Virological surveillance and antiviral resistance of human influenza virus in Argentina, 2005-2008

To describe the virological characteristics of the influenza strains circulating in Argentina in 2005-2008 and to assess the prevalence of antiviral resistance. On the basis of their geographical spread and prevalence, influenza A and B isolates grown in Madin-Darby canine kidney cells were selected...

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Veröffentlicht in:Revista panamericana de salud pública 2011-12, Vol.30 (6), p.634-640
Hauptverfasser: Pontoriero, Andrea, Baumeister, Elsa, Campos, Ana M, Savy, Vilma L
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Campos, Ana M
Savy, Vilma L
description To describe the virological characteristics of the influenza strains circulating in Argentina in 2005-2008 and to assess the prevalence of antiviral resistance. On the basis of their geographical spread and prevalence, influenza A and B isolates grown in Madin-Darby canine kidney cells were selected after antigenic and genomic characterization to be analyzed for antiviral resistance by enzymatic assay and pyrosequencing. Amantadine susceptibility was evaluated by pyrosequencing for known resistance markers on 45 strains of influenza A. Susceptibility to oseltamivir and zanamivir was evaluated by enzymatic assay of 67 influenza A and 46 influenza B strains, some of which were further analyzed by sequencing the neuraminidase gene. Resistance to amantadine was observed only on A(H3N2) strains (29/33); all of them carried the mutation S31N in their M2 sequence. Oseltamivir resistance was observed in 12 (34.3%) of the 35 A(H1N1) strains from 2008; all of them carried the mutation H275Y in their neuraminidase sequence. All these viruses remained sensitive to zanamivir. This study describes a high incidence of amantadine-resistant influenza A(H3N2) viruses since 2006 and an unprecedented increase in oseltamivir resistance detected only in influenza A(H1N1) viruses isolated in 2008. Influenza A and B viruses were more sensitive to oseltamivir than to zanamivir, and influenza A viruses were more sensitive to both neuraminidase inhibitors than the influenza B viruses. The national data generated and analyzed in this study may help increase knowledge about influenza antiviral drug resistance, which is a problem of global concern.
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On the basis of their geographical spread and prevalence, influenza A and B isolates grown in Madin-Darby canine kidney cells were selected after antigenic and genomic characterization to be analyzed for antiviral resistance by enzymatic assay and pyrosequencing. Amantadine susceptibility was evaluated by pyrosequencing for known resistance markers on 45 strains of influenza A. Susceptibility to oseltamivir and zanamivir was evaluated by enzymatic assay of 67 influenza A and 46 influenza B strains, some of which were further analyzed by sequencing the neuraminidase gene. Resistance to amantadine was observed only on A(H3N2) strains (29/33); all of them carried the mutation S31N in their M2 sequence. Oseltamivir resistance was observed in 12 (34.3%) of the 35 A(H1N1) strains from 2008; all of them carried the mutation H275Y in their neuraminidase sequence. All these viruses remained sensitive to zanamivir. This study describes a high incidence of amantadine-resistant influenza A(H3N2) viruses since 2006 and an unprecedented increase in oseltamivir resistance detected only in influenza A(H1N1) viruses isolated in 2008. Influenza A and B viruses were more sensitive to oseltamivir than to zanamivir, and influenza A viruses were more sensitive to both neuraminidase inhibitors than the influenza B viruses. 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On the basis of their geographical spread and prevalence, influenza A and B isolates grown in Madin-Darby canine kidney cells were selected after antigenic and genomic characterization to be analyzed for antiviral resistance by enzymatic assay and pyrosequencing. Amantadine susceptibility was evaluated by pyrosequencing for known resistance markers on 45 strains of influenza A. Susceptibility to oseltamivir and zanamivir was evaluated by enzymatic assay of 67 influenza A and 46 influenza B strains, some of which were further analyzed by sequencing the neuraminidase gene. Resistance to amantadine was observed only on A(H3N2) strains (29/33); all of them carried the mutation S31N in their M2 sequence. Oseltamivir resistance was observed in 12 (34.3%) of the 35 A(H1N1) strains from 2008; all of them carried the mutation H275Y in their neuraminidase sequence. All these viruses remained sensitive to zanamivir. This study describes a high incidence of amantadine-resistant influenza A(H3N2) viruses since 2006 and an unprecedented increase in oseltamivir resistance detected only in influenza A(H1N1) viruses isolated in 2008. Influenza A and B viruses were more sensitive to oseltamivir than to zanamivir, and influenza A viruses were more sensitive to both neuraminidase inhibitors than the influenza B viruses. 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purification</subject><subject>Influenza, Human - epidemiology</subject><subject>Influenza, Human - virology</subject><subject>Medical research</subject><subject>Medical treatment</subject><subject>Morbidity - trends</subject><subject>Mutation, Missense</subject><subject>Neuraminidase - antagonists &amp; inhibitors</subject><subject>Neuraminidase - genetics</subject><subject>Oseltamivir - pharmacology</subject><subject>Point Mutation</subject><subject>Population Surveillance</subject><subject>Public health</subject><subject>Resistance</subject><subject>Seasons</subject><subject>Virus Cultivation</subject><subject>Zanamivir - pharmacology</subject><issn>1020-4989</issn><issn>1680-5348</issn><issn>1680-5348</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kctOwzAQRS0EoqXwC5AdLEgZx05qL6uKl1SJBY9t5CZ2cZXExU4qwdczfbFB6sL2WHPuzPiakCsKQ5pKuHulkEDMpZAJUApAEwBI2BHp00xAnDIujjHeQz1yFsICCZoxekp6ScJSwWnaJ7MP613l5rZQVRQ6v9K2qlRT6Eg1Ja7WrqzHlNfBhnaTcCb67GrVRLYxVaebHxUh0wW8R2M_16hp1G2EE6UxbuKcnBhVBX2xOwfk_eH-bfIUT18enyfjaVxwxtpYC2okCKPMjBUcmAFFtZKCSwzLtKRcMEhkhjCnwHg24rwsmU6gFKCpYAMy3NYNhdWVyxeu8w02zDdm5f_MQsH1VrD07qvToc1rGwq9fr92XcglujRCJ9elbw6SOI-QgNZniI62aOFdCF6bfOltrfw3Qvn67w6Mc7lr0s1qXf7p9p_FfgG1QI97</recordid><startdate>201112</startdate><enddate>201112</enddate><creator>Pontoriero, Andrea</creator><creator>Baumeister, Elsa</creator><creator>Campos, Ana M</creator><creator>Savy, Vilma L</creator><general>Organización Panamericana de la Salud</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>8BJ</scope><scope>FQK</scope><scope>JBE</scope><scope>7X8</scope><scope>GPN</scope></search><sort><creationdate>201112</creationdate><title>Virological surveillance and antiviral resistance of human influenza virus in Argentina, 2005-2008</title><author>Pontoriero, Andrea ; 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On the basis of their geographical spread and prevalence, influenza A and B isolates grown in Madin-Darby canine kidney cells were selected after antigenic and genomic characterization to be analyzed for antiviral resistance by enzymatic assay and pyrosequencing. Amantadine susceptibility was evaluated by pyrosequencing for known resistance markers on 45 strains of influenza A. Susceptibility to oseltamivir and zanamivir was evaluated by enzymatic assay of 67 influenza A and 46 influenza B strains, some of which were further analyzed by sequencing the neuraminidase gene. Resistance to amantadine was observed only on A(H3N2) strains (29/33); all of them carried the mutation S31N in their M2 sequence. Oseltamivir resistance was observed in 12 (34.3%) of the 35 A(H1N1) strains from 2008; all of them carried the mutation H275Y in their neuraminidase sequence. All these viruses remained sensitive to zanamivir. This study describes a high incidence of amantadine-resistant influenza A(H3N2) viruses since 2006 and an unprecedented increase in oseltamivir resistance detected only in influenza A(H1N1) viruses isolated in 2008. Influenza A and B viruses were more sensitive to oseltamivir than to zanamivir, and influenza A viruses were more sensitive to both neuraminidase inhibitors than the influenza B viruses. The national data generated and analyzed in this study may help increase knowledge about influenza antiviral drug resistance, which is a problem of global concern.</abstract><cop>United States</cop><pub>Organización Panamericana de la Salud</pub><pmid>22358415</pmid><doi>10.1590/S1020-49892011001200023</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record>
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subjects Amantadine - pharmacology
Animals
Antiviral Agents - pharmacology
Argentina
Argentina - epidemiology
Cell Line
Data analysis
Dogs
Drug Resistance, Multiple, Viral - genetics
Drug Resistance, Viral
Drug use
Epidemiology
Health Policy & Services
Hospitals
Humans
Influenza A virus - drug effects
Influenza A virus - genetics
Influenza A virus - isolation & purification
Influenza A Virus, H1N1 Subtype - drug effects
Influenza A Virus, H1N1 Subtype - genetics
Influenza B virus - drug effects
Influenza B virus - genetics
Influenza B virus - isolation & purification
Influenza, Human - epidemiology
Influenza, Human - virology
Medical research
Medical treatment
Morbidity - trends
Mutation, Missense
Neuraminidase - antagonists & inhibitors
Neuraminidase - genetics
Oseltamivir - pharmacology
Point Mutation
Population Surveillance
Public health
Resistance
Seasons
Virus Cultivation
Zanamivir - pharmacology
title Virological surveillance and antiviral resistance of human influenza virus in Argentina, 2005-2008
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