“…This may account for an underestimate of G6PD deficiency in Hb AS and Hb SS indi viduals in the present study as well as in previous reports [28], While it has been proposed by Lewis and Iiathorn [16] that G6PD deficiency modifies the clinical sever ity of sickle cell anemia by causing an im proved fitness, this has not been demon strated [11,13]. On the contrary, it is pro posed that the increased fitness of Gd A -/H b AS individuals is accorded by the in creased G6PD enzyme levels in G6PD-deficient males in the presence of Hb S. It has been established that viral hepatitis, and perhaps other infectious agents, including influenza A virus, may induce hemolytic anemias with a more severe clinical course of hepatitis in individuals deficient in G6PD than in G6PD-normal individuals, leading to a high rate of acute hepatic coma, pro longed hyperbilirubinemia, massive intra vascular hemolysis, and death [5,12,21,22,26,27], Hepatic disease was more se vere in both G6PD-deficient males and fe males than in G6PD-normal individuals, and the highest rates of viral hepatitis were in the age group of 15-44 years [21,22]. Viral hepatitis is common in Africa, the preva lence of hepatitis B surface antigen in the general population being from 1 to 6°/o [29]; yet viral hepatitis may be only one of sev eral or many factors (including falciparum malaria) producing oxidative stress which may select against G6PD deficiency.…”