kis blood group ki immunity power sabse jyada rhrlti hai.
Answers
Explanation:
It depends on situation (infection).
Suppose,
Individuals with blood group O are more susceptible than other individuals to severe cholera,
Individuals with blood group O are more susceptible than other individuals to severe cholera, although the mechanism underlying this association is unknown. To assess the respective roles of both intrinsic host factors and adaptive immune responses that might influence susceptibility to infection with Vibrio cholerae, we prospectively followed a cohort of household contacts of patients with cholera in Bangladesh. In this study, we made the novel observation that persons with blood group O were less likely than those with other blood groups to become infected with V. cholerae O1 (odds ratio [OR], 0.67; 95% confidence interval [CI], 0.53 to 0.85; P = 0.008). Consistent with prior studies, however, household contacts with blood group O were more likely to develop severe illness if infected with V. cholerae O1 (OR, 2.3; 95% CI, 0.98 to 5.59; P = 0.05). While blood group O protected significantly against infection with V. cholerae O1, there was no evidence of protection against V. cholerae O139. A multivariate analysis demonstrated that the association between blood group O and protection from infection with V. cholerae O1 was independent of age, gender, and baseline anti-cholera toxin and vibriocidal antibody titers. Based on this epidemiologic evidence, we propose a hypothesis for understanding the association between blood group O and the risk of infection with V. cholerae O1 and O139 as well as the risk of developing severe symptoms once infected.
Vibrio cholerae is a gram-negative bacterium that causes a spectrum of infection ranging from asymptomatic colonization to rapidly fatal secretory diarrhea known as cholera gravis. V. cholerae is differentiated serologically by the O side chain of its lipopolysaccharide; the vast majority of human cholera is caused by the O1 and O139 serogroups. The O1 serogroup of V. cholerae is subclassified into two biotypes (classical and El Tor) and two major serotypes (Inaba and Ogawa) (11). Due to variations in the predominating serogroup, biotype, and serotype in circulation, the epidemiology of cholera is in constant flux. In the 1960s, the V. cholerae O1 El Tor biotype emerged as a major cause of cholera, ultimately replacing the classical biotype. In 1992, the V. cholerae O139 serogroup first appeared; after briefly predominating in South Asia, it now persists in this region, but at much lower levels than V. cholerae O1 El Tor.
Susceptibility to infection with V. cholerae is dependent on both adaptive immune responses induced by previous infection and innate host factors. The best-studied correlate of adaptive immunity to V. cholerae is the serum vibriocidal antibody, a complement-fixing bactericidal antibody. Seroepidemiologic studies in areas of endemicity have shown that vibriocidal antibody titers increase with age and that risk of disease is inversely proportional to the vibriocidal antibody titer (9, 16, 17). However, there is no threshold vibriocidal antibody titer above which complete protection from infection is achieved, and it is hypothesized that the vibriocidal antibody is a surrogate marker for a protective mucosal immune response (24). Systemic antibodies to cholera toxin have not been found to correlate with protection from cholera (9). Furthermore, infection with V. cholerae O1 does not confer protection from V. cholerae O139, even though both serogroups produce identical cholera toxins (1, 22).
Among the intrinsic host factors that influence susceptibility to cholera, the ABH histo-blood group antigens are the most studied. Multiple case-control studies in areas of cholera endemicity have demonstrated that individuals with blood group O (the blood group phenotype associated with the H antigen) are at increased risk of hospitalization due to classical and El Tor V. cholerae O1 as well as V. cholerae O139 (3, 4, 5, 7, 26). A study of North American volunteers also demonstrated increased purging in blood group O subjects infected with a high inoculum of classical V. cholerae O1 (13). It has been hypothesized that V. cholerae infection is the evolutionary force behind the low prevalence of the O blood group in the Ganges River Delta, which is a historic and current global epicenter of cholera (10, 11).
Two previous studies have addressed the question of whether blood group O is also associated with an increased risk of asymptomatic infection or mild illness due to V. cholerae in addition to the increased risk of severe illness (10, 26). Both studies concluded that there was no difference in the overall risk of infection with V. cholerae among persons with blood group O compared to those with non-blood group O antigens.