Based on phylogenetic analysis, H1N1subtypes showed some genetic drifts from vaccine strain but H3N2 subtypes were from the previous vaccine strains.24 The present study showed that out of 50 positive isolates

for human influenza A virus, 15 and 2 strains were H1N1 and H3N2, respectively. Nucleotide sequences of these 17 isolates were compared to the HA1 gene of other H1N1 and H3N2 reference virus isolates in GenBank. The H1N1 isolates were genetically close to A/Brisbane/59/2007 vaccine strain Inhibitors,research,lifescience,medical and Iranian isolates from previous years. Ten H1N1 isolates were clustered in a distinct branch close to New Caledonia/20/99 strain, and five of them were branched with two Tehran/2006 isolates (figure 3a). These subtypes were different from A/Brisbane/59/2007 vaccine virus in 5-7 amino acids whose substitutions were located in the antigenic sites B and D. The phylogenetic analysis of H3N2 HA nucleotide Inhibitors,research,lifescience,medical sequences demonstrated our H3N2 isolates were related to the A/Brisbane/10/2007 vaccine strain and cluster in a unique branch (figure 3b). These isolates varied from vaccine strain only in one amino acid, which was located in the antigenic site D.

Further analysis Inhibitors,research,lifescience,medical will be necessary to estimate the evolution of the mutational changes in the antigenic sites on the HA1 protein.25 Conclusion Human influenza A/H1N1 was predominant subtype during 2008-2009 influenza seasons in Tehran. In addition, some amino acid variations were found in Tehran/2008/H1N1 isolates from the 2008-2009 vaccine strain, however, the H3N2 isolates showed higher genetic resemblance to the vaccine strain. Acknowledgement We would like to thank Dr. Mazaheri and Ms. Shokati of Pasteur Institute of Iran, and Dr. Tafazzoli Inhibitors,research,lifescience,medical and Dr. Mofid of the Outpatient Clinic of Shahid Beheshti University for their assistance in the collection of samples. Conflict Inhibitors,research,lifescience,medical of Interest: None declared
Background: Clarithromycin resistance in CCI-779 mouse Helicbacter pylori has been found to be associated with point mutations in 23s rRNA gene leads to reduced affinity of the antibiotic to its ribosomal target

or changing the site of methylation. The aim of this study was to determine the most important point mutations in 23s rRNA gene in H. pylori that are closely related to clarithromycin resistance among such isolates. Methods: Sixty three H. pylori isolates, obtained from gastric biopsy speciemens in Kerman, Iran, were used to evaluate their susceptibility to clarithromycin by disk diffusion Thymidine kinase test, and to detect the most common point mutations in 23s rRNA gene associated with clarithromycin resistance by Polymerase chain reaction-amplification and restriction fragment length polymorphism (PCR-RFLP) and 3′-mismatch PCR. Results: 31.7% of the H. pylori isolates were resistant to clarithromycin, and each of the resistant isolate had at least one of the most common point mutations in 23s rRNA gene associated with calrithromycin resistance.