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American Journal of Epidemiology Vol. 107, No. 4: 321-327
Copyright © 1978 by The Johns Hopkins University School of Hygiene and Public Health

other

IMMUNE RESPONSE OF LEPROSY PATIENTS TO HEPATITIS B VIRUS

S. SERJEANTSON1, and D. G. WOODFIELD2

1 Department of Human Biology, John Curtin School of Medical Research P.O. Box 334, Canberra, ACT 2601 Australia
2 Auckland Centre, New Zealand Blood Transfusion Service Auckland, New Zealand

1 address for reprint requests.

The Immune responses of 323 Melanesian leprosy patients and 290 controls to hepatitis virus type B were examined by analyzing prevalence rates of hepatitis B antigen (HBsAg) and its antibody (anti-HBs) in an area of Papua New Guinea hyperendemlc for the virus. By use of multivariate techniques, extraneous variables known to be correlated with both leprosy severity and HBsAg prevalence, such as Institutionalization, age, sex and place of residence, could be statistically controlled. In multivariate analysis of HBsAg rates, after removal of the variation due to age, which was the most important single factor contributing to HBsAg carrier-status, lepromatous leprosy was a significant determinant of antigenemla. Similarly, when the series was grouped Into three Immune-response categories of HBsAg, anti-HBs or no serologic evidence of exposure to the virus, disease severity was a significant factor In determining immune response. For lepromatous and borderline lepromatous patients, the probability of responding antigenically to the virus, given that some measurable response has occurred (HBsAg/(HBsAg + anti-HBs)) was 0.42. The corresponding probability for tuberculoid patients was 0.25 and for healthy controls, 0.29. These probabilities indicate that lepromatous patients have an Impaired Immune response that not only predisposes them to the most severe form of leprosy but may also decrease their efficiency In terminating HBsAg Infection with anti-HBs.

antibodies; Australia antigen; carrier state; hepatitis virus B; leprosy


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