tetano
Editor, Senior Moderator
Infect Genet Evol. 2016 Jan 29. pii: S1567-1348(16)30022-3. doi: 10.1016/j.meegid.2016.01.022. [Epub ahead of print]
[h=1]Adaptation of influenza A(H1N1)pdm09 virus in experimental mouse models.[/h] Prokopyeva EA[SUP]1[/SUP], Sobolev IA[SUP]2[/SUP], Prokopyev MV[SUP]3[/SUP], Shestopalov AM[SUP]2[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] In the present study, three mouse-adapted variants of influenza A(H1N1)pdm09 virus were obtained by lung-to-lung passages of BALB/c, C57BL/6z and CD1 mice. The significantly increased virulence and pathogenicity of all of the mouse-adapted variants induced 100% mortality in the adapted mice. Genetic analysis indicated that the increased virulence of all of the mouse-adapted variants reflected the incremental acquisition of several mutations in PB2, PB1, HA, NP, NA, and NS2 proteins. Identical amino acid substitutions were also detected in all of the mouse-adapted variants of A(H1N1)pdm09 virus, including PB2 (K251R), PB1 (V652A), NP (I353V), NA (I106V, N248D) and NS1 (G159E). Apparently, influenza A(H1N1)pdm09 virus easily adapted to the host after serial passages in the lungs, inducing 100% lethality in the last experimental group. However, cross-challenge revealed that not all adapted variants are pathogenic for different laboratory mice. Such important results should be considered when using the influenza mice model.
Copyright ? 2015. Published by Elsevier B.V.
[h=4]KEYWORDS:[/h] BALB/c; C57BL/6z and CD1 mice; Influenza А(H1N1)pdm09 virus adaptation; Interstitial pneumonia; Lungs; Nonstructural protein PB1-F2; Protein mutation
PMID: 26829383 [PubMed - as supplied by publisher]
[h=1]Adaptation of influenza A(H1N1)pdm09 virus in experimental mouse models.[/h] Prokopyeva EA[SUP]1[/SUP], Sobolev IA[SUP]2[/SUP], Prokopyev MV[SUP]3[/SUP], Shestopalov AM[SUP]2[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] In the present study, three mouse-adapted variants of influenza A(H1N1)pdm09 virus were obtained by lung-to-lung passages of BALB/c, C57BL/6z and CD1 mice. The significantly increased virulence and pathogenicity of all of the mouse-adapted variants induced 100% mortality in the adapted mice. Genetic analysis indicated that the increased virulence of all of the mouse-adapted variants reflected the incremental acquisition of several mutations in PB2, PB1, HA, NP, NA, and NS2 proteins. Identical amino acid substitutions were also detected in all of the mouse-adapted variants of A(H1N1)pdm09 virus, including PB2 (K251R), PB1 (V652A), NP (I353V), NA (I106V, N248D) and NS1 (G159E). Apparently, influenza A(H1N1)pdm09 virus easily adapted to the host after serial passages in the lungs, inducing 100% lethality in the last experimental group. However, cross-challenge revealed that not all adapted variants are pathogenic for different laboratory mice. Such important results should be considered when using the influenza mice model.
Copyright ? 2015. Published by Elsevier B.V.
[h=4]KEYWORDS:[/h] BALB/c; C57BL/6z and CD1 mice; Influenza А(H1N1)pdm09 virus adaptation; Interstitial pneumonia; Lungs; Nonstructural protein PB1-F2; Protein mutation
PMID: 26829383 [PubMed - as supplied by publisher]