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Viruses Isolated (viruse + isolated)
Selected AbstractsFine antigenic variation within H5N1 influenza virus hemagglutinin's antigenic sites defined by yeast cell surface displayEUROPEAN JOURNAL OF IMMUNOLOGY, Issue 12 2009Jian Li Abstract Fifteen strains of mAb specific for HA of the A/Hong Kong/482/97 (H5N1) influenza virus were generated. The HA antigenic sites of the human A/Hong Kong/482/97 (H5N1) influenza virus were defined by using yeast cell surface-displaying system and anti-H5 HA mAb. Evolution analysis of H5 HA identified residues that exhibit diversifying selection in the antigenic sites and demonstrated surprising differences between residue variation of H5 HA and H3 HA. A conserved neutralizing epitope in the H5 HA protein recognized by mAb H5M9 was found using viruses isolated from 1997,2006. Seven single amino acid substitutions were introduced into the HA antigenic sites, respectively, and the alteration of antigenicity was assessed. The structure obtained by homology-modeling and molecular dynamic methods showed that a subtle substitution at residue 124 propagates throughout its nearby loop (152,159). We discuss how the structural changes caused by point mutation might explain the altered antigenicity of the HA protein. The results demonstrate the existence of immunodominant positions in the H5 HA protein, alteration of these residues might improve the immunogenicity of vaccine strains. [source] Phenotypic characteristics of novel swine-origin influenza A/California/07/2009 (H1N1) virusINFLUENZA AND OTHER RESPIRATORY VIRUSES, Issue 1 2010Irina Kiseleva Background, The 2009 novel A(H1N1) virus appears to be of swine origin. This strain causing the current outbreaks is a new virus that has not been seen previously either in humans or animals. We have previously reported that viruses causing pandemics or large outbreaks were able to grow at a temperature above the normal physiological range (temperature resistance, non-ts phenotype), were found to be inhibitor resistant and restricted in replication at suboptimal temperature (sensitivity to grow at low temperature, non-ca phenotype). In this study, we performed phenotypic analysis of novel A(H1N1) virus to evaluate its pandemic potential and its suitability for use in developing a live attenuated influenza vaccine. Objectives, The goal of this study is to identify phenotypic properties of novel A(H1N1) influenza virus. Methods, A/California/07/2009 (H1N1) swine-origin influenza virus was studied in comparison with some influenza A viruses isolated in different years with respect to their ability to grow at non-permissive temperatures. We also analyzed its sensitivity to gamma-inhibitors of animal sera and its ability to agglutinate chicken, human and guinea pig erythrocytes. Results, Swine-origin A/California/07/2009 (H1N1) virus was found to be non-ts and inhibitor resistant and was not able to grow at 25°C (non-ca). We did not find any difference in the ability of the hemagglutinin of A/California/07/2009 (H1N1) virus to bind to erythrocytes of different origin. Conclusion, The novel swine-origin A(H1N1) virus displays a phenotype typical of the past pandemic and epidemic viruses. This finding suggests that this virus might be a good wild type parental prototype for live vaccine for potential use for controlling pandemic influenza. [source] Non-random reassortment in human influenza A virusesINFLUENZA AND OTHER RESPIRATORY VIRUSES, Issue 1 2008Raul Rabadan Background, The influenza A virus has two basic modes of evolution. Because of a high error rate in the process of replication by RNA polymerase, the viral genome drifts via accumulated mutations. The second mode of evolution is termed a shift, which results from the reassortment of the eight segments of this virus. When two different influenza viruses co-infect the same host cell, new virions can be released that contain segments from both parental strains. This type of shift has been the source of at least two of the influenza pandemics in the 20th century (H2N2 in 1957 and H3N2 in 1968). Objectives, The methods to measure these genetic shifts have not yet provided a quantitative answer to questions such as: what is the rate of genetic reassortment during a local epidemic? Are all possible reassortments equally likely or are there preferred patterns? Methods, To answer these questions and provide a quantitative way to measure genetic shifts, a new method for detecting reassortments from nucleotide sequence data was created that does not rely upon phylogenetic analysis. Two different sequence databases were used: human H3N2 viruses isolated in New York State between 1995 and 2006, and human H3N2 viruses isolated in New Zealand between 2000 and 2005. Results, Using this new method, we were able to reproduce all the reassortments found in earlier works, as well as detect, with very high confidence, many reassortments that were not detected by previous authors. We obtain a lower bound on the reassortment rate of 2,3 events per year, and find a clear preference for reassortments involving only one segment, most often hemagglutinin or neuraminidase. At a lower frequency several segments appear to reassort in vivo in defined groups as has been suggested previously in vitro. Conclusions, Our results strongly suggest that the patterns of reassortment in the viral population are not random. Deciphering these patterns can be a useful tool in attempting to understand and predict possible influenza pandemics. [source] Genetic characterization of hantaviruses isolated from Guizhou, China: Evidence for spillover and reassortment in natureJOURNAL OF MEDICAL VIROLOGY, Issue 6 2008Yang Zou Abstract To gain more insights into the epidemiology of hantaviruses in the Guizhou province, China, rodents were captured in Guizhou during the period from 2001 to 2003. In addition, serum sample was collected from one patient. Virus isolation was attempted from human serum and rodent samples. Four hantaviruses were isolated successfully in cell culture from one human, two A. agrarius, and one R. norvegicus. The nucleotide sequences for the entire S and M and partial L segment were determined from these four isolates as well as six viruses isolated in 1980s. Phylogenetic analysis revealed that the S segment from all isolates belong to the Hantaan virus (HTNV) clade, regardless of the sources from which they were derived. According to the S sequences, these viruses could be divided into three distinct phylogroups, showing geographical clustering. Analysis of the entire M and the partial L segment sequences demonstrated that 8 out of the 10 isolates belong to the HTNV clade. However, two isolates (CGRn8316 and CGRn9415) isolated from R. norvegicus belong to the Seoul virus (SEOV) clade. In addition, these two isolates were distinct from other known members of SEOV clade. Together, the data suggest that at least three groups of HTNV are co-circulating and one new variant of SEOV may be present in Guizhou. Our results also suggest that HTNV from A. agrarius spilled over to R. norvegicus and natural reassortment between HTNV and SEOV occurred during or after the spillover. J. Med. Virol. 80:1033,1041, 2008. © 2008 Wiley-Liss, Inc. [source] Distinct patterns of evolution between respiratory syncytial virus subgroups A and B From New Zealand isolates collected over thirty-seven years,JOURNAL OF MEDICAL VIROLOGY, Issue 10 2006James W. Matheson Abstract Respiratory syncytial virus (RSV) is the most important cause of viral lower respiratory tract infections in infants and children worldwide. In New Zealand, infants with RSV disease are hospitalized at a higher rate than other industrialized countries, without a proportionate increase in known risk factors. The molecular epidemiology of RSV in New Zealand has never been described. Therefore, we analyzed viral attachment glycoprotein (G) gene sequences from 106 RSV subgroup A isolates collected in New Zealand between 1967 and 2003, and 38 subgroup B viruses collected between 1984 and 2004. Subgroup A and B sequences were aligned separately, and compared to sequences of viruses isolated from other countries during a similar period. Genotyping and clustering analyses showed RSV in New Zealand is similar and temporally related to viruses found in other countries. By quantifying temporal clustering, we found subgroup B viruses clustered more strongly than subgroup A viruses. RSV B sequences displayed more variability in stop codon usage and predicted protein length, and had a higher degree of predicted O-glycosylation site changes than RSV A. The mutation rate calculated for the RSV B G gene was significantly higher than for RSV A. Together, these data reveal that RSV subgroups exhibit different patterns of evolution, with subgroup B viruses evolving faster than A. J. Med. Virol. 78:1354,1364, 2006. © 2006 Wiley-Liss, Inc. [source] | ||||||||||