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      Molecular findings from influenza A(H1N1)pdm09 detected in patients from a Brazilian equatorial region during the pandemic period

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          Abstract

          After the World Health Organization officially declared the end of the first pandemic of the XXI century in August 2010, the influenza A(H1N1)pdm09 virus has been disseminated in the human population. In spite of its sustained circulation, very little on phylogenetic data or oseltamivir (OST) resistance is available for the virus in equatorial regions of South America. In order to shed more light on this topic, we analysed the haemagglutinin (HA) and neuraminidase (NA) genes of influenza A(H1N1)pdm09 positive samples collected during the pandemic period in the Pernambuco (PE), a northeastern Brazilian state. Complete HA sequences were compared and amino acid changes were related to clinical outcome. In addition, the H275Y substitution in NA, associated with OST resistance, was investigated by pyrosequencing. Samples from PE were grouped in phylogenetic clades 6 and 7, being clustered together with sequences from South and Southeast Brazil. The D222N/G HA gene mutation, associated with severity, was found in one deceased patient that was pregnant. Additionally, the HA mutation K308E, which appeared in Brazil in 2010 and was only detected worldwide the following year, was identified in samples from hospitalised cases. The resistance marker H275Y was not identified in samples tested. However, broader studies are needed to establish the real frequency of resistance in this Brazilian region.

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          Functional balance between haemagglutinin and neuraminidase in influenza virus infections.

          Ralf Wagner, Mikhail Matrosovich, Hans-Dieter Klenk (2002)
          Influenza A and B viruses carry two surface glycoproteins, the haemagglutinin (HA) and the neuraminidase (NA). Both proteins have been found to recognise the same host cell molecule, sialic acid. HA binds to sialic acid-containing receptors on target cells to initiate virus infection, whereas NA cleaves sialic acids from cellular receptors and extracellular inhibitors to facilitate progeny virus release and to promote the spread of the infection to neighbouring cells. Numerous studies performed recently have revealed that an optimal interplay between these receptor-binding and receptor-destroying activities of the surface glycoproteins is required for efficient virus replication. An existing balance between the antagonistic HA and NA functions of individual viruses can be disturbed by various events, such as reassortment, virus transmission to a new host, or therapeutic inhibition of neuraminidase. The resulting decrease in the viral replicative fitness is usually overcome by restoration of the functional balance due to compensatory mutations in HA, NA or both proteins. Copyright 2002 John Wiley & Sons, Ltd.
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            Global transmission of oseltamivir-resistant influenza.

            Anne Moscona (2009)
            Article 0 comments Cited 163 times – based on 0 reviews     Review now
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              Infections with oseltamivir-resistant influenza A(H1N1) virus in the United States.

              Nila J. Dharan (2009)
              During the 2007-2008 influenza season, oseltamivir resistance among influenza A(H1N1) viruses increased significantly for the first time worldwide. Early surveillance data suggest that the prevalence of oseltamivir resistance among A(H1N1) viruses will most likely be higher during the 2008-2009 season. To describe patients infected with oseltamivir-resistant influenza A(H1N1) virus and to determine whether there were any differences between these patients and patients infected with oseltamivir-susceptible A(H1N1) virus in demographic or epidemiological characteristics, clinical symptoms, severity of illness, or clinical outcomes. Influenza A(H1N1) viruses that were identified and submitted to the Centers for Disease Control and Prevention by US public health laboratories between September 30, 2007, and May 17, 2008, and between September 28, 2008, and February 19, 2009, were tested as part of ongoing surveillance. Oseltamivir resistance was determined by neuraminidase inhibition assay and pyrosequencing analysis. Information was collected using a standardized case form from patients with oseltamivir-resistant A(H1N1) infections and a comparison group of patients with oseltamivir-susceptible A(H1N1) infections during 2007-2008. Demographic and epidemiological information as well as clinical information, including symptoms, severity of illness, and clinical outcomes. During the 2007-2008 season, influenza A(H1N1) accounted for an estimated 19% of circulating influenza viruses in the United States. Among 1155 influenza A(H1N1) viruses tested from 45 states, 142 (12.3%) from 24 states were resistant to oseltamivir. Data were available for 99 oseltamivir-resistant cases and 182 oseltamivir-susceptible cases from this period. Among resistant cases, median age was 19 years (range, 1 month to 62 years), 5 patients (5%) were hospitalized, and 4 patients (4%) died. None reported oseltamivir exposure before influenza diagnostic sample collection. No significant differences were found between cases of oseltamivir-resistant and oseltamivir-susceptible influenza in demographic characteristics, underlying medical illness, or clinical symptoms. Preliminary data from the 2008-2009 influenza season identified resistance to oseltamivir among 264 of 268 influenza A(H1N1) viruses (98.5%) tested. Oseltamivir-resistant A(H1N1) viruses circulated widely in the United States during the 2007-2008 influenza season, appeared to be unrelated to oseltamivir use, and appeared to cause illness similar to oseltamivir-susceptible A(H1N1) viruses. Circulation of oseltamivir-resistant A(H1N1) viruses will continue, with a higher prevalence of resistance, during the 2008-2009 season.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Mem Inst Oswaldo Cruz
                Journal ID (iso-abbrev): Mem. Inst. Oswaldo Cruz
                Title: Memórias do Instituto Oswaldo Cruz
                Publisher: Instituto Oswaldo Cruz, Ministério da Saúde
                ISSN (Print): 0074-0276
                ISSN (Electronic): 1678-8060
                Publication date (Print and electronic): November 2014
                Publication date (Print): November 2014
                Volume: 109
                Issue: 7
                Pages: 912-917
                Affiliations
                [1 ] Setor de Virologia, Laboratório Central de Saúde Pública de Pernambuco, Recife, PE, Brasil
                [2 ] Programa de Pós-Graduação em Medicina Tropical, Universidade Federal de Pernambuco, Recife, PE, Brasil
                [3 ] Laboratório de Vírus Respiratórios e do Sarampo, Instituto Oswaldo Cruz-Fiocruz, Rio de Janeiro, RJ, Brasil
                [4 ] Instituto Evandro Chagas, Belém, PA, Brasil
                Author notes
                [+ ] Corresponding author: fcm@ 123456ioc.fiocruz.br
                Article
                DOI: 10.1590/0074-0276140210
                PMC ID: 4296496
                PubMed ID: 25410995
                SO-VID: c81acb7e-4ebc-4f88-9e74-ba341a85ccc6
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 11 June 2014
                Date accepted : 8 September 2014
                Page count
                Figures: 1, Tables: 2, References: 36, Pages: 6
                Categories
                Subject: Articles

                Keywords: influenza a(h1n1)pdm09,haemagglutinin,oseltamivir resistance,pyrosequencing
                Data availability:
                Keywords: influenza a(h1n1)pdm09, haemagglutinin, oseltamivir resistance, pyrosequencing

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