Genetic susceptibility to cholera

Levine, Myron M.; Nalin, David R.; Rennels, M B; Hornick, R. B.; Sotman, Steven B.; Blerk, G Van; Hughes, Timothy P.; O'Donnell, S; Barua, D

doi:10.1080/03014467900003751

Cited by 77 publications

(40 citation statements)

References 12 publications

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“…HBGA phenotype also appears to influence susceptibility to bacterial enteropathogens [86,87], including V. cholerae [88,89]. Nonsecretors are more likely to suffer from severe cholera than secretors [90].…”

Section: Histo Blood Group Antigensmentioning

confidence: 99%

“…Causes of impaired oral vaccine efficacy in developing countries Review colonized by V. cholerae [89], but are more likely, upon colonization, to develop severe symptoms [88,89]. The extent to which HBGA phenotype influences cholera vaccine response remains uncertain.…”

Section: Genetic Risk Factorsmentioning

confidence: 99%

“…Nonsecretors are more likely to suffer from severe cholera than secretors [90]. Somewhat paradoxically, individuals with blood group O are less likely to be (1) future science groupCauses of impaired oral vaccine efficacy in developing countries Review colonized by V. cholerae [89], but are more likely, upon colonization, to develop severe symptoms [88,89]. The extent to which HBGA phenotype influences cholera vaccine response remains uncertain.…”

mentioning

confidence: 99%

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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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Section: Histo Blood Group Antigensmentioning

confidence: 99%

Section: Genetic Risk Factorsmentioning

confidence: 99%

mentioning

confidence: 99%

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Causes of Impaired Oral Vaccine Efficacy in Developing Countries

et al. 2017

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“…For example, persons with blood group O are at increased risk of developing severe symptoms when infected with Vibrio cholerae O1 (8,63,105), although a recent study has suggested that people with this blood group are less likely to be infected with this organism (74). Similarly, individuals with the blood group O phenotype are at increased risk of developing disease due to norovirus, as demonstrated in two independent challenge studies (87,107).…”

Section: Epidemiologymentioning

confidence: 87%

Prevention and self-treatment of travelers' diarrhea

Diemert

2002

Primary Care: Clinics in Office Practice

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“…In addition, blood group O has been associated with severe cholera in Calcutta (25, 112), the Philippines (9), Bangladesh (27, 51), Peru (116), and among North American volunteers (76). The prevalence of blood group O varies considerably among different human populations.…”

Section: Cholera Resistance Genesmentioning

confidence: 99%

Host-Pathogen Interactions in Emerging and Re-emerging Infectious Diseases: A Genomic Perspective of Tuberculosis, Malaria, Human Immunodeficiency Virus Infection, Hepatitis B, and Cholera

McNicholl

Downer

Udhayakumar

et al. 2000

Annu. Rev. Public Health

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On exposure to a pathogen, a host may resist infection, become subclinically infected, or progress through several stages from mild to severe infection. Chronic sequelae may or may not occur. Host factors, particularly host genes, influence many of these stages. We have used a model of the continuum of pathogenesis of infectious diseases to consider the effect of host genes on five pathogens of significant public health burden: Mycobacterium tuberculosis, Plasmodium species, human immunodeficiency virus, hepatitis B virus, and Vibrio cholerae. The relationships between these infections and polymorphisms in human leukocyte antigen, cytokines, other immune response, or pathogen receptor genes are reviewed. We discuss gene-gene interactions and their effects in complex settings, such as coinfections with several pathogens. Priorities for prevention and control of these pathogens include vaccines and antimicrobial drugs. Research on how host genes can influence vaccine responses and the efficacy of drugs or other interventions, as well as further research into the relationship of host genes to infectious disease outcomes, may lead to new strategies for prevention and control.

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Genetic susceptibility to cholera

Cited by 77 publications

References 12 publications

Causes of Impaired Oral Vaccine Efficacy in Developing Countries

Causes of Impaired Oral Vaccine Efficacy in Developing Countries

Prevention and self-treatment of travelers' diarrhea

Host-Pathogen Interactions in Emerging and Re-emerging Infectious Diseases: A Genomic Perspective of Tuberculosis, Malaria, Human Immunodeficiency Virus Infection, Hepatitis B, and Cholera

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