tetano
Editor, Senior Moderator
J Infect Dis. 2015 Jul 9. pii: jiv375. [Epub ahead of print]
[h=1]Outcomes and Susceptibility to Neuraminidase Inhibitors in Individuals Infected with Different Influenza B Lineages: the Influenza Resistance Information Study.[/h] van der Vries E[SUP]1[/SUP], Ip DK[SUP]2[/SUP], Cowling BJ[SUP]2[/SUP], Zhang JD[SUP]3[/SUP], Tong X[SUP]4[/SUP], Wojtowicz K[SUP]5[/SUP], Schutten M[SUP]1[/SUP], Boucher CA[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] [h=4]BACKGROUND:[/h] Little is known about how influenza infections caused by B/Victoria and B/Yamagata virus lineages compare with respect to disease course and susceptibility to antiviral therapy.
[h=4]METHODS:[/h] Data from patients with influenza B infections from the first 5 years (2009-13) of the prospective Influenza Resistance Information Study (IRIS, NCT00884117) were evaluated. Cultured viruses were phenotypically tested for neuraminidase inhibitor (NAI) sensitivity, and sequenced to determine virus lineage (B/Victoria or B/Yamagata). Differences in clinical outcomes (viral clearance and symptom resolution) between virus lineages were assessed using Kaplan-Meier analysis.
[h=4]RESULTS:[/h] In all, 914 patients were positive for influenza B by reverse transcriptase polymerase chain reaction (RT-PCR: B/Victoria, 586; B/Yamagata, 289; not subtyped, 39); 474 were treated with antivirals. No phenotypic resistance to oseltamivir or zanamivir was found in B/Victoria or B/Yamagata viruses. Of 15 predefined resistance mutations, 2 were detected by neuraminidase sequencing: I221T had reduced sensitivity to oseltamivir, and I221V was sensitive to NAI inhibition. No consistent differences between virus lineages in times to viral clearance or to symptom or fever resolution were found in adults and adolescents or in children.
[h=4]CONCLUSIONS:[/h] Influenza B virus lineage had no notable effect on disease outcomes or antiviral susceptibility in this population.
? The Author 2015. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.
PMID: 26160744 [PubMed - as supplied by publisher]
[h=1]Outcomes and Susceptibility to Neuraminidase Inhibitors in Individuals Infected with Different Influenza B Lineages: the Influenza Resistance Information Study.[/h] van der Vries E[SUP]1[/SUP], Ip DK[SUP]2[/SUP], Cowling BJ[SUP]2[/SUP], Zhang JD[SUP]3[/SUP], Tong X[SUP]4[/SUP], Wojtowicz K[SUP]5[/SUP], Schutten M[SUP]1[/SUP], Boucher CA[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] [h=4]BACKGROUND:[/h] Little is known about how influenza infections caused by B/Victoria and B/Yamagata virus lineages compare with respect to disease course and susceptibility to antiviral therapy.
[h=4]METHODS:[/h] Data from patients with influenza B infections from the first 5 years (2009-13) of the prospective Influenza Resistance Information Study (IRIS, NCT00884117) were evaluated. Cultured viruses were phenotypically tested for neuraminidase inhibitor (NAI) sensitivity, and sequenced to determine virus lineage (B/Victoria or B/Yamagata). Differences in clinical outcomes (viral clearance and symptom resolution) between virus lineages were assessed using Kaplan-Meier analysis.
[h=4]RESULTS:[/h] In all, 914 patients were positive for influenza B by reverse transcriptase polymerase chain reaction (RT-PCR: B/Victoria, 586; B/Yamagata, 289; not subtyped, 39); 474 were treated with antivirals. No phenotypic resistance to oseltamivir or zanamivir was found in B/Victoria or B/Yamagata viruses. Of 15 predefined resistance mutations, 2 were detected by neuraminidase sequencing: I221T had reduced sensitivity to oseltamivir, and I221V was sensitive to NAI inhibition. No consistent differences between virus lineages in times to viral clearance or to symptom or fever resolution were found in adults and adolescents or in children.
[h=4]CONCLUSIONS:[/h] Influenza B virus lineage had no notable effect on disease outcomes or antiviral susceptibility in this population.
? The Author 2015. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.
PMID: 26160744 [PubMed - as supplied by publisher]