Each Influenza Virus Type Varies
Each influenza virus type varies from origin to host infection. The three different influenza virii discussed in the paper operate on these characteristics: structure variation, origin, target infector, and which is closely related to swine influenza. Orthomyxoviridae is a family of RNA virii comprised of three genera that can cause influenza. The Orthomyxoviridae family contain: influenza A, B, and influenza C. The three virus types can be distinguished from one another on the basis of antigenic differences between their nucleoproteins (NP) and matrix (M) proteins (Heinen 2003). The internal antigens (M1 and NP proteins) are the type-specific proteins (type-specific antigens) used to determine if a particular virus is A, B or C (Hunt 2009).
Influenza can affect vertebrates, including birds, humans, seals, pigs, and other mammals. Influenza virii have evolved into a number of host-specific lineages that are exemplified by the NP gene and include equine Prague/56, recent equine strains, classical swine and human strains, H13 gull strains, and all other avian strains (Webster et. al. 1992). H1N1 is a subtype of influenza A virii.
Mutation plays a significant role in the life cycle of virii. Mutation of a virus can cause unimmunized response and allow virii to enter the body, thus causing epidemics, pandemics, and future new diseases and virii. It is important for our society to be aware of the mutation and evolution of these virii, as well as the different species of hosts which can carry them. If we fail to remain vigilant, then our species could be easily be eradicated by a virus that assaults something that we all share, such as mitochondria.Influenza virii are significant human respiratory pathogens that cause both seasonal, endemic infections and periodic, unpredictable pandemics (Taubenberger and Morens 2007).
Influenza B and C virii are almost exclusively isolated from man, although influenza C virus has also been isolated from pigs and influenza B has recently been isolated from seals. Influenza A virii, in contrast, infect a wide range of avian and mammalian species, with the latter group including man, pigs, horses and aquatic mammals (Easterday 1975). It is important for our society to be aware of the mutation and evolution of these virii, as well as the different species of hosts which can carry them.
If we fail to remain vigilant, then our species could be easily be eradicated by a virus that assaults something that we all share, such as mitochondria.The genome of influenza A virii consists of 8 single-stranded RNA segments (genes) of negative polarity (Scholtissek 1994). The type A virii are further divided into subtypes, based on the antigenic nature of their surface glycoproteins haemagglutinin (HA) and neuraminidase (NA). So far, 15 different HAs (H1 to 15) and 9 NAs (N1 to 9) have been identified among all influenza virii (Heinen 2003). Influenza A virii originate in aquatic avian, including migrating water fowl and shorebirds.There are 3 ways influenza can invade the human body: antigenic drift, antigenic shift, and direct or indirect introduction of an avian influenza virus into the human population.
Antigenic drift is caused by mutation and selection of variants under the selection pressure of the immune system. Antigenic shift is caused by replacement of at least the hemagglutinin gene of the prevailing human strain by the allelic gene of an avian influenza virus by reassortment (Scholtissek 1994). An example would be swine influenza; this virus was first recorded as the Spanish flu (H1N1) in 1918.
This virus mutated over several decades and reappeared in the 2009 flu pandemic within pigs. The target infector for influenza A is in humans and water fowl, but there is an exception: virii in humans do not infect avian population and vice versa, with the exception of pigs, which are able to be infected by both types of virii. Swine Influenza, also known as H1N1 is a subtype of influenza A.Influenza A has been the cause of a number of outbreaks: H1N1, Spanish flu in 1918 and the 2009 flu pandemic, H2N2, Asian flu in 1957, H3N2, Hong Kong flu in 1968, H5N1, current pandemic threat, H7N7, H1N2, endemic in humans and pigs, H9N2, H7N2, H7N3, and H10N7.Influenza A virii differ from influenza B and C by, first, causing the most diseases.
Secondly, influenza A virii is faster than influenza B and C. Influenza A has been the known virus of B and C to have renounced pandemics. Influenza A can cause pandemica, influena B can cause epidemics but not pandemics, and influenza C can cause neither panademics nor pandemics.Influenza B virus is a human pathogen whose origin and possible reservoir in nature are not known. An influenza B virus was isolated from a naturally infected harbor seal (Phoca vitulina) and was found to be infectious to seal kidney cells in vitro (Osterhaus 2000). Influenza B virions have four proteins in the envelope: HA, NA, NB, and BM2. Also, Influenza B does not cause pandemics and inhabit humans and seals as hosts.
Influenza B is not classified in subtypes, but can cause morbidity and mortality among humans.Influenza C virii are different than influenza A and B virii. Influenza C virion contains 7 RNA segments, not 8 RNAs like influenza A and B virii. Influenza C is commonly found as a host in humans and pigs.
Influenza C virii generally do not cause disease, although it is a virus. Influenza C is not classified according to subtypes.ConclusionInfluenza virii: Influenza A, B and C all vary in orientation, origin, host of infection, and common subtypes affecting humans. Swine influenza is a subtype of influenza A virii. Influenza A and B virii contain 8 RNAs, where influenza C virii contain only 7 RNA segments. All three influenzas can or have inhabited humans as hosts and another form of mammal.
Influenza virii have been found around the world in varies outbreaks of pandemics and epidemics. Antigenic drift is the leading factor of deaths and subtypes of influenza. With a mutation of the virii evolving, detection is vital to the prevention of future epidemics.DiscussionIt is important for our society to be aware of the mutation and evolution of these virii, as well as the different species of hosts which can carry them. If we fail to remain vigilant, then our species could be easily be eradicated by a virus that assaults something that we all share, such as mitochondria.
Influenza virii can vary and occasionally go undetected. These virii can mutate, thus making the determination of the virus more challenging. When a pandemic occurs in one decade and is recorded and controlled, a virus can and has mutated or harbored until decades later and begun another pandemic, determination if the virus is the same can be complex.
Vaccinations are updated yearly in order to keep up with the antigenic drift (mutation). The different origins of each influenza strains found in vertebrates can be missed or unstudied. Influenza could have infected other vertebrates that were not known to human research.
Without this knowledge, humans could not learn as much about the disease and if strain could intertwine with the humans strain another outbreak may occur. The reason there are so many different strains and continuous outbreaks and deaths is because the vaccinations humans use are for the unmutated strains of influenza. Without the through research on the mutated strain of influenza, a vaccination cannot be made.
As a result, either a detect upon vertebrate animals with the virus must be made and used, or the outbreak of the virus among humans must take place.Literature CitedEasterday, B.C. (1975) Animal Influenza. In: The influenza virii and influenza (Ed. Kilbourne, E.D.) Academic Press, Orlando. 449-481Heinen, Paul. 2003.
Swine influenza: a zoonosis. Veterinary Sciences Tomorrow.<http://www.vetscite.org/publish/articles/000041/print.html>Hunt, Dr. Margaret. 2009. Influenza Virus (Orthomyxovirus). Virology. <http://pathmicro.med.sc.edu/mhunt/flu.htm>A. D.ÂM.ÂE. Osterhaus, G. F. Rimmelzwaan, 1 B. E.ÂE. Martina, 2 T. M. Bestebroer, 1 R. A.ÂM. Fouchier. 2000. Influenza B Virus in Seals. Science. 288(5568): 1051-1053Scholtissek, Christoph. 1994. Source of influenza pandemics. European journal of epidemiology 10: 455-458Jeffery K. Taubenberger and David M. Morens. 2007. The Pathology of Influenza Virus Infections. Annual Review of Pathology: Mechanisms of Disease Vol. 3: 499-522.R G Webster, W J Bean, O T Gorman, T M Chambers and Y Kawaoka. 1992. Evolution and Ecology of Influenza A virii. Microbiol Mol Biol Rev. 56(1): 152-179
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