Doctor of Philosophy, Case Western Reserve University, 1994, Epidemiology and Biostatistics
Since clearance of HBV infection is dependent on normally functioning cell-mediated immunity, it is possible that immunological dysfunction induced by HIV-1 infection leads to poor clearance of HBV. Consequently, HIV infection is expected to promote the spread of HBV infection. To determine whether HIV infection has the potential to promote the spread of HBV infection, a hospital-based cross-sectional study was conducted in Uganda. Information was collected on respondent's demographic characteristics, risk factors for, and clinical features of HBV infection. In addition, blood was obtained for HIV-1 and hepatitis tests. The overall prevalence of HBsAg, anti-HBs, anti-HBc and total HBV infection was 15.7%, 54.0%, 42.9% and 66.9% respectively. 64.4% of subjects with detectable levels of anti-HBs had "protective levels" of the antibody. Of 1392 subjects tested for all the three key markers of HBV infection (HBsAg, anti-HBs and anti-HBc), 463 (33.2%) had no evidence of infection, 51 (3.7%) were in a serologic window period, 210 (15.1%) had evidence of infection that occurred in the distant past, 450 (32.3%) were i n convalescence, and 218 (15.5%) had active infection. Of 218 subjects with active infection, 111 (50.9%) were in the early phases of infection, 96 (44.1%) had either acute or chronic hepatitis, and 11 (5.0%) had reinfections. 43 subjects had concurrent circulation of HBsAg and anti-HBs. The overall prevalence of HBV chronic carriage was 4.9%. HIV positive individuals were more likely than those negative to have chronic carriage (P = 0.0007). After controlling for other variables, being HIV positive was associated with a 3.66 fold increase in the likelihood of chronic carriage. Being a male or having both fever and fatigue were independently predictive of HBV chronic carriage. Of 172 HBsAg positive subjects tested for anti-HD, 4 (2.3%) had the antibody. Of 152 HBsAg positive subjects tested for HBeAg, 23 (15.1%) had the antigen. There was no difference in HBeA (open full item for complete abstract)
Committee: Edward Mortimer, Jr. (Advisor)
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