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We examined the impact of a lamivudine-containing highly active antiretroviral therapy (HAART) regimen on 164 hepatitis B virus/HIV co-infected individuals starting their first HAART. Lamivudine-treated patients (accounting for 73% of the study population) showed a significantly lower level of alanine aminotransferase over follow-up [-81.1 mU/ml mean difference; 95% confidence intervals (95% CI): -30.3; -131.7, P=0.003] and a significantly reduced risk of liver-related morbidity/mortality [Relative hazard (RH)=0.07; 95% CI: 0.01-0.38, P=0.002] than those starting a lamivudine sparing-regimen.

Background: The effect of chronic coinfection with hepatitis viruses on the response to therapy against human immunodeficiency virus 1 (HIV-1) remains debated., Methods: In a prospective cohort study, the effect of hepatitis B virus (HBV) and hepatitis C virus (HCV) serostatus on the outcome of potent HIV-1 therapy was analyzed in HIV-1-infected patients previously naive to antiretroviral therapy. Changes from baseline CD4+ cell counts and HIV RNA levels over time were analyzed by linear regression models. Time to clinical progression and time to reach virologic and immunologic response were analyzed by multivariate Cox proportional hazards regression models., Results: We studied 1320 patients, among whom 600 were HCV antibody-positive and 90 were HBV surface antigen-positive. During a median follow-up of 37 months (range, 1-48 months), clinical progression was observed in 99 patients (56 new acquired immunodeficiency syndrome-defining events and 43 deaths). In multivariate models, HCV-positive HBV-negative patients showed a shorter time to clinical progression (hazard ratio, 1.55; 95% confidence interval, 1.00-2.41). Patients who were HCV-positive also showed mean CD4+ recoveries over time that were at least 30 cells/ micro L fewer than those of seronegative patients. Hepatitis virus serostatus did not affect the virologic response to HIV-1 therapy., Conclusions: Clinical progression of HIV-1 disease after starting potent antiretroviral therapy is accelerated by concomitant infection with HCV. Compared with patients without coinfection, coinfected patients showed impaired CD4+ cell recovery, despite similar virologic response to HIV-1 therapy. These findings may have important implications for the treatment of HCV and for the timing of initiation of HIV-1 therapy in coinfected individuals.

Object: To assess the prevalence and the incidence of the anti-HCV and HBV markers in extracorporeal dialysis patients., Method: From 1990 to 1993, every six months, anti-HCV and anti-HBV markers were determined in 88 dialyzed patients, in 24 health workers from the Nephrology and Dialysis Departments and checked with 4143 blood donors. ALT values were also checked monthly., Results: A 13.6 prevalence of anti-HCV was found while no new anti-HCV case was seen in the three-year observation period. Data referring to HBV infection were affected by vaccination. Statistical survey has shown a significant relation between anti-HCV and blood transfusions and between anti-HBV infection and duration of dialysis. The incidence of HCV infection was 4.1% among health workers who were all HBV vaccinated in the year before the research., Comment: We strongly recommend the observance of such rules as hygiene and prophylaxis, disinfection, sterilization and the use of disposable material. Also, a reduction of the number of transfusions seems to cut down the incidence of hematic infections.

The long-term persistence of anti-HBsAg above 10 mUI is conventionally believed to protect against natural infection with hepatitis B virus, while it is not yet clear what is the clinical significance of the fall to below 10 mUI in antibody levels. In our opinion, an important method for evaluating the effectiveness of the vaccine lies in comparing the duration of vaccine-immunity with that following the disease, the later being held to provide life-long protection. In this view, we examined the sera samples of 69 subjects (56 healthy people, and 13 drug-addicts) previously affected from HBV infection looking for anti-HBsAg with an Elisa method. The subjects were aged between 4 months and 73 years and had all suffered from acute fully recovered icteric hepatitis in the previous 2 to 10 years. All the drug addicts (13 males) and 4 healthy children from the group had no or negligible levels of antibodies; 3 out of 8 old people (60 or more yrs old) showed no antibodies only 4-5 yrs after having been infected. In the remaining group of 44 healthy people 14 cases were observed which had antibody levels 10 mUI, regardless of age, sex or occupation; the greater the time between the infection and the test, the greater the probability of finding negligible antibody levels. We conclude that the reduction in antibody levels may not be indicative of a loss of immunity: many of our cases have shown low or undetectable antibody levels, a few years after full recovery from an acute attack of hepatitis B.

IgM antibody against hepatitis B core antigen (IgM anti-HBc), a marker of recent hepatitis B virus infection, was sought by radioimmunoassay in sera diluted 1/4000 from 376 patients presenting to four centres in Italy with acute, apparently type B hepatitis (hepatitis B surface antigen (HBsAg) positive). In 320 patients (85%) a positive IgM anti-HBc test result confirmed that hepatitis was due to primary infection with hepatitis B virus. In the remaining 56 patients absence of the IgM marker indicated that they were previously unrecognised long term carriers of HBsAg. Further serum analysis often showed delta infection and occasionally hepatitis A or cytomegalovirus infection as the true cause of their illness. After six to eight months circulating HBsAg persisted in 38 of 45 patients (84%) without IgM anti-HBc but in only six of 150 patients (4%) with the IgM antibody (p less than 0.0001). A negative IgM anti-HBc test result in patients with acute HBsAg positive hepatitis points to a factor other than hepatitis B virus as the cause of the liver damage and predicts the carriage of HBsAg.

The Authors have studied the correlation between serum HBeAg and the presence of hepatitis B "core" and "surface" antigens in liver tissue. The histological pictures of the bioptic specimens of patients affected by HBV were classified as: chronic persisting hepatitis, chronic active hepatitis, cirrhosis and minimal aspecific changes. HBcAg was detected in liver cells nuclei in all the patients resulted positive for serum HBeAg. In some of these subjects HBsAg was found to be localized on the hepatocyte membranes, and this seems to be related in some way to the presence of HBcAg in liver nuclei. No presence of hepatitis B associated antigens was observed in biopsies from subjects who were negative for serum HbsAg.

HBsAg bound to IgM was measured in the serum of HBsAg carriers with acute hepatitis using a radioimmunoassay based on selective absorption of IgM on solid phase coated with antiserum to human IgM. HBsAg/IgM was detected in 94 (100%) patients with acute type B hepatitis during the acute phase of infection and persisted after the fourth week only in 13 of them, who developed chronic liver disease. HBsAg/IgM was detected only in 1 patient out of 15 carriers of the HBsAg with superimposed non-B hepatitis. No activity was found in serum of 20 patients with acute HBsAg-negative hepatitis. The nature of the IgM component of the complex is uncertain, however, blocking experiments of the HBsAg/IgM reaction with polymerized human albumin suggest that the IgM component of the complex might represent antibody to the denatured protein. Persistent HBsAg/IgM complex detection in patients with acute type B hepatitis provides a useful tool to predict transition of HBV infection to chronicity. Its absence in patients with acute HBsAg-positive hepatitis is indicative of non-B hepatitis in chronic carriers of the HBsAg.

Sera from seventy patients suffering for HBsAg positive hepatitis, twenty-five HBsAg blood-donors, and eighty-four healthy subjects with no history of hepatitis, negative for all markers of HBV infection, were tested for circulating IgM/HBsAg complexes by a radioimmunoassay. IgM/HBsAg complexes, present in acute hepatitis patients at admission, progressively decreased and could not be demonstrated in sera of the convalescent phase. No complexes were found in sera from subjects negative for HBV markers. The results obtained from sera from HBsAg positive blood donors are compared with HBeAg/anti-HBe system. The absence of IgM/HBsAg complexes seems to be a sign of good prognosis in HBV infection.

Infection with the hepatitis B surface antigen (HBsAg)-associated delta agent (delta) was determined in a series of Italian patients with a diagnosis of acute hepatitis B (HBsAg-positive) progressive to chronicity. Twenty-two of 27 (81%) and 12 of 18 (67%) patients collected, respectively, in Naples and Cagliari, where delta is highly endemic, developed immunoglobulin M antibody to delta and/or rising titers of immunoglobulin G anti-delta during the initial acute phase of the disease. In each of them, anti-delta increased to a high-titered plateau indicative of chronic delta infection. Delta markers were found in none of the 13 patients collected in Siena, where the prevalence of delta infection is low. The great majority of the patients with anti-delta and a progressive form of HBsAg-positive hepatitis lacked the IgM antibody to hepatitis B core antigen. They were presumably unrecognized carriers of HBsAg who became infected by delta and developed hepatitis induced by this agent. In areas where delta is endemic, it may represent the true cause of seemingly type B hepatitis progressing to chronic HBsAg-positive liver disease.

The prevalence of Hepatitis B Virus (HBV) markers was studied in 350 staff members from a Psychiatric Hospital, where a high prevalence of HBV markers was observed among patients. The prevalence of HBsAg, anti-HBs plus anti-HBc, anti-HBc alone and anti-HBs alone were determined to be: 2%, 15.1%, 4% and 0.3%, respectively. The prevalence of HBV markers was greater (although not significant) among women (24.7%) as compared to men (17.8%) (p greater than 0.05), and in the personnel with more than 20 years of employment (24.1%), as compared to those with less than 20 years (20% (p greater than 0.05). The highest prevalence of infection was observed in the department in which were admitted children and young adults. The overall prevalence of HBV markers was higher among staff members than in the blood donors of our area. Hospital personnel must know such epidemiologic conditions: active immunization with the Hepatitis B vaccine must be offered to hospital employees, firstly in those institutions in which a high prevalence of HBV infection has been documented.

Hepatitis B surface antigen (HBsAg) bound to immunoglobulin M (IgM) was detected in sera of HBsAg carriers by a radioimmunoassay based on selective absorption of the immunoglobulin on a solid phase coated with antiserum to human IgM. Isopycnic banding and rate-zonal sedimentation have shown that the reaction is related to particulate forms of the HBsAg complexed with IgM. The binding of IgM possibly occurred because of a selective affinity of these molecules to the surface of HBsAg particles. HBsAg/IgM was found transiently in 24 of 25 (96%) patients with acute self-limited hepatitis B and persistently in 6 of 25 patients whose acute hepatitis B progressed to chronicity. It was also found in 20 of 39 (51%) chronic HBsAg carriers with inactive and asymptomatic infection. The HBsAg/IgM phenomenon is not dependent on replication of hepatitis B virions; its persistence in patients with acute hepatitis B may provide complementary evidence of transition of the infection to chronicity.