As most published studies on precore mutants have been carried out on isolates from patients with liver diseases, and it is unclear whether HBsAg carriers with viraemia in the absence of HBeAg are also generally infected by such mutants, it was decided to sequence the precore region in some HBV-DNA isolated from HBsAg-positive carriers. Precore sequences of HBV-DNA from 43 HBsAg carriers in Malaysia were studied. Three HBV subtypes were identified according to the nucleotide sequence of the precore region. Most of the carriers were found to be infected by the subtype adr. Mutations were detected in the precore regions. The most common conserved mutation was a silent mutation involving conversion from T to C (CCT to CCC) at position 1858 at codon 15 (proline). It was found that 4/43 (9.3%) had a mutation at the penultimate codon where TGG was changed to TAG. All 4 isolates with the TAG mutation had nt T at position 1858. Of the 4 carriers who were infected by these mutant viruses, 2 were coinfected with the wild type, 1 was infected only by a variant with the mutation at position 1896, while another was infected by a variant with mutations at positions 1896 and 1899. Three of the 4 were anti-HBe positive while 1 was HBeAg positive. Alanine aminotransaminase activities in all 4 carriers were normal. This study therefore demonstrated that variants with stop codons at the penultimate codon could be found in asymptomatic carriers in Malaysia.
110 normal, healthy adults were tested for antibody to hepatitis A (anti-HA) type IgG and 86 (78.2%) were found to be positive. An age-specific prevalence wasfound to be lowest in the lower agegroup and highest in the higher age-group. Out of 24 IgG positive individuals, only one was found to have type IgM. No significant difference in the incidence ofanti-HA type IgG was found between 42 patients in the Urology Unit, General Hospital, Kuala Lumpur and normal individuals (P > 0.1). 15 patients diagnosed as viral hepatitis were investigated for HA V IgG and IgM antibodies. 13 (86.7%) were positive for type IgG. Of this, only five (33%) were positive for the type IgM, suggesting that HA V is the cause of acute viral hepatitis in 33% of cases admitted to hospital as viral hepatitis.
The incidence of HBsAg in random blood donors was found to be twice that of the prisoner population. The anti-HBe however, was about twice that in the prisoners when compared with the random blood donors. Both the random blood donors and the prisoners had similar incidence of HBeAg. The percentage frequency of HBsAg positivity with anti-HBe positivity was also similar in both groups. The 18 normal non-blood donors did not have HBsAg, HBeAg or anti-HBe.
The infectiousness with regard to HBV Infection of staff and patients in various units of the General Hospital, Kuala Lumpur
was assessed. It was found that all units, with the exception of the obstetric unit, were equally high risk areas. At least 50% of the patients in all these units had one or more of the markers. Among the medical staff, the anaesthetists had the highest
incidence of HBV markers (100%) while medical officers who had worked for three years or more were more likely to have to
have the HBV markers. The degree of infectiousness of the nurses In HDU and ICU/OT was found to be similar.
HBV-DNA were analysed in 330 HBsAg-positive carriers in Malaysia by dot-blot hybridization and polymerase chain reaction. Seventy-three (22.12%) were positive for the virus. Of these, 65 (89%) were males and 8 (11%) were females. Statistically, there was no significant difference (P = 0.13). No significant decline in HBV-DNA with age in the Malay and Chinese males was observed (P = 0.2). Prevalence of HBV-DNA was higher in the Chinese carriers than in the Malay carriers for most age groups in both sexes. Sixty-one HBV-DNA-positive carriers were also positive for HBeAg. However, three individuals were positive only for anti-HBe, one was positive for both HBeAg and anti-HBe, and eight were negative for both HBeAg and anti-HBe. Fifty-seven were positive for HBeAg but negative for HBV-DNA. No relation was observed between raised alanine aminotransaminase and aspartate aminotransaminase levels and the presence of HBV-DNA (P = 0.4).