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      Full-Genome Sequences of Influenza H3N2 Virus Strains Isolated from Finnish Patients during the 2012-2013 Epidemic Season

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          Abstract

          Here, we sequenced 10 influenza A(H3N2) virus genomes isolated from Finnish patients diagnosed with flu-like illness during the 2012-2013 influenza season. The alignment showed a high number of amino acid substitutions (238 in total) in only 10 samples, proving that a high mutation rate exists in seasonal influenza A viruses.

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          Detection of E119V and E119I mutations in influenza A (H3N2) viruses isolated from an immunocompromised patient: challenges in diagnosis of oseltamivir resistance.

          Margaret Okomo-Adhiambo, Gail J. Demmler-Harrison, Varough M Deyde … (2010)
          The clinical use of the neuraminidase inhibitor (NAI) oseltamivir is associated with the emergence of drug resistance resulting from subtype-specific neuraminidase (NA) mutations. The influenza A/Texas/12/2007 (H3N2) virus isolated from an oseltamivir-treated immunocompromised patient exhibited reduced susceptibility to oseltamivir in the chemiluminescent neuraminidase inhibition (NI) assay (approximately 60-fold increase in its 50% inhibitory concentration [IC(50)] compared to that for a control virus). When further propagated in cell culture, the isolate maintained reduced susceptibility to oseltamivir in both chemiluminescent and fluorescent NI assays (approximately 50- and 350-fold increases in IC(50), respectively). Sequencing analysis of the isolate revealed a mix of nucleotides coding for amino acids at position 119 of the NA [E119(V/I)]. Plaque purification of the isolate yielded E119V and E119I variants, both exhibiting reduced susceptibility to oseltamivir. The E119I variant also showed decreased susceptibility to zanamivir and the investigational NAIs peramivir and A-315675. The emergence of E119V variants in oseltamivir-treated patients has been previously reported; however, the E119I mutation detected here is a novel one which reduces susceptibility to several NAIs. Both mutations were not detected in unpropagated original clinical specimens using either conventional sequencing or pyrosequencing, suggesting that these variants were present in very low proportions (<10%) in clinical specimens and gained dominance after virus propagation in MDCK cells. All virus isolates recovered from the patient were resistant to adamantanes. Our findings highlight the potential for emergence and persistence of multidrug-resistant influenza viruses in oseltamivir-treated immunocompromised subjects and also highlight challenges for drug resistance diagnosis due to the genetic instability of the virus population upon propagation in cell culture.
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            A Single E627K Mutation in the PB2 Protein of H9N2 Avian Influenza Virus Increases Virulence by Inducing Higher Glucocorticoids (GCs) Level

            Jin Tian, Wenbao Qi, Xiaokang Li … (2012)
            While repeated infection of humans and enhanced replication and transmission in mice has attracted more attention to it, the pathogenesis of H9N2 virus was less known in mice. PB2 residue 627 as the virulent determinant of H5N1 virus is associated with systemic infection and impaired TCR activation, but the impact of this position in H9N2 virus on the host immune response has not been evaluated. In this study, we quantified the cellular immune response to infection in the mouse lung and demonstrate that VK627 and rTsE627K infection caused a significant reduction in the numbers of T cells and inflammatory cells (Macrophage, Neutrophils, Dendritic cells) compared to mice infected with rVK627E and TsE627. Further, we discovered (i) a high level of thymocyte apoptosis resulted in impaired T cell development, which led to the reduced amount of mature T cells into lung, and (ii) the reduced inflammatory cells entering into lung was attributed to the diminished levels in pro-inflammatory cytokines and chemokines. Thereafter, we recognized that higher GCs level in plasma induced by VK627 and rTsE627K infection was associated with the increased apoptosis in thymus and the reduced pro-inflammatory cytokines and chemokines levels in lung. These data demonstrated that VK627 and rTsE627K infection contributing to higher GCs level would decrease the magnitude of antiviral response in lung, which may be offered as a novel mechanism of enhanced pathogenicity for H9N2 AIV.
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              Full-Genome Sequences of Influenza A(H1N1)pdm09 Viruses Isolated from Finnish Patients from 2009 to 2013

              Triin Lakspere, Janne Tynell, Minttu Kaloinen … (2014)
              Here we report full-length sequencing of the first large set of influenza A(H1N1)pdm09 virus genomes isolated in Finland between the years 2009 and 2013 and discuss the advantages and needs of influenza virus sequencing efforts.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Genome Announc
                Journal ID (iso-abbrev): Genome Announc
                Journal ID (hwp): ga
                Journal ID (pmc): ga
                Journal ID (publisher-id): GA
                Title: Genome Announcements
                Publisher: American Society for Microbiology (1752 N St., N.W., Washington, DC )
                ISSN (Electronic): 2169-8287
                Publication date (Electronic): 27 March 2014
                Publication date Collection: Mar-Apr 2014
                Volume: 2
                Issue: 2
                Electronic Location Identifier: e00039-14
                Affiliations
                [a ]The Institute for Molecular Medicine Finland (FIMM), Helsinki, Finland
                [b ]Helsinki University Hospital Laboratory, HUSLAB, Helsinki, Finland
                [c ]Helsinki University Central Hospital, HUCS, Helsinki, Finland
                Author notes
                Address correspondence to Laura Kakkola, laura.kakkola@ 123456utu.fi .
                Article
                Publisher ID: genomeA00039-14
                DOI: 10.1128/genomeA.00039-14
                PMC ID: 3968323
                PubMed ID: 24675845
                SO-VID: 27117dfe-8afe-428e-8ed6-d8d4d028701b
                Copyright © Copyright © 2014 Lakspere et al.
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution 3.0 Unported license.

                History
                Date received : 16 January 2014
                Date accepted : 6 March 2014
                Page count
                Pages: 1
                Categories
                Subject: Viruses
                Custom metadata
                cover-date March/April 2014
                access-type free

                ScienceOpen disciplines: Genetics
                Data availability:
                ScienceOpen disciplines: Genetics

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