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Influenza A virus causes influenza in birds and some mammals, and is the only species of the genus Alphainfluenzavirus of the virus family Orthomyxoviridae.[1]Occasionally, viruses are transmitted from wild aquatic birds to domestic poultry, and this may cause an outbreak or give rise to human influenza pandemics.[2][3]The influenza A virus subtypes that have been confirmed in humans, are H1N1 which caused the Spanish flu in 1918 and the 2009 swine flu pandemic.[4]


The virus particle is 80 to 120 nanometers in diameter such that the smallest virions adopt an elliptical shape.[5][6] The length of each particle varies considerably, owing to the fact that influenza is pleomorphic, and can be in excess of many tens of micrometers, producing filamentous virions.[7]


The genome is made up of the following segments-PB2, PB1, PA, HA, NP, NA ,M and finally segment 8 encodes two distinct non-structural proteins (NS1 and NEP) by using different reading frames from the same RNA segment.[8][9]


Typically influenza is transmitted from infected birds through their droppings. Out of a host, flu viruses can remain infectious for about one week at human body temperature, over 30 days at 0 degrees celsius, and indefinitely at very low temperatures.[10][11][12]


The viruses bind to a cell through interactions between its hemagglutinin glycoprotein and sialic acid sugars on the surfaces of epithelial cells in the lung and throat.[13] The cell imports the virus by endocytosis. In the acidic endosome, part of the hemagglutinin protein fuses the viral envelope with the vacuole's membrane, releasing the viral RNA molecules, accessory proteins and RNA-dependent RNA polymerase into the cytoplasm .[14]

Multiplicity reactivation

Influenza virus is able to undergo multiplicity reactivation after inactivation by UV radiation, or by ionizing radiation. When two or more damaged viruses infect the same cell, viable progeny viruses can be produced provided each of the eight genomic segments is present in at least one undamaged copy.[15][16][17][18]


Some of the influenza A virus subtypes that have been confirmed in humans are the following: H1N1 (Spanish flu) 1917[19], H1N1 (Swine flu) 2009[20], H2N2 (Asian flu) 1957[21], H3N2 (Hong Kong flu) 1968[22], H5N1 2006[23], H7N9[24], H7N7[25][26] and H1N2[27].


H1N1 was responsible for the 2009 pandemic in both human and pig populations. A variant of H1N1 was responsible for the Spanish flu pandemic, that killed some 50 million to 100 million people worldwide over about a year in 1918 and 1919.[28]


H3N2 is endemic in both human and pig populations. It evolved from H2N2 by antigenic shift and caused the Hong Kong flu pandemic of 1968, and 1969, that killed up to three quarters of a million people.[29] A severe form of the H3N2 virus killed several children in the United States in late 2003.[30]


Globally the toll of influenza virus is estimated at two hundred ninety thousand to six hundred forty five thousand deaths annually.[31]The annually updated, trivalent influenza vaccine consists of hemagglutinin (HA) surface glycoprotein components from influenza H3N2, H1N1, and B influenza viruses.[32]


All influenza A pandemics since the Spanish flu pandemic, and indeed almost all cases of influenza A worldwide excepting human infections from avian viruses such as H5N1 and H7N7, have been caused by descendants of the 1918 virus, including drifted H1N1 viruses and reassorted H2N2 and H3N2 viruses.[33]


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  8. Eisfeld, Amie J.; Neumann, Gabriele; Kawaoka, Yoshihiro (January 2015). "At the centre: influenza A virus ribonucleoproteins". Nature Reviews Microbiology. 13 (1): 28–41. doi:10.1038/nrmicro3367. PMID 25417656. Retrieved 2 May 2022.
  9. Dadonaite, B; Gilbertson, B; Knight, ML; Trifkovic, S; Rockman, S; Laederach, A; Brown, LE; Fodor, E; Bauer, DLV (November 2019). "The structure of the influenza A virus genome". Nature microbiology. 4 (11): 1781–1789. doi:10.1038/s41564-019-0513-7. PMID 31332385. Retrieved 2 May 2022.
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  16. Henle W, Liu OC (October 1951). "Studies on host-virus interactions in the chick embryo-influenza virus system. VI. Evidence for multiplicity reactivation of inactivated virus". The Journal of Experimental Medicine. 94 (4): 305–22. doi:10.1084/jem.94.4.305. PMC 2136114. PMID 14888814.
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  29. Detailed chart of its evolution here Archived 9 May 2009 at the Wayback Machine at PDF called Ecology and Evolution of the Flu
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