Epidemiology of peste des petits ruminants virus in Ethiopia and molecular studies on virulence
2005
Abraham Gopilo
Peste des petits ruminants (PPR) is a one of the most important economical diseases in Ethiopia. Clinical PPR is confirmed in Ethiopian goats, however, its circulation in other animals was not described. The results of the present work showed that the antibody seroprevalence in camel, cattle, goat and sheep confirmed natural transmission in these animals without clinical disease. The absence of pathogenicity in these animals might be due to host resistance or loss of virulence of the virus strain. We investigated the latter point by in vitro studies on PPRV comparing strains from Ethiopia and other countries with the vaccine strain attenuated after several cell culture passages. Virulence of PPRV was monitored in cell culture system and the use of virus specific monoclonal antibodies enabled to detect differences in virulence between PPRV and RPV. Vero (primate origin) and 293T (human cell lines supported virus replication permitting the in vitro growth of PPRV and RPV. In contrast to RPV, B95a (marmoset B) cells infected with PPRV were non-permissive. The capability of cells to support active virus replication, which may result in intercellular spread and induce damages in infected cells, has implications on the pathogenesis and epidemiology. Cellular receptors are major determinants of host range and tissue tropism of a virus. The difference in infectivity of PPRV and RPV might have depended on H protein epitopes and their cellular receptors. Therefore, the amino acid epitope of H protein of PPRV was compared with that of other morbilliviruses. We sequenced and compared genome and antigenome promoters of a vaccine strain with field strains of PPRV. The promoters contained the polymerase binding sites to initiate and generate the positive-strand replication and transcription of mRNAs. Nucleotide base change differences between vaccine strain and field strains would provide molecular basis for attenuation. Alignment of the genome promoter sequences revealed seven nucleotide mutations at certain positions. Our finding on nucleotide mutation on PPRV are in agreement agreed with nucleotide changes in finderpest virus and other morbillivirus promoter regions between vaccine strain and wild type virus. Certain mutations were specific to PPRV. The promoter sequences were clustered around the geographic origin of the viruses and were lineage specific. Phylogenetic analysis of PPRV promoters was used for PPR phylogeograhy and for comparison with other paramyxoviruses.
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