RESUMEN
Phylogenetic analysis of 19 complete VZV genomic sequences resolves wild-type strains into 5 genotypes (E1, E2, J, M1, and M2). Complete sequences for M3 and M4 strains are unavailable, but targeted analyses of representative strains suggest they are stable, circulating VZV genotypes. Sequence analysis of VZV isolates identified both shared and specific markers for every genotype and validated a unified VZV genotyping strategy. Despite high genotype diversity no evidence for intra-genotypic recombination was observed. Five of seven VZV genotypes were reliably discriminated using only four single nucleotide polymorphisms (SNP) present in ORF22, and the E1 and E2 genotypes were resolved using SNP located in ORF21, ORF22 or ORF50. Sequence analysis of 342 clinical varicella and zoster specimens from 18 European countries identified the following distribution of VZV genotypes: E1, 221 (65%); E2, 87 (25%); M1, 20 (6%); M2, 3 (1%); M4, 11 (3%). No M3 or J strains were observed.
Asunto(s)
Varicela/virología , Herpes Zóster/virología , Herpesvirus Humano 3/clasificación , Herpesvirus Humano 3/genética , Polimorfismo de Nucleótido Simple , Varicela/epidemiología , Europa (Continente)/epidemiología , Genotipo , Herpes Zóster/epidemiología , Herpesvirus Humano 3/aislamiento & purificación , Humanos , Epidemiología Molecular , Datos de Secuencia Molecular , Filogenia , Análisis de Secuencia de ADN , Homología de SecuenciaRESUMEN
During 2005-2006, nine measles virus (MV) genotypes were identified throughout the World Health Organization European Region. All major epidemics were associated with genotypes D4, D6, and B3. Other genotypes (B2, D5, D8, D9, G2, and H1) were only found in limited numbers of cases after importation from other continents. The genetic diversity of endemic D6 strains was low; genotypes C2 and D7, circulating in Europe until recent years, were no longer identified. The transmission chains of several indigenous MV strains may thus have been interrupted by enhanced vaccination. However, multiple importations from Africa and Asia and virus introduction into highly mobile and unvaccinated communities caused a massive spread of D4 and B3 strains throughout much of the region. Thus, despite the reduction of endemic MV circulation, importation of MV from other continents caused prolonged circulation and large outbreaks after their introduction into unvaccinated and highly mobile communities.
