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      Guidance for practitioners on the use of antiviral drugs to control influenza outbreaks in long-term care facilities in Canada, 2014–2015 season

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          Abstract

          The AMMI Canada Guidelines document ‘The use of antiviral drugs for influenza: A foundation document for practitioners’, published in the Autumn 2013 issue of the Journal, outlines the recommendations for the use of antiviral drugs to treat influenza. This article, which represents the first of two updates to these guidelines published in the current issue of the Journal, aims to inform health care professionals of the increased risk for influenza in long-term care facilities due to a documented mismatch between the components chosen for this season’s vaccine and currently circulating influenza strains. Adjusted recommendations for the use of antiviral drugs for influenza in long-term care facilities for this season are provided.

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          Most cited references17

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          Low 2012–13 Influenza Vaccine Effectiveness Associated with Mutation in the Egg-Adapted H3N2 Vaccine Strain Not Antigenic Drift in Circulating Viruses

          Background Influenza vaccine effectiveness (VE) is generally interpreted in the context of vaccine match/mismatch to circulating strains with evolutionary drift in the latter invoked to explain reduced protection. During the 2012–13 season, however, detailed genotypic and phenotypic characterization shows that low VE was instead related to mutations in the egg-adapted H3N2 vaccine strain rather than antigenic drift in circulating viruses. Methods/Findings Component-specific VE against medically-attended, PCR-confirmed influenza was estimated in Canada by test-negative case-control design. Influenza A viruses were characterized genotypically by amino acid (AA) sequencing of established haemagglutinin (HA) antigenic sites and phenotypically through haemagglutination inhibition (HI) assay. H3N2 viruses were characterized in relation to the WHO-recommended, cell-passaged vaccine prototype (A/Victoria/361/2011) as well as the egg-adapted strain as per actually used in vaccine production. Among the total of 1501 participants, influenza virus was detected in 652 (43%). Nearly two-thirds of viruses typed/subtyped were A(H3N2) (394/626; 63%); the remainder were A(H1N1)pdm09 (79/626; 13%), B/Yamagata (98/626; 16%) or B/Victoria (54/626; 9%). Suboptimal VE of 50% (95%CI: 33–63%) overall was driven by predominant H3N2 activity for which VE was 41% (95%CI: 17–59%). All H3N2 field isolates were HI-characterized as well-matched to the WHO-recommended A/Victoria/361/2011 prototype whereas all but one were antigenically distinct from the egg-adapted strain as per actually used in vaccine production. The egg-adapted strain was itself antigenically distinct from the WHO-recommended prototype, and bore three AA mutations at antigenic sites B [H156Q, G186V] and D [S219Y]. Conversely, circulating viruses were identical to the WHO-recommended prototype at these positions with other genetic variation that did not affect antigenicity. VE was 59% (95%CI:16–80%) against A(H1N1)pdm09, 67% (95%CI: 30–85%) against B/Yamagata (vaccine-lineage) and 75% (95%CI: 29–91%) against B/Victoria (non-vaccine-lineage) viruses. Conclusions These findings underscore the need to monitor vaccine viruses as well as circulating strains to explain vaccine performance. Evolutionary drift in circulating viruses cannot be regulated, but influential mutations introduced as part of egg-based vaccine production may be amenable to improvements.
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            Influenza vaccine effectiveness in the community and the household.

            There is a recognized need to determine influenza vaccine effectiveness on an annual basis and a long history of studying respiratory illnesses in households. We recruited 328 households with 1441 members, including 839 children, and followed them during the 2010-2011 influenza season. Specimens were collected from subjects with reported acute respiratory illnesses and tested by real-time reverse transcriptase polymerase chain reaction. Receipt of influenza vaccine was defined based on documented evidence of vaccination in medical records or an immunization registry. The effectiveness of 2010-2011 influenza vaccination in preventing laboratory-confirmed influenza was estimated using Cox proportional hazards models adjusted for age and presence of high-risk condition, and stratified by prior season (2009-2010) vaccination status. Influenza was identified in 78 (24%) households and 125 (9%) individuals; the infection risk was 8.5% in the vaccinated and 8.9% in the unvaccinated (P = .83). Adjusted vaccine effectiveness in preventing community-acquired influenza was 31% (95% confidence interval [CI], -7% to 55%). In vaccinated subjects with no evidence of prior season vaccination, significant protection (62% [95% CI, 17%-82%]) against community-acquired influenza was demonstrated. Substantially lower effectiveness was noted among subjects who were vaccinated in both the current and prior season. There was no evidence that vaccination prevented household transmission once influenza was introduced; adults were at particular risk despite vaccination. Vaccine effectiveness estimates were lower than those demonstrated in other observational studies carried out during the same season. The unexpected findings of lower effectiveness with repeated vaccination and no protection given household exposure require further study.
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              Differential neutralization efficiency of hemagglutinin epitopes, antibody interference, and the design of influenza vaccines.

              It is generally assumed that amino acid mutations in the surface protein, hemagglutinin (HA), of influenza viruses allow these viruses to circumvent neutralization by antibodies induced during infection. However, empirical data on circulating influenza viruses show that certain amino acid changes to HA actually increase the efficiency of neutralization of the mutated virus by antibodies raised against the parent virus. Here, we suggest that this surprising increase in neutralization efficiency after HA mutation could reflect steric interference between antibodies. Specifically, if there is a steric competition for binding to HA by antibodies with different neutralization efficiencies, then a mutation that reduces the binding of antibodies with low neutralization efficiencies could increase overall viral neutralization. We use a mathematical model of virus-antibody interaction to elucidate the conditions under which amino acid mutations to HA could lead to an increase in viral neutralization. Using insights gained from the model, together with genetic and structural data, we predict that amino acid mutations to epitopes C and E of the HA of influenza A/H3N2 viruses could lead on average to an increase in the neutralization of the mutated viruses. We present data supporting this prediction and discuss the implications for the design of more effective vaccines against influenza viruses and other pathogens.
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                Author and article information

                Journal
                Can J Infect Dis Med Microbiol
                Can J Infect Dis Med Microbiol
                PGI
                The Canadian Journal of Infectious Diseases & Medical Microbiology
                Pulsus Group Inc
                1712-9532
                1918-1493
                Jan-Feb 2015
                : 26
                : 1
                : e1-e4
                Affiliations
                [1 ]Professor of Medicine, Medical Microbiology and Pharmacology & Therapeutics, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba;
                [2 ]Professor, Department of Pediatrics & Institute of Health Policy, Management and Evaluation; Senior Associate Scientist, Research Institute; Chief, Division of Infectious Diseases, Department of Pediatrics, Hospital for Sick Children, University of Toronto, Toronto, Ontario;
                [3 ]Professor Emeritus of Medicine, Division of Infectious Diseases, Department of Medicine, University of British Columbia, Vancouver, British Columbia;
                [4 ]Department of Microbiology-Infectious Disease, Hopital Maisonneuve-Rosemont, Montreal, Quebec;
                [5 ]Epidemiology Lead, Influenza & Emerging Respiratory Pathogens, BC Centre for Disease Control, Vancouver, British Columbia;
                [6 ]Professor of Medicine, Biomedical & Molecular Sciences and Pathology & Molecular Medicine; Chair, Division of Infectious Diseases, Department of Medicine, Kingston General Hospital, Queen’s University, Kingston, Ontario
                Author notes
                Correspondence: Dr Fred Y Aoki, 510-745 Bannatyne Avenue, Winnipeg, Manitoba R3E 0J9. E-mail fred.aoki@ 123456umanitoba.ca
                Article
                idmm-26-e1
                10.1155/2015/613068
                4353273
                25798158
                e374496f-9d4a-4e02-8a09-fc912e3cd103
                Copyright© 2015 Pulsus Group Inc. All rights reserved

                This open-access article is distributed under the terms of the Creative Commons Attribution Non-Commercial License (CC BY-NC) ( http://creativecommons.org/licenses/by-nc/4.0/), which permits reuse, distribution and reproduction of the article, provided that the original work is properly cited and the reuse is restricted to noncommercial purposes. For commercial reuse, contact support@ 123456pulsus.com

                History
                Categories
                AMMI Canada Guidelines

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