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Hepatitis B virus DNA was determined in the sera of 198 chronic hepatitis B surface antigen (HBsAg) carriers by the spot hybridization technique. The results were correlated with hepatitis Be antigen (HBeAg) and antibody (anti-HBe), delta antibody (anti-HD) and liver histology. All subjects had a liver biopsy. The prevalence of HBV DNA was 63% in HBeAg-positive subjects and 8.8% in anti-HBe positives. HBV DNA was not found more frequently in chronic HBsAg carriers who had histological evidence of liver disease than in carriers without such evidence. Anti-HD was detected in 48.5% of subjects, with an increasing trend (p less than 0.001) according to the severity of liver disease. Among patients with more severe liver disease (CAH and cirrhosis), HBV DNA and HBeAg were detected less frequently in anti-HD-positive than in anti-HD-negative subjects (7% vs. 42.3%, p less than 0.001 and 7% vs. 34.4%, p less than 0.005, respectively). These findings indicate that HDV infection jointly affects both HBeAg status and HBV DNA.

In January 1989, the prevalence of antibodies to hepatitis A virus (anti-HAV) was determined by ELISA in 702 apparently healthy children 5-14 years old in Kumba City, Cameroon. Children were recruited from those attending six different primary schools, representative of the socio-demographic characteristics of the inhabitants, using a systematic random sampling. The overall IgG anti-HAV prevalence was 96.9%, reaching 100% by the age of 11 years. In primary school beginners the prevalence was very high, 94.0%, contrary to what has been observed in developed countries. The anti-HAV prevalence was not associated with family size, but was related to parent's occupation, children from the lower class having a 5.9 fold risk (C.I. = 1.9-18.3) of past exposure to HAV. These results suggest a persistently high prevalence of anti-HAV in children despite improving hygienic conditions. The spread of HAV in this population may be the result of domestic water and/or food contamination.

A pilot survey conducted in Cameroon comprising 702 children of primary school age revealed that 58.5% of the children were positive for at least one HBV marker. An overall HBsAg prevalence of 19.9% was observed. Both any HBV marker and HBsAg prevalences increased with age (P less than 0.01). Of the HBsAg-positive subjects, 28.4% were positive for HBV-DNA; none was positive for anti-HDV. There was no significant difference among sexes for either any HBV marker or for HBsAg prevalence. However, a significant difference by sex was found in the percentage ratio HBsAg+/and any marker + (41.0% in males against 28.2% in females; P less than 0.05). No significant difference with respect to the father's occupation and family size was observed. When the zone of location of school was taken into consideration it was observed that suburban school children had a higher prevalence of any HBV marker as compared to central town school children (73.9% vs. 56.6%; P less than 0.001). These results place Cameroon among countries of high endemicity for HBV. The results also indicate an early acquisition of infection, a high infectivity, and probably continuous infection even in the primary school ages.

The serum kinetics of preS1 and preS2 antigens has been evaluated in 38 serial samples from eight patients with chronic active (CAH) or chronic persistent (CPH) hepatitis, followed for 2-7 years (mean 4.4 years) in whom liver biopsy was performed at intervals, and in 46 samples from ten asymptomatic HBsAg carriers followed for 4-5 years (mean 4.6 years). Four patterns of preS behaviour have been observed: (1) persistently positive preS1 and preS2; (2) disappearance of preS2; (3) disappearance of both preS1 and preS2; and (4) persistently negative preS1 and preS2. Pattern 4 has been observed exclusively among healthy carriers, while seven out of eight chronic patients exhibited either pattern 1 or 2. Among the chronic patients, preS2 disappearance was accompanied or followed by alanine aminotransferase (ALT) normalization. The correlation of preS antigens with conventional viral replication markers showed that 100% of hepatitis B virus (HBV)-DNA-positive and 86.6% of HBeAg-positive sera were preS1/preS2 positive, while 61% of HBV-DNA-negative and 64% of HBeAg-negative sera were preS1/preS2 negative. Our data suggest that continuous monitoring of preS antigens in follow-up sera will allow for an improved prognostic evaluation of chronic HBV infection.

A population of 488 HBsAg carrier individuals, from central Italy, classified on the basis of biochemical, clinical and histological parameters, was analysed for the presence of HBV-DNA in serum and its relationship with HBeAg/anti-HBe markers. The prevalence of HBV-DNA was 32.8% in chronic patients with biopsy-proven liver disease, and 20 and 4.3% respectively in asymptomatic carriers with and without altered ALT levels. The values in chronic patients were correlated with the histological activity. Concordance of HBV-DNA presence and HBeAg positivity was observed in only 61.4% of cases. However HBV-DNA prevalence in sera of anti-HBe positive individuals was very low in asymptomatic carriers with normal ALT levels (2.5%). Higher values were observed in anti-HBe positive chronic patients (15.8%) and in carriers occasionally found with changes in ALT without any other clinical sign of illness (16.7%). These data would indicate that HBV-DNA is the serological marker which is most closely related to liver disease.

A seroepidemiological survey of a group of 291 intravenous drug abusers (IVDAs), 45 household contacts of IVDAs, and 39 laboratory workers has been carried out to determine the prevalence of HIV-1, HIV-2, HTLV-1, and HBV antibodies in the sera, as well as to evaluate the role of various risk factors. Among i.v. drug abusers, the prevalence was 32.3% for HIV-1 and 6.6% for HTLV-1. For both viruses, the total figures did not significantly change from 1985 through 1987, accounting for a slow viral circulation in this group. No seropositivity (HIV-1, HTLV-1) was found among laboratory workers, whereas one subject was found seropositive for HIV-1 among household contacts. From 1985 to 1986, 5 out of 58 subjects seronegative for HIV-1 and 5 out of 82 seronegative for HTLV-1 seroconverted (incidence rates of 8.6 and 6.1%, respectively). From 1986 to 1987, none out of 11 seronegatives for HIV and 1 out of 16 seronegatives for HTLV-1 seroconverted. The total figures for hepatitis B markers were 79.2% among IVDAs, 24.4% among household contacts, and 25.6% among laboratory workers. A significant correlation was found between presence of HBV markers and seropositivity for HIV and HTLV-1. A significant association with HIV-1 seropositivity was found for history of sexual intercourse with HIV-1 seropositive partners and for sexual promiscuity. These data emphasize the important role played by sexual behavior in addition to needle-sharing in the spreading of multiple infections among drug abusers.

In May 1988, the hepatitis A antibody (anti-HAV) and hepatitis B virus (HBV) markers were studied by radioimmunoassay in 484 apparently healthy children between the ages of 7 and 12, attending a primary school in Naples, Italy. The overall anti-HAV prevalence was 11.2%, increasing from 5.2 in 7-year-old children to 28.2% in children between the ages of 11 and 12 years old. The overall prevalence of the hepatitis B surface antigen (HBsAg) and of other HBV markers were 0.8 and 6.8 respectively. Compared with a similar previous study conducted in Naples in 1980, the results show a significant reduction in the prevalence of anti-HAV in each of the two age-groups (P less than 0.01), in the prevalence of any HBV marker in the 11 to 12-year-old group, as well as in the total population (P less than 0.05). The findings of the present study indicate that today, children in Naples are less exposed to the hepatitis A virus than in the past, most likely because of improvements in both the socioeconomic conditions and in health education during recent years. These same reasons, as well as decreased family size and a lower prevalence of HBeAg among HBsAg carriers could explain the decline, although to a lesser degree, of exposure to HBV infection.