Abrupt increases of alanine transaminase were observed in 6 of 23 non-treated, male homosexuals with chronic hepatitis associated with hepatitis B virus. Before this occurrence, all subjects had hepatitis B e antigen (HBeAg) and elevated DNA polymerase activity. Within 3 months, HBeAg was nondetectable in 3 subjects and elevated DNA polymerase disappeared in 4. These serologic events were not always sustained, however. In 3 subjects, reactivation of hepatitis B virus infection occurred within the subsequent 6-month period. Serologic testing for cytomegalovirus, Epstein-Barr virus, delta agent, and hepatitis B surface antigen (HBsAg) subtype showed that episodes of clearance and reactivation were not explainable by secondary infection with these agents or infection with a different HBsAg subtype. Spontaneous clearance and reactivation of hepatitis B virus infection may commonly occur among male homosexuals with chronic type B hepatitis. These phenomena should be considered when evaluating the need for treatment or interpreting the results of investigations that use anti-viral therapy.
The prevalence of hepatitis B virus markers was studied among employees and clients at a nonresidential public school for the mentally handicapped and at a privately operated residential facility. In the residential institution, 73 (80%) of 91 clients and 15 (16%) of 92 workers had positive tests for hepatitis B virus markers. Twenty-three clients, including six carriers of hepatitis B surface antigen (subtype ayw), received their education their education at the public school. Only two students (4%) who did not live at the residential institution and one employee (2%) had positive tests for hepatitis B virus markers. One of these students had acute hepatitis B infection, with hepatitis B surface antigen subtype ayw; the subtyping suggested that he had acquired the infection from one of the six carriers from the residential institution. Testing for IgM antibody to hepatitis B core antigen in single serum samples facilitated the identification of acute and chronic hepatitis B infection in children and staff of both facilities. The results show hepatitis B can be transmitted in this setting, and vaccination may be warranted for susceptible students and staff.
We have observed the disappearance of rosette inhibitory factor (RIF) from the serum of 19 patients with acute hepatitis B virus infection. This occurred at a time coinciding with the detection of anti-HBs. In addition, levels of RIF activity were significantly greater (p < 0.001) in 35 HBsAg carriers who lacked anti-HBs when compared to 15 carriers who regularly demonstrated this antibody. In all instances, RIF effect was partial affecting some, but not all, T-lymphocytes from forming erythrocyte rosettes.To define if RIF exhibits an effect on specific T-lymphocyte subpopulations, lymphocytes from healthy donors were separated into TM (helper), TG (suppressor), and To (null) subpopulations by an immunoglobulin-ox-cell rosette depletion method. The effect of RIF on erythrocyte rosette formation and Fc-receptor expression in these subpopulations was assessed. TG-lymphocytes were found to be refractory to RIF-mediated suppression of erythrocyte rosette formation while TM-lyrnphocytes demonstrated an enhanced sensitivity to RIF. Incubation of Tc-and To-lymphocytes, potential TM-precursor cells, with RIF resulted in a decreased expression of new IgM-Fc receptors. In order to determine if any functional significance could be derived from these findings, the effect of RIF on in uitro immunoglobulin secretion was tested. Using pokeweed mitogen-stimulated mononuclear cell cultures, purified RIF-low density lipoprotein was shown to suppress IgM, IgG, and IgA secretion by 75.3, 74.3, and 59.3%, respectively.These data are consistent with the hypothesis that RIF is a potential immunoregulatory protein which could contribute to the lack of anti-HBs noted during the acute phase of hepatitis B and in the majority of HBsAg carriers.Rosette inhibitory factor (RIF) is a unique serum, lowdensity lipoprotein (LDL) which is detectable during infection with hepatitis A, B, and non-A, non-B viruses (1-3). This factor inhibits healthy T-lymphocytes from forming sheep erythrocyte rosettes (E rosette), a marker for the functional integrity of T-cells. It has been suggested that RIF may behave as an immunoregulatory molecule (4) but direct evidence for this assumption is lacking. Studies from our laboratory support the sugges-
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