Molecular epidemiology of measles virus before and after the 2003 mass vaccination campaign for measles/rubella in Iran

Molecular epidemiology of measles virus [MV] is important, not only to measure the success of measles vaccination programs but also to monitor the circulation and elimination of the virus worldwide. In this study, we compared MV obtained from patients before the 2003 mass vaccination MR campaign and viruses detected after 2003 until 2008 in Iran. The nucleoprotein [N] gene of 29 MV strains circulating in Iran between 2002 and 2008 were amplified by RT-PCR and subjected to sequence and phylogenetic analysis. Molecular characterization of MV studied here revealed that although the outbreaks in Iran were associated with MV genotype D4, the isolated viruses clearly belonged to several different lineages. Maximum and minimum homology within the 29 Iranian strains in our study was100% and 94.9% within the carboxyl terminus of the N gene, respectively. Using Clustal X program, the alignment of Iranian MV sequences showed nine lineages. This study provides the usefulness of MV sequence analysis for the demonstration of local interruption of indigenous strain transmission as well as providing a valuable means for monitoring the elimination processes of MV control

[Novel mutations in LAMA2 gene responsible for a severe phenotype of congenital muscular dystrophy in two tunisian families]

Congenital muscular dystrophies are a group of common genetically determined disorders often transmitted with a recessive mode of inheritance. In recent years, several deficiencies of proteins from the muscle membrane, extra cellular matrix, sarcomere, muscle cytosol and the nucleus have been described to cause CMD. The occidental type of CMD [MDC1A] in which the primary defect is a deficiency in laminin alpha 2 chain [merosin] encoded by LAMA2 gene, accounts for 30-40% of cases. The clinical course of CMD with complete laminin alpha 2 chain deficiency may be variable but most often; severe forms characterized by hypotonia at birth, profound muscle weakness, marked delay in motor milestones are observed. Since the identification of the first LAMA2 gene mutations leading to merosin deficiency in 1995, several mutations have subsequently been reported in many exons of this gene without any "hotspot" region. In this work, we report two novel homozygous mutations c.8005delT and C.8244+1G>A in the LAMA2 gene in four Tunisian patients with a severe MDC1A phenotype belonging to two unrelated consanguineous families