Characterization of hepatitis E virus (HEV) from Algeria and Chad by partial genome sequence

Abstract

The purpose of this study was to analyze partial nucleotide sequences and derived peptide sequences of hepatitis E virus (HEV) from two outbreaks of hepatitis E in Africa (Chad 1983-1984; Algeria 1978-1980). A portion of ORF3 and the major portion of ORF2 were amplified by Reverse Transcriptase-Polymerase Chain Reaction (RT-PCR). The PCR products were sequenced directly or after cloning into the pCRII vector. Sequences were then compared to the corresponding regions of reported full length HEV sequences. In the ORF2 and ORF3 regions, the homology between the Algerian and the Chad isolates at the nucleic acid level was 92 and 95%, respectively. At the peptide level the homology was 98% in both regions. In these regions, both strains are more related to Asian strains at the nucleic acid level (89 to 95%) and at the amino acid level (95 to 100%) than to the Mexico strain. At the peptide level the differences are less apparent. Both African isolates have amino acid changes in common with some reference strains although the Chad isolate has three unique changes. These African strains of HEV, based on the ORF2 and ORF3 phylogenetic trees, appear to be a distinct phylogenetic group, separate from the Mexican and Asian strains.

An outbreak of hepatitis E in Northern Namibia, 1983.

“…30 More recent reports of hepatitis E have emerged from many other African countries. [3][4][5][6][7][8][9][10][11] In southern Africa, surveys in South Africans and in Mozambican refugees living in Swaziland have shown serologic evidence of HEV infection, [35][36][37] but no actual disease has been documented by detection of HEV in clinical specimens. This report of hepatitis E in southern Africa is the first to unambiguously document cases by detection of HEV in patient specimens.…”

“…Primers used for detection of the HEV genome were derived from the ORF-2 and ORF-3 of the HEV Burma sequence. 10 The amplified products were analyzed using 1% agarose gel electrophoresis. A specimen was considered positive for HEV if independent amplifications of ORF-3 and ORF-2 were positive, and assay controls (n ϭ 5) gave expected results.…”

“…1 In the past decade, hepatitis E has been shown to be the cause of sporadic and epidemic hepatitis across central and south Asia, 2 and in northern and subSaharan Africa. [3][4][5][6][7][8][9][10][11] One of the largest outbreaks of hepatitis E, in Delhi, India (1955) was identified retrospectively by identification of antibodies to HEV in archived serum specimens. 12 Polymerase chain reaction (PCR) tests to detect HEV RNA 8,13,14 and improved serology for HEV [15][16][17][18] have greatly increased the ability of reference laboratories to identify hepatitis E disease.…”

Infección simultánea por el virus de la hepatitis E y de otras hepatitis virales en Colombia y su caracterización genotípica

“…En Suramérica se han reportado casos aislados en Venezuela, Uruguay y Argentina (7). El genotipo 2 se ha identificado en pacientes en México, Chad y Nigeria (6,8,9). El genotipo 3 se ha encontrado en casos de hepatitis autóctona en muchas regiones desarrolladas y tiene una alta prevalencia en poblaciones de cerdos en todo el mundo (10).…”

Short report: phylogenetically distinct hepatitis E viruses in Pakistan.

“…We determined the consensus sequence of HEV isolate Abb-2B (7,143 nucleotides) from cDNA using methods previously reported. 10,11 We performed phylogenetic analysis of Abb-2B and all other full-length HEV genomes (n ϭ 15) in the GenBank database (Table 1) using PHYLIP and PAUP programs in GCG release 10.0 (University of Wisconsin, Madison, WI) as previously described. 2 Both methods of phylogenetic analysis placed the Abb-2B isolate in the South Asian cluster of genotype I, whereas Sar-55, the other Pakistan isolate, was placed in the Central Asia cluster of genotype I (Figure 1).…”