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Early emergence of an H275Y mutation in a hematopoietic cell transplant recipient treated with intravenous peramivir
Author(s) -
Renaud C.,
Pergam S.A.,
Polyak C.,
Jain R.,
Kuypers J.,
Englund J.A.,
Corey L.,
Boeckh M.J.
Publication year - 2010
Publication title -
transplant infectious disease
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.69
H-Index - 67
eISSN - 1399-3062
pISSN - 1398-2273
DOI - 10.1111/j.1399-3062.2010.00582.x
Subject(s) - virology , medicine , oseltamivir , resistance mutation , population , neuraminidase , mutation , drug resistance , reverse transcriptase , virus , polymerase chain reaction , microbiology and biotechnology , biology , covid-19 , gene , genetics , disease , infectious disease (medical specialty) , environmental health
C. Renaud, S.A. Pergam, C. Polyak, R. Jain, J. Kuypers, J.A. Englund, L. Corey, M.J. Boeckh. Early emergence of an H275Y mutation in a hematopoietic cell transplant recipient treated with intravenous peramivir.
Transpl Infect Dis 2010: 12: 513–517. All rights reserved Abstract: Oseltamivir resistance in pandemic 2009 influenza A/H1N1 is caused by the neuraminidase mutation H275Y. This mutation has also been associated with in vitro resistance to peramivir, but few clinical cases have been described to date. Using allele‐specific real‐time reverse transcriptase polymerase chain reaction assay for the H275Y mutation, we were able to identify resistant H1N1 in a hematopoietic cell transplant recipient receiving intravenous peramivir therapy, and through serial testing we determined the molecular evolution of resistance. This case demonstrates that an H275Y mutant population can emerge early and replicate in vivo under peramivir antiviral pressure to become the major viral population.