Amantadine susceptibility in influenza A virus isolates: determination methods and lack of resistance in a Canadian sample, 1991–1994

Prud'homme, Isabelle; Zoueva, Olga; Weber, J

doi:10.1016/s0928-0197(97)00011-1

Cited by 26 publications

(12 citation statements)

References 16 publications

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“…The reaction products were sequenced using an automatic sequencer (ALF DNA Sequencer: Pharmacia Biotech). The presence of amantadine-resistant viruses with changes at amino acids 26, 27, 30, or 31 of the M2 protein was investigated by comparing the corresponding codons on the reverse complement of the sequence obtained for the sequence of known sensitive and resistant isolates (19).…”

Section: Methodsmentioning

confidence: 99%

Incidence of Amantadine‐Resistant Influenza A Viruses in Sentinel Surveillance Sites and Nursing Homes in Niigata, Japan

Masuda

Sano

Oshitani

et al. 2000

Microbiology and Immunology

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Section: Methodsmentioning

confidence: 99%

Incidence of Amantadine‐Resistant Influenza A Viruses in Sentinel Surveillance Sites and Nursing Homes in Niigata, Japan

Masuda

Sano

Oshitani

et al. 2000

Microbiology and Immunology

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“…4,5,16,17,19 A thorough literature search and our previous reports indicated that 70% to 80% of substitutions in resistant viruses occur at position 31, around 10% each at positions 27 and 30, and 1% to 2% at position 26, in vitro and in clinical samples. 4,5,11,12,[17][18][19][20][21][22] (Table 2).…”

Section: Screening Of Resistant Virusesmentioning

confidence: 99%

Emergence of amantadine-resistant influenza A viruses: epidemiological study

Sano

Saito

Masuda

et al. 2003

Journal of Infection and Chemotherapy

173

137

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“…5,[8][9][10] Despite rapid emergence of drug-resistant mutants following treatment with adamantanes and the ability of drug-resistant mutants to transmit, 11 the incidence of adamantane resistance among viruses circulating in communities had been low (<1%) for decades. [12][13][14][15][16] At CDC, representative community isolates collected in various geographic regions during a given influenza season are tested for antiviral resistance. A dramatic rise in the frequency of adamantane resistance associated with an S31N mutation in the M2 protein was first reported for influenza A(H3N2) viruses circulating in Asia in 2000 17 which was followed by the spread of resistant A(H3N2) viruses to different parts of the world in subsequent seasons.…”

Section: Introductionmentioning

confidence: 99%

Genomic events underlying the changes in adamantane resistance among influenza A(H3N2) viruses during 2006–2008

Deyde¹,

Garten²,

Sheu

et al. 2009

Influenza Resp Viruses

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Background Adamantanes resistance in H3N2 viruses has been increasing since 2000, and in 2005–2006 reached nearly 100% in most countries, with the circulation of the N‐lineage. In 2006–2007, however, a significant decrease in resistance was observed in many regions. Objectives To explore potential links between adamantane resistance and the A(H3N2) viruses that circulated between 2006 and 2008. Methods A total of 1451 Influenza A (H3N2) viruses collected globally in 2001–2008 were screened for the presence of adamantane resistance markers. A subset of 100 viruses representing the broad genetic and geographic spectrum of these viruses was selected for complete genome sequencing and phylogenetic analyses. Results Full genome sequence analysis of 2006–2007 viruses revealed co‐circulation of four distinct genotypes, designated A–D. Phylogenetic analyses demonstrated reassortment between viruses from the N‐lineage and other viruses that had circulated in prior seasons, including those bearing an adamantane sensitive marker. Genotype D viruses became dominant in late 2006–2007 and continued to be the main H3N2 genotype in 2007–2008. Viruses of this genotype retained all N‐lineage genome segments except PB2 and NP, which were acquired through reassortment. Conclusions The decrease in adamantane resistance at that time was due to transient co‐circulation of genotypes that emerged through reassortment. Our findings emphasize the importance of complete genome sequencing in understanding the complex nature of the relationship between influenza virus evolution and antiviral resistance. The recent emergence of the pandemic multi‐reassortant H1N1 virus underscores the importance of whole genome sequence monitoring for rapid detection of such unusual and novel strains.

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Amantadine susceptibility in influenza A virus isolates: determination methods and lack of resistance in a Canadian sample, 1991–1994

Cited by 26 publications

References 16 publications

Incidence of Amantadine‐Resistant Influenza A Viruses in Sentinel Surveillance Sites and Nursing Homes in Niigata, Japan

Incidence of Amantadine‐Resistant Influenza A Viruses in Sentinel Surveillance Sites and Nursing Homes in Niigata, Japan

Emergence of amantadine-resistant influenza A viruses: epidemiological study

Genomic events underlying the changes in adamantane resistance among influenza A(H3N2) viruses during 2006–2008

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