Influenza A virus (A/Puerto Rico/8/1934(H1N1))


Alias: Influenza A virus (A/Puerto Rico/8/34(H1N1)), Influenza A virus ( A/Puerto Rico/8/1934(H1N1)), Influenza A virus (A/PR 8/34 (H1N1)), Influenza A virus (A/PR/8/1934(H1N1)), Influenza A virus (A/PR/8/34(H0N1)), Influenza A virus (A/PR/8/34(H1N1)), Influenza A virus (A/PR/8/34(HON1)), Influenza A virus (A/PR8/1934(H1N1)), Influenza A virus (A/Puerto Rico/8/1934(H0N1)), Influenza A virus (A/Puerto Rico/8/34), Influenza A virus (STRAIN A/PUERTO RICO/8/34), nfluenza A virus (A/PR 8/34(H1N1))

Top Publications

  1. Taubenberger J, Reid A, Lourens R, Wang R, Jin G, Fanning T. Characterization of the 1918 influenza virus polymerase genes. Nature. 2005;437:889-93 pubmed
    ..The sequence changes identified here may be important in the adaptation of influenza viruses to humans. ..
  2. Mibayashi M, Martinez Sobrido L, Loo Y, Cardenas W, Gale M, Garcia Sastre A. Inhibition of retinoic acid-inducible gene I-mediated induction of beta interferon by the NS1 protein of influenza A virus. J Virol. 2007;81:514-24 pubmed
    ..Our results indicate that, in addition to sequestering dsRNA, the NS1 of influenza A virus binds to RIG-I and inhibits downstream activation of IRF-3, preventing the transcriptional induction of IFN-beta. ..
  3. Newcomb L, Kuo R, Ye Q, Jiang Y, Tao Y, Krug R. Interaction of the influenza a virus nucleocapsid protein with the viral RNA polymerase potentiates unprimed viral RNA replication. J Virol. 2009;83:29-36 pubmed publisher
  4. Sugiyama K, Obayashi E, Kawaguchi A, Suzuki Y, Tame J, Nagata K, et al. Structural insight into the essential PB1-PB2 subunit contact of the influenza virus RNA polymerase. EMBO J. 2009;28:1803-11 pubmed publisher
    ..This novel interface is surprisingly small, yet, it has a crucial function in regulating the 250 kDa polymerase complex and is completely conserved among avian and human influenza viruses. ..
  5. McAuley J, Zhang K, McCullers J. The effects of influenza A virus PB1-F2 protein on polymerase activity are strain specific and do not impact pathogenesis. J Virol. 2010;84:558-64 pubmed publisher
    ..Alternate mechanisms besides alterations to replication are likely responsible for the enhanced virulence in mammalian hosts attributed to PB1-F2 in previous studies. ..
  6. Chutinimitkul S, Herfst S, Steel J, Lowen A, Ye J, van Riel D, et al. Virulence-associated substitution D222G in the hemagglutinin of 2009 pandemic influenza A(H1N1) virus affects receptor binding. J Virol. 2010;84:11802-13 pubmed publisher
    ..Altered receptor specificity of the virus with D222G thus affected interaction with cells of the human lower respiratory tract, possibly explaining the observed association with enhanced disease in humans. ..
  7. Le Goffic R, Leymarie O, Chevalier C, Rebours E, Da Costa B, Vidic J, et al. Transcriptomic analysis of host immune and cell death responses associated with the influenza A virus PB1-F2 protein. PLoS Pathog. 2011;7:e1002202 pubmed publisher
    ..Collectively, these data demonstrate that PB1-F2 strongly influences the early host response during IAV infection and provides new insights into the mechanisms by which PB1-F2 mediates virulence. ..
  8. Abed Y, Pizzorno A, Bouhy X, Rhéaume C, Boivin G. Impact of potential permissive neuraminidase mutations on viral fitness of the H275Y oseltamivir-resistant influenza A(H1N1)pdm09 virus in vitro, in mice and in ferrets. J Virol. 2014;88:1652-8 pubmed publisher
    ..Permissive mutations may enhance the fitness of A(H1N1)pdm09 H275Y viruses in vitro and in vivo. The emergence of such variants should be carefully monitored. ..
  9. Fields S, Winter G. Nucleotide sequences of influenza virus segments 1 and 3 reveal mosaic structure of a small viral RNA segment. Cell. 1982;28:303-13 pubmed
    ..We propose that the small segment is generated during positive strand synthesis as a result of the viral polymerase pausing at uridine-rich sequences in the template and reinitiating synthesis at another site. ..

More Information

Publications116 found, 100 shown here

  1. de Wit E, Spronken M, Bestebroer T, Rimmelzwaan G, Osterhaus A, Fouchier R. Efficient generation and growth of influenza virus A/PR/8/34 from eight cDNA fragments. Virus Res. 2004;103:155-61 pubmed
    ..In conclusion, high-titer virus stocks of recombinant influenza A/PR/8/34 virus can be produced as well as virus stocks with much lower titers, but without the requirement of virus amplification through replication. ..
  2. Bruns K, Studtrucker N, Sharma A, Fossen T, Mitzner D, Eissmann A, et al. Structural characterization and oligomerization of PB1-F2, a proapoptotic influenza A virus protein. J Biol Chem. 2007;282:353-63 pubmed
    ..The consequences of the strong oligomerization and helical propensities of the molecule are discussed and used to formulate a hypothetical model of its interaction with the mitochondrial membrane. ..
  3. Guo Z, Chen L, Zeng H, Gomez J, Plowden J, Fujita T, et al. NS1 protein of influenza A virus inhibits the function of intracytoplasmic pathogen sensor, RIG-I. Am J Respir Cell Mol Biol. 2007;36:263-9 pubmed
    ..These results provide further information on the mechanism by which IAV NS1 antagonizes the host antiviral response. ..
  4. Obayashi E, Yoshida H, Kawai F, Shibayama N, Kawaguchi A, Nagata K, et al. The structural basis for an essential subunit interaction in influenza virus RNA polymerase. Nature. 2008;454:1127-31 pubmed publisher
    ..The carboxy-terminal domain of PA forms a novel fold, and forms a deep, highly hydrophobic groove into which the amino-terminal residues of PB1 can fit by forming a 3(10) helix. ..
  5. Gack M, Albrecht R, Urano T, Inn K, Huang I, Carnero E, et al. Influenza A virus NS1 targets the ubiquitin ligase TRIM25 to evade recognition by the host viral RNA sensor RIG-I. Cell Host Microbe. 2009;5:439-49 pubmed publisher
    ..Our findings reveal a mechanism by which influenza virus inhibits host IFN response and also emphasize the vital role of TRIM25 in modulating antiviral defenses. ..
  6. Gannage M, Dormann D, Albrecht R, Dengjel J, Torossi T, Rämer P, et al. Matrix protein 2 of influenza A virus blocks autophagosome fusion with lysosomes. Cell Host Microbe. 2009;6:367-80 pubmed publisher
    ..We propose that influenza A virus, which also encodes proapoptotic proteins, is able to determine the death of its host cell by inducing apoptosis and also by blocking macroautophagy. ..
  7. Mehle A, Doudna J. Adaptive strategies of the influenza virus polymerase for replication in humans. Proc Natl Acad Sci U S A. 2009;106:21312-6 pubmed publisher
    ..These data reveal a strategy used by the 2009 H1N1 influenza A virus and identify other pathways by which avian and swine-origin viruses may evolve to enhance replication, and potentially pathogenesis, in humans. ..
  8. Graef K, Vreede F, Lau Y, McCall A, Carr S, Subbarao K, et al. The PB2 subunit of the influenza virus RNA polymerase affects virulence by interacting with the mitochondrial antiviral signaling protein and inhibiting expression of beta interferon. J Virol. 2010;84:8433-45 pubmed publisher
    ..Overall this study implicates the PB2 protein in the regulation of host antiviral innate immune pathways and suggests an important role for the mitochondrial association of the PB2 protein in determining virulence. ..
  9. Iwai A, Shiozaki T, Kawai T, Akira S, Kawaoka Y, Takada A, et al. Influenza A virus polymerase inhibits type I interferon induction by binding to interferon beta promoter stimulator 1. J Biol Chem. 2010;285:32064-74 pubmed publisher
    ..These findings demonstrate that the viral polymerase plays an important role for regulating host anti-viral response through the binding to IPS-1 and inhibition of IFN? production. ..
  10. Liu Y, Childs R, Matrosovich T, Wharton S, Palma A, Chai W, et al. Altered receptor specificity and cell tropism of D222G hemagglutinin mutants isolated from fatal cases of pandemic A(H1N1) 2009 influenza virus. J Virol. 2010;84:12069-74 pubmed publisher
    ..These features of 222G mutants may contribute to exacerbation of disease. ..
  11. Abed Y, Pizzorno A, Bouhy X, Boivin G. Role of permissive neuraminidase mutations in influenza A/Brisbane/59/2007-like (H1N1) viruses. PLoS Pathog. 2011;7:e1002431 pubmed publisher
    ..In conclusion, the Q222R reversion mutation compromised Bris07-like H1N1 virus in vitro and in vivo. Thus, the R222Q NA mutation present in the WT virus may have facilitated the emergence of NAI-resistant Bris07 variants. ..
  12. Meunier I, von Messling V. PB1-F2 modulates early host responses but does not affect the pathogenesis of H1N1 seasonal influenza virus. J Virol. 2012;86:4271-8 pubmed publisher
    ..However, the three viruses did not differ in their virulence or clinical course in ferrets, supporting speculations that PB1-F2 is of limited importance for the pathogenesis of primary viral infection with human seasonal H1N1 viruses. ..
  13. Varga Z, Grant A, Manicassamy B, Palese P. Influenza virus protein PB1-F2 inhibits the induction of type I interferon by binding to MAVS and decreasing mitochondrial membrane potential. J Virol. 2012;86:8359-66 pubmed publisher
    ..Interestingly, PB1-F2 66S affected the MMP more efficiently than wild-type PB1-F2. In summary, the results of our study identify the molecular mechanism by which the influenza virus PB1-F2 N66S protein increases virulence. ..
  14. Shin Y, Li Y, Liu Q, Anderson D, Babiuk L, Zhou Y. SH3 binding motif 1 in influenza A virus NS1 protein is essential for PI3K/Akt signaling pathway activation. J Virol. 2007;81:12730-9 pubmed
    ..Activation of PI3K/Akt pathway is beneficial for virus replication by inhibiting virus induced apoptosis through phosphorylation of caspase-9. ..
  15. Hale B, Batty I, Downes C, Randall R. Binding of influenza A virus NS1 protein to the inter-SH2 domain of p85 suggests a novel mechanism for phosphoinositide 3-kinase activation. J Biol Chem. 2008;283:1372-80 pubmed
    ..Overall, these data suggest a model by which NS1 activates PI3K catalytic activity by masking a normal regulatory element specific to the p85beta inter-SH2 domain. ..
  16. Mazur I, Anhlan D, Mitzner D, Wixler L, Schubert U, Ludwig S. The proapoptotic influenza A virus protein PB1-F2 regulates viral polymerase activity by interaction with the PB1 protein. Cell Microbiol. 2008;10:1140-52 pubmed publisher
    ..Thus, we have identified a novel function of PB1-F2 as an indirect regulator of the influenza virus polymerase activity via its interaction with PB1. ..
  17. Li Z, Watanabe T, Hatta M, Watanabe S, Nanbo A, Ozawa M, et al. Mutational analysis of conserved amino acids in the influenza A virus nucleoprotein. J Virol. 2009;83:4153-62 pubmed publisher
    ..The respective conserved amino acids in NP may thus be critical for the assembly and/or incorporation of sets of eight vRNA segments. ..
  18. Yamada S, Hatta M, Staker B, Watanabe S, Imai M, Shinya K, et al. Biological and structural characterization of a host-adapting amino acid in influenza virus. PLoS Pathog. 2010;6:e1001034 pubmed publisher
    ..These differences may affect the protein's interaction with viral and/or cellular factors, and hence its ability to support virus replication in mammals. ..
  19. Varga Z, Ramos I, Hai R, Schmolke M, Garcia Sastre A, Fernandez Sesma A, et al. The influenza virus protein PB1-F2 inhibits the induction of type I interferon at the level of the MAVS adaptor protein. PLoS Pathog. 2011;7:e1002067 pubmed publisher
    ..In summary, we have characterized the anti-interferon function of PB1-F2 and we suggest that this activity contributes to the enhanced pathogenicity seen with PB1-F2 N66S- expressing influenza viruses. ..
  20. Dudek S, Wixler L, Nordhoff C, Nordmann A, Anhlan D, Wixler V, et al. The influenza virus PB1-F2 protein has interferon antagonistic activity. Biol Chem. 2011;392:1135-44 pubmed publisher
    ..In summary, we demonstrate that the PB1-F2 protein of IAVs exhibits a type I IFN-antagonistic function by interfering with the RIG-I/MAVS complex, which contributes to an enhanced pathogenicity in vivo. ..
  21. Liu Q, Qiao C, Marjuki H, Bawa B, Ma J, Guillossou S, et al. Combination of PB2 271A and SR polymorphism at positions 590/591 is critical for viral replication and virulence of swine influenza virus in cultured cells and in vivo. J Virol. 2012;86:1233-7 pubmed publisher
    ..These results suggest that a combination of 271A with the 590/591 SR polymorphism is critical for pH1N1 and triple-reassortant SIVs for efficient replication and adaptation in mammals...
  22. Weeks Gorospe J, Hurtig H, Iverson A, Schuneman M, Webby R, McCullers J, et al. Naturally occurring swine influenza A virus PB1-F2 phenotypes that contribute to superinfection with Gram-positive respiratory pathogens. J Virol. 2012;86:9035-43 pubmed publisher
    ..These findings support efforts to increase influenza virus surveillance to consider viral genotypes that could be used to predict increased severity of superinfections with specific Gram-positive respiratory pathogens...
  23. Jagger B, Wise H, Kash J, Walters K, Wills N, Xiao Y, et al. An overlapping protein-coding region in influenza A virus segment 3 modulates the host response. Science. 2012;337:199-204 pubmed publisher
    ..Thus, we have identified a previously unknown IAV protein that modulates the host response to infection, a finding with important implications for understanding IAV pathogenesis. ..
  24. Shi M, Jagger B, Wise H, Digard P, Holmes E, Taubenberger J. Evolutionary conservation of the PA-X open reading frame in segment 3 of influenza A virus. J Virol. 2012;86:12411-3 pubmed publisher
    ..Notably, truncated forms of PA-X evolved convergently in swine and dogs, suggesting a strong species-specific effect. ..
  25. Zhu C, Peng G, Yi W, Song H, Liu F, Liu X. The Influenza A Virus Non-structural Protein NS1 Upregulates The Expression of Collagen Triple Helix Repeat Containing 1 Protein. Scand J Immunol. 2016;84:365-369 pubmed publisher
    ..The activation function had a dose-dependent effect, indicating that influenza virus upregulated CTHRC1 expression through its NS1 protein. ..
  26. Nogales A, Rodriguez L, DeDiego M, Topham D, Martínez Sobrido L. Interplay of PA-X and NS1 Proteins in Replication and Pathogenesis of a Temperature-Sensitive 2009 Pandemic H1N1 Influenza A Virus. J Virol. 2017;91: pubmed publisher
  27. Winter G, Fields S. Nucleotide sequence of human influenza A/PR/8/34 segment 2. Nucleic Acids Res. 1982;10:2135-43 pubmed
    ..The sequence of segment 2 completes the sequence of the virus (total 13,588 nucleotides). ..
  28. Ksenofontov A, Dobrov E, Fedorova N, Radiukhin V, Badun G, Arutiunian A, et al. [Disordered regions in C-domain structure of influenza virus M1 protein]. Mol Biol (Mosk). 2011;45:689-96 pubmed
    ..It is suggested, that influenza virus M1 polyfunctionality in infected cell is determined by its tertiary structure plasticity which in its turn results from the presence of unstructured regions. ..
  29. Wang C, Zhang Y, Wu B, Liu S, Xu P, Lu Y, et al. Evolutionary characterization of the pandemic H1N1/2009 influenza virus in humans based on non-structural genes. PLoS ONE. 2013;8:e56201 pubmed publisher
    ..The two genotypes of the virus presented distinctive clustering features in their geographic distributions. These results provide additional insight into the genetics and evolution of human pandemic influenza H1N1. ..
  30. Wang S, Zhao Z, Bi Y, Sun L, Liu X, Liu W. Tyrosine 132 phosphorylation of influenza A virus M1 protein is crucial for virus replication by controlling the nuclear import of M1. J Virol. 2013;87:6182-91 pubmed publisher
    ..The present study reveals a pivotal role of this tyrosine phosphorylation in the intracellular transportation of M1, which controls the process of viral replication. ..
  31. Kim J, Lee I, Park S, Hwang M, Bae J, Lee S, et al. Genetic requirement for hemagglutinin glycosylation and its implications for influenza A H1N1 virus evolution. J Virol. 2013;87:7539-49 pubmed publisher
  32. Song M, Hee Baek Y, Kim E, Park S, Kim S, Lim G, et al. Increased virulence of neuraminidase inhibitor-resistant pandemic H1N1 virus in mice: potential emergence of drug-resistant and virulent variants. Virulence. 2013;4:489-93 pubmed publisher
    ..Collectively, our findings highlight the potential emergence of A(H1N1)pdm09 drug-resistant variants with increased virulence and the need for rapid development of novel antiviral drugs. ..
  33. Suptawiwat O, Jeamtua W, Boonarkart C, Kongchanagul A, Puthawathana P, Auewarakul P. Effects of the Q223R mutation in the hemagglutinin (HA) of egg-adapted pandemic 2009 (H1N1) influenza A virus on virus growth and binding of HA to human- and avian-type cell receptors. Acta Virol. 2013;57:333-8 pubmed
  34. Beale R, Wise H, Stuart A, Ravenhill B, Digard P, Randow F. A LC3-interacting motif in the influenza A virus M2 protein is required to subvert autophagy and maintain virion stability. Cell Host Microbe. 2014;15:239-47 pubmed publisher
    ..IAV therefore subverts autophagy by mimicking a host short linear protein-protein interaction motif. This strategy may facilitate transmission of infection between organisms by enhancing the stability of viral progeny...
  35. Butler J, Hooper K, Petrie S, Lee R, Maurer Stroh S, Reh L, et al. Estimating the fitness advantage conferred by permissive neuraminidase mutations in recent oseltamivir-resistant A(H1N1)pdm09 influenza viruses. PLoS Pathog. 2014;10:e1004065 pubmed publisher
    ..Our findings suggest that recent A(H1N1)pdm09 viruses are now more permissive to the acquisition of H275Y than earlier A(H1N1)pdm09 viruses, increasing the risk that OR A(H1N1)pdm09 will emerge and spread worldwide...
  36. Mallajosyula V, Citron M, Ferrara F, Lu X, Callahan C, Heidecker G, et al. Influenza hemagglutinin stem-fragment immunogen elicits broadly neutralizing antibodies and confers heterologous protection. Proc Natl Acad Sci U S A. 2014;111:E2514-23 pubmed publisher
    ..Soluble, bacterial expression of such designed immunogens allows for rapid scale-up during pandemic outbreaks. ..
  37. Dong H, Fiorin G, Degrado W, Klein M. Proton release from the histidine-tetrad in the M2 channel of the influenza A virus. J Phys Chem B. 2014;118:12644-51 pubmed publisher
    ..Our calculations also suggest that the M2 protein would seem to exclude the entrance of anions into the central channel through a special mechanism, due to the latter's potential inhibitory effect on proton conduction. ..
  38. Nacken W, Wixler V, Ehrhardt C, Ludwig S. Influenza A virus NS1 protein-induced JNK activation and apoptosis are not functionally linked. Cell Microbiol. 2017;19: pubmed publisher
  39. Kawaguchi A, Momose F, Nagata K. Replication-coupled and host factor-mediated encapsidation of the influenza virus genome by viral nucleoprotein. J Virol. 2011;85:6197-204 pubmed
    ..These findings demonstrate that replication of the virus genome is followed by its encapsidation by NP in collaboration with its chaperone...
  40. Tu J, Guo J, Zhang A, Zhang W, Zhao Z, Zhou H, et al. Effects of the C-terminal truncation in NS1 protein of the 2009 pandemic H1N1 influenza virus on host gene expression. PLoS ONE. 2011;6:e26175 pubmed publisher
  41. Xu R, Zhu X, McBride R, Nycholat C, Yu W, Paulson J, et al. Functional balance of the hemagglutinin and neuraminidase activities accompanies the emergence of the 2009 H1N1 influenza pandemic. J Virol. 2012;86:9221-32 pubmed publisher
    ..Thus, a functional match between the hemagglutinin and neuraminidase appears to be necessary for efficient transmission between humans and may be an indicator of the pandemic potential of zoonotic viruses...
  42. El Moussi A, Ben Hadj Kacem M, Pozo F, Ledesma J, Cuevas M, Casas I, et al. Genetic diversity of HA1 domain of heammaglutinin gene of influenza A(H1N1)pdm09 in Tunisia. Virol J. 2013;10:150 pubmed publisher
    ..However it also reveals a trend of 2010 strains to accumulate amino acid variation and form new phylogenetic clade with three specific amino acid substitutions: V47I, E172K and K308E. ..
  43. Gao H, Sun H, Hu J, Qi L, Wang J, Xiong X, et al. Twenty amino acids at the C-terminus of PA-X are associated with increased influenza A virus replication and pathogenicity. J Gen Virol. 2015;96:2036-49 pubmed publisher
    ..Furthermore, aa 233-252 at the C terminus of PA-X strongly suppressed co-transfected gene expression by ∼ 50%, suggesting that these terminal 20 aa could play a role in enhancing viral replication and contribute to virulence. ..
  44. Nakada R, Hirano H, Matsuura Y. Structure of importin-α bound to a non-classical nuclear localization signal of the influenza A virus nucleoprotein. Sci Rep. 2015;5:15055 pubmed publisher
    ..These results suggest that a modest inhibitor with low affinity to importin-α could have anti-influenza activity with minimal cytotoxicity. ..
  45. Xia C, Wolf J, Vijayan M, Studstill C, Ma W, Hahm B. Casein Kinase 1? Mediates the Degradation of Receptors for Type I and Type II Interferons Caused by Hemagglutinin of Influenza A Virus. J Virol. 2018;92: pubmed publisher
    ..Thus, this study unveils a novel strategy employed by IAV to evade IFN-mediated antiviral activities. These findings may provide new insights into the interplay between IAV and host immunity to impact influenza virus pathogenicity. ..
  46. Winter G, Fields S. Cloning of influenza cDNA ino M13: the sequence of the RNA segment encoding the A/PR/8/34 matrix protein. Nucleic Acids Res. 1980;8:1965-74 pubmed
    ..In addition, there is a second long reading frame which partly overlaps the reading frame of the matrix protein...
  47. Cheung T, Guan Y, Ng S, Chen H, Wong C, Peiris J, et al. Generation of recombinant influenza A virus without M2 ion-channel protein by introduction of a point mutation at the 5' end of the viral intron. J Gen Virol. 2005;86:1447-54 pubmed publisher
    ..These results also indicated that the M2 ion-channel protein is critical, but not essential, for virus replication in cell culture. This approach may provide a new way of producing attenuated influenza A virus...
  48. Ludwig S, Wolff T. Influenza A virus TRIMs the type I interferon response. Cell Host Microbe. 2009;5:420-1 pubmed publisher
    ..For influenza viruses, a unique strategy has now been unraveled, as the viral nonstructural protein 1 was shown to inhibit activation of the pathogen recognition receptor RIG-I by binding the ubiquitin ligase TRIM25...
  49. Ma W, Liu Q, Bawa B, Qiao C, Qi W, Shen H, et al. The neuraminidase and matrix genes of the 2009 pandemic influenza H1N1 virus cooperate functionally to facilitate efficient replication and transmissibility in pigs. J Gen Virol. 2012;93:1261-8 pubmed publisher
    ..These results demonstrate that the right combination of NA and M genes is critical for the replication and transmissibility of influenza viruses in pigs...
  50. Watanabe T, Tisoncik Go J, Tchitchek N, Watanabe S, Benecke A, Katze M, et al. 1918 Influenza virus hemagglutinin (HA) and the viral RNA polymerase complex enhance viral pathogenicity, but only HA induces aberrant host responses in mice. J Virol. 2013;87:5239-54 pubmed publisher
  51. Martínez Romero C, de Vries E, Belicha Villanueva A, Mena I, Tscherne D, Gillespie V, et al. Substitutions T200A and E227A in the hemagglutinin of pandemic 2009 influenza A virus increase lethality but decrease transmission. J Virol. 2013;87:6507-11 pubmed publisher
  52. Han N, Mu Y. Locking the 150-cavity open: in silico design and verification of influenza neuraminidase inhibitors. PLoS ONE. 2013;8:e73344 pubmed publisher
    ..Our study provides a prospective way to design novel inhibitors for controlling the spread of influenza virus. ..
  53. Ai H, Zhang L, Chang A, Wei H, Che Y, Liu H. Virtual screening of potential inhibitors from TCM for the CPSF30 binding site on the NS1A protein of influenza A virus. J Mol Model. 2014;20:2142 pubmed publisher
    ..These two compounds could be modified to achieve higher binding affinity, so that they may be used as potential leads in the development of new anti-influenza drugs. ..
  54. Gooskens J, Zevenhoven Dobbe J, Claas E, Kroes A, Posthuma C. Mass spectrometry-based comparative sequence analysis for the genetic monitoring of influenza A(H1N1)pdm09 virus. PLoS ONE. 2014;9:e92970 pubmed publisher
    ..The low sensitivity for the detection of H275Y mutation in mixed viral populations suggests that MSCSA is not suitable for antiviral resistance monitoring in the clinical setting. ..
  55. Yamada H, Nagao C, Haredy A, Mori Y, Mizuguchi K, Yamanishi K, et al. Dextran sulfate-resistant A/Puerto Rico/8/34 influenza virus is associated with the emergence of specific mutations in the neuraminidase glycoprotein. Antiviral Res. 2014;111:69-77 pubmed publisher
    ..These results suggested that DS is an NA inhibitor with a different mechanism of action from the currently used NA inhibitors and that DS could be used in combination with these inhibitors to treat influenza virus infections. ..
  56. Gnirß K, Zmora P, Blazejewska P, Winkler M, Lins A, Nehlmeier I, et al. Tetherin Sensitivity of Influenza A Viruses Is Strain Specific: Role of Hemagglutinin and Neuraminidase. J Virol. 2015;89:9178-88 pubmed publisher
  57. Kuznetsova S, Isakova Sivak I, Kuznetcova V, Petukhova G, Losev I, Donina S, et al. [Effect of Point Mutations in the Polymerase Genes of the Influenza A/PR/8/34 (H1N1) Virus on the Immune Response in a Mouse Model]. Vopr Virusol. 2015;60:25-30 pubmed
    ..The ts-mutations in PB1, PB2, and PA genes are mostly involved in the modulation of the humoral immunity, but also have a moderate effect on the cellular adaptive immune response. ..
  58. Little K, Leang S, Butler J, Baas C, Harrower B, Mosse J, et al. Zanamivir-resistant influenza viruses with Q136K or Q136R neuraminidase residue mutations can arise during MDCK cell culture creating challenges for antiviral susceptibility monitoring. Euro Surveill. 2015;20: pubmed publisher
  59. Kathum O, Schräder T, Anhlan D, Nordhoff C, Liedmann S, Pande A, et al. Phosphorylation of influenza A virus NS1 protein at threonine 49 suppresses its interferon antagonistic activity. Cell Microbiol. 2016;18:784-91 pubmed publisher
    ..Because phosphorylation was shown to occur at later stages of infection, we hypothesize that at this stage other functions of the multifunctional NS1 beyond its interferon-antagonistic activity are needed. ..
  60. Bhowmick S, Chakravarty C, Sellathamby S, Lal S. The influenza A virus matrix protein 2 undergoes retrograde transport from the endoplasmic reticulum into the cytoplasm and bypasses cytoplasmic proteasomal degradation. Arch Virol. 2017;162:919-929 pubmed publisher
    ..The migration of M2 through this pathway inside the infected cell suggests possible new roles that the M2 protein may have in the host cytoplasm, apart from its previously described functions. ..
  61. Pereira C, Read E, Wise H, Amorim M, Digard P. Influenza A Virus NS1 Protein Promotes Efficient Nuclear Export of Unspliced Viral M1 mRNA. J Virol. 2017;91: pubmed publisher
  62. Kuzuhara T, Kise D, Yoshida H, Horita T, Murazaki Y, Utsunomiya H, et al. Crystallization and X-ray diffraction analysis of the RNA primer/promoter-binding domain of influenza A virus RNA-dependent RNA polymerase PB2. Acta Crystallogr Sect F Struct Biol Cryst Commun. 2009;65:144-6 pubmed publisher
    ..The SeMet-derivative crystals were found to belong to the same space group, with unit-cell parameters a = b = 52.6, c = 156.4 A. Attempts are being made to solve the structure by multi-wavelength anomalous dispersion phasing. ..
  63. Wang B, Dwyer D, Blyth C, Soedjono M, Shi H, Kesson A, et al. Detection of the rapid emergence of the H275Y mutation associated with oseltamivir resistance in severe pandemic influenza virus A/H1N1 09 infections. Antiviral Res. 2010;87:16-21 pubmed publisher
    ..In the light of emerging resistance, close monitoring and understanding of the nature and dynamics of resistance mutations in newly emerging strains should be a priority...
  64. Wang W, Castel n Vega J, Jim nez Alberto A, Vassell R, Ye Z, Weiss C. A mutation in the receptor binding site enhances infectivity of 2009 H1N1 influenza hemagglutinin pseudotypes without changing antigenicity. Virology. 2010;407:374-80 pubmed publisher
    ..None of these modifications affected neutralization. These findings provide information for increasing 2009 H1N1HA-pseudotype titers without altering antigenicity and offer insights into receptor use...
  65. Suppiah J, Yusof M, Othman K, Saraswathy T, Thayan R, Kasim F, et al. Monitoring of the h275y mutation in pandemic influenza A(H1N1) 2009 strains isolated in Malaysia. Southeast Asian J Trop Med Public Health. 2011;42:100-4 pubmed
    ..The sequencing analysis did not yield mutation at residue 275 for all 67 isolates indicating that our viral isolates belong to the wild type and do not confer resistance to oseltamivir. ..
  66. Tse H, Kao R, Wu W, Lim W, Chen H, Yeung M, et al. Structural basis and sequence co-evolution analysis of the hemagglutinin protein of pandemic influenza A/H1N1 (2009) virus. Exp Biol Med (Maywood). 2011;236:915-25 pubmed publisher
    ..Our findings provide a useful reference for follow-up studies in monitoring the ongoing evolution of the pandemic influenza A H1N1 (2009) virus...
  67. Trapp S, Soubieux D, Marty H, Esnault E, Hoffmann T, Chandenier M, et al. Shortening the unstructured, interdomain region of the non-structural protein NS1 of an avian H1N1 influenza virus increases its replication and pathogenicity in chickens. J Gen Virol. 2014;95:1233-43 pubmed publisher
  68. Cooper D, Banerjee S, Chakrabarti A, García Sastre A, Hesselberth J, Silverman R, et al. RNase L targets distinct sites in influenza A virus RNAs. J Virol. 2015;89:2764-76 pubmed publisher
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