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George_Herbert_Mead's.../Present-Past-and-Future... Cachedby CGH Mead’s - ‎Cited by 117 - ‎Related articles George Herbert Mead, the American pragmatist philosopher and. Clinical Issues Influenza epidemiology—past, present, and future Philippe R. Lagace´-Wiens, MD, DTM&H, FRCPC; Ethan Rubinstein, MD, LLB; Abba Gumel, Ph D In April 2009, Mexican, American, and Canadian authorities announced that a novel influenza virus with pandemic potential had been identified in large segments of the psychof content distribution, such as file sharing, real-time appli- cations and media streaming; ... Within weeks, it became apparent that the world was dealing with the first influenza pandemic in 40 yrs.Other genes, including nucleoprotein, M1 (matrix), M2 (ion pore), NS1, NS2, PA, PB1, PB1-F2, and PB2, encode for proteins critical for structure, reproduction, and virulence, and may also be used as diagnostic targets by polymerase chain reaction or antigen detection (e.g., M1 or nucleoprotein) and may be studied to predict virulence in certain nonhuman hosts (2– 4).HA and NA genes encode surface proteins that are involved in attachment to and budding of the virus from host cells.Antigenic shift, which may result in pandemic spread because of lack of partial immunity within the population, occurs when a sufficiently antigenically distinct HA (with or without a new NA) emerges (1, 6).Antigenic shift may occur either as a result of a reassortment event between human-adapted influenza and animal-adapted strains within a coinfected host, resulting in a progeny virus capable of sustained human transmission, or if a new human-adapted HA arises when an animal or avian influenza A virus is transmitted without reassortment from an animal reservoir to humans (1, 3, 4).

Influenza: Virology, Antigenic Evolution, and Ecology Influenza viruses are members of the orthomyxovirus viruses that encode a segmented RNA genome.lubricants and fuels, and labour in the form of slavery on a vast new scales, The ru-. It appeared first in Mexico and quickly, over the course of 3 months, was reported from practically all countries, regardless of the season.As of October 11, 2009, which was the end of the first wave of this epidemic and the beginning of the second wave, close to 400,000 laboratory-identified H1N1 influenza cases and ⬎4735 deaths had From Department of Medical Microbiology and Infectious Diseases (PRSL-W), Faculty of Medicine, University of Manitoba and Clinical Microbiology Department, Saint-Boniface General Hospital, Diagnostic Services of Manitoba, Manitoba, Canada; Department of Medical Microbiology (ER), Internal Medicine and the Section of Infectious Diseases, Faculty of Medicine, University of Manitoba and Section of Infectious Diseases, Department of Internal Medicine, Health Sciences Centre, Manitoba, Canada; Institute of Industrial Mathematical Sciences (AG), Faculty of Science, University of Manitoba, Manitoba, Canada. Rubinstein holds stock options and has consulted for Biond Vax Pharmaceuticals, and he received honoraria from Merck.On the other hand, influenza A is responsible for most seasonal influenza and all known pandemics (2). Influenza A virus contains an RNA genome comprising eight RNA segments encoding 11 genes.

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Of these, the hemagglutinin (HA), which binds to the cellular receptor sialic acid, and neuraminidase (NA), which cleaves sialic acid residues from budding viruses, are of particular importance to the epidemiology of influenza (1–3).The human specificity is largely attributable to the receptor specificity of hemagglutinin to target structures of sialic acid present in human cells (1).Both these surface proteins undergo significant variation over the course of their replication and during repeated epidemics as a result of influenza’s errorprone RNA polymerase (1, 3, 5–7).Over the course of epidemics, insertions, deletions, and changes in the sequence of these genes result in polymorphisms of NA and HA structures, although they are of insufficient magnitude to change their antigenic nomenclature; these polymorphisms are termed antigenic drift (1, 3, 7).

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