RESUMEN
<p><b>OBJECTIVE</b>To investigate characteristics of the whole-genome of influenza A H1N1 virus circulated in Qingdao from year 2009 to 2011.</p><p><b>METHODS</b>RNA of 35 influenza A H1N1 virus isolates circulated in Qingdao between year 2009 and 2011 was extracted and all segments were amplified by RT-PCR. The sequence was then detected and assembled by software Sequencher.25 HA full-length sequences published on GenBank were selected as reference. While MEGA 5.0 software package was explored for phylogenetic analysis to characterize the molecular feature with reference to the whole-genome sequence and the hemagglutinin (HA).1068 HA sequences of influenza A H1N1 virus isolated worldwide from August 2010 to March 2011 were downloaded for amino acid mutation analysis.</p><p><b>RESULTS</b>On the HA genes phylogenetic tree, the virus were separately divided into 4 clades in 2009-2010 and 2010-2011 surveillance season, each with a preponderant epidemic clade. The homogeneity of nucleotide and amino acids of HA isolates were 99.6%-99.9% and 99.1%-99.8% respectively in 2009-2010 surveillance season; 99.1%-99.6% and 98.2%-99.1% respectively in 2010-2011 surveillance season. The homogeneity of nucleotide and amino acids of the preponderant isolates were separately 98.8%-99.8% and 98.0%-99.6%. Compared with the vaccine strain, there were separately 14 and 12 variant amino acids of virus HA in the two surveillance season, involving 10 antigen sites and 5 positive selected sites. The sequence analysis of neuraminidase protein showed that the positions 247, 274 presented serine and histidine(S247, H274) respectively. The sequence analysis of M2 protein showed that the isolated A H1N1 viruses presented asparagine in amino acid site 31 (N31).</p><p><b>CONCLUSION</b>All the A H1N1 influenza virus circulated in Qingdao from year 2009 to 2011 presented continual variation and therefore caused antigenic drift. All the isolations were adamantane-resistance, but susceptible to inhibitors of neuraminidase.</p>
Asunto(s)
Humanos , Secuencia de Aminoácidos , China , Epidemiología , Genoma Viral , Glicoproteínas Hemaglutininas del Virus de la Influenza , Genética , Subtipo H1N1 del Virus de la Influenza A , Clasificación , Genética , Gripe Humana , Epidemiología , Virología , Neuraminidasa , Genética , Filogenia , ARN Viral , Análisis de Secuencia de ProteínaRESUMEN
Objective To assess the heritability of serum uric acid in adult,using the classic twin design.Methods Adult Twins were recruited from the Qingdao Twin Registry.Uric acid,height,weight were measured.Zygosity in all the same-sex twin pairs was determined by 16 polymorphic markers.Heritability was assessed by structural equation models,with age,gender and body mass index(BMI) included as covariates.Results In total,687 twin pairs were available for data analyses,including 420 pairs of monozygotic and 267 pairs of dizygotic twins.After logarithm transformed,uric acid in males ( 17.47±1.91 ) was significantly higher than in females ( 15.22±1.70,P＜0.0001 ).After adjustment on age,sex and BMI,intraclass correlations for uric acid were 0.70 for monozygotic twins and 0.40 for dizygotic twins.The sex-limitation AE model,combining additive genetic and unique environmental factors,could produce the best fit for the data.Heritability estimate for uric acid was 70.5% (95% CI:65.9-74.6),with the proportion of unique environmental effects as 29.5%(95%CI:25.4-34.2).Conclusion Additive genetic effects appeared to be the major contributor to the variation of uric acid in this twins sample being studied.