Severe Life-Threatening Cholera Associated with Blood Group 0 in Peru: Implications for the Latin American Epidemic

Swerdlow, David L.; Mintz, Eric D.; Rodriguez, Marcela; Tejada, E. Fernández; Ocampo, Cecilia Vera; Espejo, L. A.; Barrett, Timothy J.; Petzelt, Judy; Bean, Nancy H.; Seminario, Luis; Tauxe, Robert V.

doi:10.1093/infdis/170.2.468

Cited by 95 publications

(70 citation statements)

References 11 publications

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“…This frequency dependence will maintain host polymorphism when several mutational changes are required for bacteria to adapt to particular host genotypes. Evidence for these assumptions comes from the observation that the severity of disease is associated with ABO phenotype in several highly pathogenic bacteria, including Vibrio cholerae (Glass et al 1985;Swerdlow et al 1994), Escherichia coli O157 (Blackwell et al 2002), Campylobacter jejuni (Ruiz-Palacios et al 2003) and Shigella species (Sinha et al 1991). Some mucosal bacteria express terminal glycan-specific glycosidases that in Shigella have been shown to correlate with virulence (Prizont & Reed 1991).…”

Section: Discussionmentioning

confidence: 99%

Evolution of the human ABO polymorphism by two complementary selective pressures

Seymour

Allan

Pomiankowski

et al. 2004

Proc. R. Soc. Lond. B

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The best-known example of terminal-glycan variation is the ABO histo-blood group polymorphism in humans. We model two selective forces acting on histo-blood group antigens that may account for this polymorphism. The first is generated by the invasion of opportunistic bacterial or other pathogens that interact with the epithelial-mucosal surfaces. The bacteria adapt to the microenvironments of common host phenotypes and so create frequency-dependent selection for rarer host alleles. The second is generated by intracellular viruses, and accounts for the observed differentials between the ABO-phenotype frequencies. It is thought that viruses acquire histo-blood group structures as part of their envelope from their previous host. The presence of host antigens on the viral envelope causes differential transmission of the virus between host types owing to the asymmetric action of ABO natural antibodies. Our model simulations show that these two forces acting together can account for the major features of the ABO polymorphism in humans.

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Section: Discussionmentioning

confidence: 99%

Evolution of the human ABO polymorphism by two complementary selective pressures

Seymour

Allan

Pomiankowski

et al. 2004

Proc. R. Soc. Lond. B

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“…It seems likely that this phenomenon represents an example of a balanced polymorphism in the human population because blood group O is thought to confer susceptibility to diseases such as cholera (36) and other diarrheal diseases (37-39) that may be a significant selective force in many malarious countries. The global distribution of ABO blood group types is complex and may be influenced by selection imposed by a variety of pathogenic microorganisms (40,41).…”

mentioning

confidence: 99%

Blood group O protects against severe Plasmodium falciparum malaria through the mechanism of reduced rosetting

Rowe¹,

Handel²,

Thera³

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

274

254

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Malaria has been a major selective force on the human population, and several erythrocyte polymorphisms have evolved that confer resistance to severe malaria. Plasmodium falciparum rosetting, a parasite virulence phenotype associated with severe malaria, is reduced in blood group O erythrocytes compared with groups A, B, and AB, but the contribution of the ABO blood group system to protection against severe malaria has received little attention. We hypothesized that blood group O may confer resistance to severe falciparum malaria through the mechanism of reduced rosetting. In a matched case-control study of 567 Malian children, we found that group O was present in only 21% of severe malaria cases compared with 44 -45% of uncomplicated malaria controls and healthy controls. Group O was associated with a 66% reduction in the odds of developing severe malaria compared with the non-O blood groups (odds ratio 0.34, 95% confidence interval 0.19 -0.61, P < 0.0005, severe cases versus uncomplicated malaria controls). In the same sample set, P. falciparum rosetting was reduced in parasite isolates from group O children compared with isolates from the non-O blood groups (P ‫؍‬ 0.003, Kruskal-Wallis test). Statistical analysis indicated a significant interaction between host ABO blood group and parasite rosette frequency that supports the hypothesis that the protective effect of group O operates through the mechanism of reduced P. falciparum rosetting. This work provides insights into malaria pathogenesis and suggests that the selective pressure imposed by malaria may contribute to the variable global distribution of ABO blood groups in the human population.ABO ͉ erythrocyte ͉ pathogenesis ͉ rosette formation ͉ virulence

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“…The proportion of infected people who develop severe cholera is determined by several factors, including the infecting dose, gastric acidity, and immunity conferred by previous infection (116). 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).…”

Section: Cholera Resistance Genesmentioning

confidence: 99%

“…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%

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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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Severe Life-Threatening Cholera Associated with Blood Group 0 in Peru: Implications for the Latin American Epidemic

Cited by 95 publications

References 11 publications

Evolution of the human ABO polymorphism by two complementary selective pressures

Evolution of the human ABO polymorphism by two complementary selective pressures

Blood group O protects against severe Plasmodium falciparum malaria through the mechanism of reduced rosetting

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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