Carvalho

Gill

2018

Human Vaccines & Immunotherapeutics

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The difference noted in Rotavirus vaccine efficiency between high and low income countries correlates with the lack of universal access to clean water and higher standards of hygiene. Overcoming these obstacles will require great investment and also time, therefore more effective vaccines should be developed to meet the needs of those who would benefit the most from them. Increasing our current knowledge of mucosal immunity, response to Rotavirus infection and its modulation by circadian rhythms could point at actionable pathways to improve vaccination efficacy, especially in the case of individuals affected by environmental enteropathy. Also, a better understanding and validation of Rotavirus entry factors as well as the systematic monitoring of dominant strains could assist in tailoring vaccines to individual's needs. Another aspect that could improve vaccine efficiency is targeting to M cells, for which new ligands could potentially be sought. Finally, alternative mucosal adjuvants and vaccine expression, storage and delivery systems could have a positive impact in the outcome of Rotavirus vaccination.

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Rotavirus P[8] Infections in Persons with Secretor and Nonsecretor Phenotypes, Tunisia

Cited by 42 publications

References 15 publications

Molecular basis of P[6] and P[8] major human rotavirus VP8* domain interactions with histo-blood group antigens

Molecular basis of P[6] and P[8] major human rotavirus VP8* domain interactions with histo-blood group antigens

Causes of Impaired Oral Vaccine Efficacy in Developing Countries

Rotavirus vaccine efficacy: current status and areas for improvement

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