The complete nucleotide sequence was determined for a hepatitis B virus genome of subtype adw (pFDW294) isolated and cloned from the plasma sample of a Philippino. The genome was 3221 base‐pair long with a point mutation at the 1376th nucleotide that affected the coding capacity of the P and X genes. There was a wide range of sequence divergence among pFDW294 and the reported three genomes of the same subtype (1.1–9.9%), occurring more often in the pre‐S region and the S gene than in the pre‐C region and the C gene.

Hepatitis B virus markers were studied in 2,842 Philippine rural subjects from four villages in 1979-1982. The prevalence of hepatitis B surface antigen (HBsAg) and all markers for hepatitis B virus averaged 12% and 58%, respectively, in these rural populations. It is estimated that five million Filipinos are HBsAg positive. The rural age-specific HBsAg prevalence shows an "early peak" (in persons 3-4-years-old) in two communities and a "late peak" (in persons 30-40-years-old) in the other two communities. Family studies suggest that the prevalence of HBsAg and hepatitis B e antigen (HBeAg) among parents of the young children in an "early peak" and a "late peak" village cannot fully account for the difference in the patterns of prevalence of all markers, or the HBsAg marker. Horizontal intrafamilial and extrafamilial transmission may also be significant. Further research is needed on risk factors for hepatitis B virus infection.

A method has been developed for the analysis of hepatitis B surface antigen (HBsAg) antigenic structure at the molecular level that creates "fingerprints" or "signatures" of various hepatitis B viral (HBV) strains. This technique employs high affinity IgM and IgG monoclonal antibodies (anti-HBs) directed against distinct and separate determinants on HBsAg. In performing this antigenic structural analysis, separate binding curves for different monoclonal anti-HBs are generated by measuring immunoreactivity in serial dilutions of HBsAg-positive serum by radioimmunoassay. Since the HBsAg concentration in serum is unknown, the binding profiles of groups of samples are aligned by an iterative least-squares procedure to generate the numerical signature characteristic of the viral strain. The numerical signatures are then displayed on a computer-graphic plot. The signature profiles of HBsAg subtypes are a true reflection of their antigenic structure, and in vertical and horizontal transmission studies the molecular characteristics of the viral epitopes are conserved. By signature analysis we found substantial antigenic heterogeneity among the ayw3 strain both in the U. S. and France, as well as in populations of the Far East and Africa. Populations in Ethiopia, Gambia, and the Philippines were infected with two antigenically distinct HBV strains. In some newly identified HBV strains, it was found that epitopes identified by some monoclonal antibodies were absent or substantially reduced, which suggested that a genetic mutation may have occurred. Thus this study suggests that there is far more antigenic heterogeneity in HBV than previously recognized. These variants are antigenically distinct from each other at the epitope level, and were heretofore unrecognized by polyvalent anti-HBsAg antibodies.

The hepatitis B virus (HBV) profile was investigated in 104 age-grouped hepatocellular carcinoma (HCC) patients and 84 controls from the Philippines. The HCC-control percent positivities of the HBV parameters are: HBsAg: 70-18; anti-HBs: 25-37; anti-HBs: 25-37; anti-HBc: 94-35; HBeAg: 5-2; anti-HBe: 60-30; HBV exposure rate: 97-57; current infection: 80-31. Male HCC anti-HBs positivity is significantly lower than in controls. Female HCC patients' anti-HBs are also lower than controls, but this difference is not statistically significant. Simultaneous presence of HBsAg and anti-HBs was found only in male HCC patients. The mean anti-HBc titer of anti-HBs-positive HCC is higher than that of controls. That of HCC patients negative for both HBsAg and anti-HBs is also higher than the corresponding controls. Anti-HBe positivities of infected and noninfected but previously exposed HCC patients are not significantly different, in contrast to noninfected previously exposed controls whose anti-HBe is lower than those with current infection. The exposure rate prevalence of current infection, and the antibody responses to HBV of HCC patients suggested a close relationship between the two conditions in the Philippines.