The preS2/S genes of hepatitis B virus isolated from 29 acutely or chronically infected individuals in the Gauteng province of South Africa were sequenced. Phylogenetic analysis of these sequences in comparison with global isolates from the GenBank database showed that 24 sequences clustered with genotypic group A, three with genotypic group D and one each with genotypic groups B and C. Group A isolates had greater identity with groups D (variation of 6n6 %) and E (6n8 %) than with the Eastern groups B (7n4 %) and C (8n1 %) and were most different from group F (11n0 %). Of the South

Hepatitis B virus (HBV) was partitioned into type, subtype and isolate categories and the average evolutionary distances within and between categories was plotted at each of 54 points along the genome. The graphs showed alternating variable and conserved domains within and between HBV subtypes and revealed that some specimens assigned to different groups are more similar across several contiguous intervals than specimens belonging to the same group. Isolates were screened individually to determine their conformation to type and mosaic structure was identified in 14/65 specimens. Two entire clades (six specimens) of genotype B had a B/C sequence switch in the core gene region, whereas six genotype D specimens showed D/A switching in one or more regions of the genome. Genotype E was not separate from genotype D in the X and C subgenomic regions. The nature and distribution of polymorphic sites in mosaic regions was mapped at both the nucleotide and protein levels and the position of the variant fragments was related to mutational hot spots and linear epitopes of HBV. Mosaic structure was demonstrated statistically in 11 isolates using bootstrap resampling and recombination, rather than random change, appeared to be the mechanism responsible. The sequence between and including the two DR regions was represented in all putative recombinants. The distribution of genetic distances over subgenomic regions showed that substitution rates are not constant among the lineages of HBV in the preS regions. Genotype F is the most diverse group. Only genotypes A, C and F partition consistently into subtypes.

Endemic circulation of hepatitis E virus (HEV) in Namibia was suspected from serological data during an outbreak of non-A, non-B hepatitis in Rundu in 1995. The source of the outbreak was suspected to be the water supply, which had been compromised approximately 6 months earlier. Four HEV isolates from four different persons in this outbreak were successfully amplified, sequenced and analysed over a 451 bp region of a subgenomic fragment from the 39 end of the genome in ORF2. Phylogenetic analysis showed that the four Namibian HEV isolates clustered with a Mexican isolate in genotype II and shared 85?8-86?3 % nucleotide identity with the 1987 Mexican isolate, but were only 77?6-79?6 % similar to other African isolates. HEV isolated from the same region of Namibia in 1983 was reported to cluster in genotype I. However, virus isolates from sporadic cases of HEV isolated in 1997/8 in Nigeria were also from genotype II.Hepatitis E virus (HEV), previously referred to as enterically transmitted non-A, non-B hepatitis, is a non-enveloped virus approximately 32-34 nm in diameter, with a positivesense, single-stranded RNA genome of approximately 7?5 kb (Purcell, 1996;Krawczynski et al., 2000). HEV is the leading cause of enterically transmitted, non-A hepatitis worldwide and is responsible for major outbreaks of acute hepatitis in developing countries, especially in tropical and subtropical regions of the world where outbreaks are usually associated with faecally contaminated drinking water (Irshad, 1999). Sporadic cases of HEV are common in endemic regions and appear to be rare in industrialized countries, where they tend to be imported. However, not all isolated reports of HEV-associated hepatitis in developed nations include a history of travel to regions endemic for HEV (Zaaijer et al., 1993;Zanetti et al., 1994;Tassopoulos et al., 1994;Hsieh et al., 1998;Schlauder et al., 1998Schlauder et al., , 2000Worm et al., 2000;Takahashi et al., 2002).HEV is prevalent in Africa and epidemics have been identified in Algeria, the Ivory Coast, Sudan, Somalia (Bradley, 1992) and Djibouti (Coursaget et al., 1996), with smaller outbreaks reported in Morocco (Benjelloun et al., 1997), Ethiopia (Tsega et al., 1991), Chad (van CuyckGandre et al., 1996) and Kenya (Mast et al., 1994), while sporadic cases of HEV have been identified in Egypt (Tsarev et al., 1999), Nigeria (Buisson et al., 2000) and Tunisia (Coursaget et al., 1996).The first report of hepatitis E in southern Africa was the published account of a typical waterborne outbreak with 273 cases and at least four deaths in Maun, northern Botswana, in 1985(Byskov et al., 1989. The disease appeared to have affected 1-2 % of the population and pregnant women were most severely affected. An earlier outbreak in southern Africa, which occurred in Namibia's Kavango region in 1983 and affected people living in settlements lacking potable water and waste disposal facilities, was only recently characterized and identified by molecular methods as epidemic HEV . The disease was usually m...

We have investigated the efficacy of a relatively prolonged course of recombinant leukocyte interferon treatment in 14 chronic HBsAg-, HBeAg-, hepatitis B virus DNA- and DNA polymerase-positive carriers. alpha-Interferon was administered for 9 weeks. Six of 14 treated carriers have a sustained loss of HBeAg, hepatitis B virus DNA and DNA polymerase. Four subsequently lost HBsAg (28.5%). Elevated pretreatment SGPT concentrations, histologic chronic active hepatitis, an exacerbation of chronic hepatitis with an increase in SGPT concentrations in the last weeks of treatment and possibly recent onset of the carrier state was associated with complete inhibition of viral replication. None of 11 matched, untreated HBsAg-, HBeAg-, hepatitis B virus DNA- and DNA polymerase-positive carriers monitored during the same period lost HBsAg. The effect of recombinant leukocyte interferon may require an appropriate host-immune response. The efficacy of recombinant leukocyte interferon therapy is restricted, but it may be of benefit in a proportion of carriers, if these carriers can be precisely identified.