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__NOTOC__ | __NOTOC__ | ||
{{Avian influenza}} | {{Avian influenza}}'''For more information about seasonal human influenza virus that is not associated with animal exposure, see [[Influenza]]''' | ||
For more details about the avian influenza transmission, replication, and mechanism of infection in humans, click [[Avian influenza pathophysiology|here]] | '''For more details about the avian influenza transmission, replication, and mechanism of infection in humans, click [[Avian influenza pathophysiology|here]]''' | ||
<br><br> | <br><br> | ||
{{CMG}}; {{AE}} {{YD}} | {{CMG}}; {{AE}} {{YD}} | ||
==Overview== | ==Overview== | ||
Avian influenza is caused by '''influenza A virus'''. Neither influenza B nor influenza C causes avian influenza. Influenza belongs to the ''Orthomyxoviridae'' family. Influenza is an enveloped, pleomorphic (spherical and filamentous forms) virus that contains a linear, segmented (8 segments), negative-sense, single-stranded RNA genome. The genome is composed of 8 segmented genes that encode 11 proteins. | Avian influenza is caused by '''influenza A virus'''. Neither [[influenza B]] nor [[influenza C]] causes avian influenza. Influenza belongs to the ''[[Orthomyxoviridae]]'' family. Influenza is an [[enveloped]], [[pleomorphic]] ([[spherical]] and [[filamentous]] forms) virus that contains a [[linear]], [[segmented]] (8 segments), [[negative-sense]], [[single-stranded]] [[RNA]] genome. The genome is composed of 8 segmented genes that encode 11 proteins. | ||
== | ==Causes== | ||
Avian influenza is caused by '''influenza A virus'''. Neither influenza B nor influenza C causes avian influenza. | Avian influenza is caused by '''influenza A virus'''. Neither influenza B nor influenza C causes avian influenza. | ||
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*'''Neuraminidase (NA)''': Cleaves progeny virions from host cell receptors.<ref name="pmid18403604">{{cite journal| author=Korteweg C, Gu J| title=Pathology, molecular biology, and pathogenesis of avian influenza A (H5N1) infection in humans. | journal=Am J Pathol | year= 2008 | volume= 172 | issue= 5 | pages= 1155-70 | pmid=18403604 | doi=10.2353/ajpath.2008.070791 | pmc=PMC2329826 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18403604 }} </ref> | *'''Neuraminidase (NA)''': Cleaves progeny virions from host cell receptors.<ref name="pmid18403604">{{cite journal| author=Korteweg C, Gu J| title=Pathology, molecular biology, and pathogenesis of avian influenza A (H5N1) infection in humans. | journal=Am J Pathol | year= 2008 | volume= 172 | issue= 5 | pages= 1155-70 | pmid=18403604 | doi=10.2353/ajpath.2008.070791 | pmc=PMC2329826 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18403604 }} </ref> | ||
*'''Polymerase proteins''': PB1, PB2, PA, and PB1-F2. These proteins form the polymerase complex. Together with the NP protein, form the ribonucleoprotein (RNP) complex to induce replication and transcription. Additionally, PB1-F2 has a role in inducing apoptosis.<ref name="pmid18403604">{{cite journal| author=Korteweg C, Gu J| title=Pathology, molecular biology, and pathogenesis of avian influenza A (H5N1) infection in humans. | journal=Am J Pathol | year= 2008 | volume= 172 | issue= 5 | pages= 1155-70 | pmid=18403604 | doi=10.2353/ajpath.2008.070791 | pmc=PMC2329826 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18403604 }} </ref><ref name="pmid11546875">{{cite journal| author=Hatta M, Gao P, Halfmann P, Kawaoka Y| title=Molecular basis for high virulence of Hong Kong H5N1 influenza A viruses. | journal=Science | year= 2001 | volume= 293 | issue= 5536 | pages= 1840-2 | pmid=11546875 | doi=10.1126/science.1062882 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11546875 }} </ref> | *'''Polymerase proteins''': PB1, PB2, PA, and PB1-F2. These proteins form the polymerase complex. Together with the NP protein, form the ribonucleoprotein (RNP) complex to induce replication and transcription. Additionally, PB1-F2 has a role in inducing apoptosis.<ref name="pmid18403604">{{cite journal| author=Korteweg C, Gu J| title=Pathology, molecular biology, and pathogenesis of avian influenza A (H5N1) infection in humans. | journal=Am J Pathol | year= 2008 | volume= 172 | issue= 5 | pages= 1155-70 | pmid=18403604 | doi=10.2353/ajpath.2008.070791 | pmc=PMC2329826 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18403604 }} </ref><ref name="pmid11546875">{{cite journal| author=Hatta M, Gao P, Halfmann P, Kawaoka Y| title=Molecular basis for high virulence of Hong Kong H5N1 influenza A viruses. | journal=Science | year= 2001 | volume= 293 | issue= 5536 | pages= 1840-2 | pmid=11546875 | doi=10.1126/science.1062882 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11546875 }} </ref> | ||
*'''NP''': Together with the polymerase proteins, NP forms the RNP complex to induce replication and transcription.<ref name="pmid18403604">{{cite journal| author=Korteweg C, Gu J| title=Pathology, molecular biology, and pathogenesis of avian influenza A (H5N1) infection in humans. | journal=Am J Pathol | year= 2008 | volume= 172 | issue= 5 | pages= 1155-70 | pmid=18403604 | doi=10.2353/ajpath.2008.070791 | pmc=PMC2329826 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18403604 }} </ref> | *'''Nucleoprotein (NP)''': Together with the polymerase proteins, NP forms the RNP complex to induce replication and transcription.<ref name="pmid18403604">{{cite journal| author=Korteweg C, Gu J| title=Pathology, molecular biology, and pathogenesis of avian influenza A (H5N1) infection in humans. | journal=Am J Pathol | year= 2008 | volume= 172 | issue= 5 | pages= 1155-70 | pmid=18403604 | doi=10.2353/ajpath.2008.070791 | pmc=PMC2329826 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18403604 }} </ref> | ||
*'''Non-structural proteins''': NS1 and NS2. NS1 processes mRNA and helps the virus evade the host immune responses. NS2 controls the exporting process of RNP from the host nucleus.<ref name="pmid18403604">{{cite journal| author=Korteweg C, Gu J| title=Pathology, molecular biology, and pathogenesis of avian influenza A (H5N1) infection in humans. | journal=Am J Pathol | year= 2008 | volume= 172 | issue= 5 | pages= 1155-70 | pmid=18403604 | doi=10.2353/ajpath.2008.070791 | pmc=PMC2329826 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18403604 }} </ref> | *'''Non-structural proteins''': NS1 and NS2. NS1 processes mRNA and helps the virus evade the host immune responses. NS2 controls the exporting process of RNP from the host nucleus.<ref name="pmid18403604">{{cite journal| author=Korteweg C, Gu J| title=Pathology, molecular biology, and pathogenesis of avian influenza A (H5N1) infection in humans. | journal=Am J Pathol | year= 2008 | volume= 172 | issue= 5 | pages= 1155-70 | pmid=18403604 | doi=10.2353/ajpath.2008.070791 | pmc=PMC2329826 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18403604 }} </ref> | ||
*'''Matrix proteins''': M1 and M2. M1 has a role in viral assembly. M2 controls pH in the Golgi body.<ref name="pmid18403604">{{cite journal| author=Korteweg C, Gu J| title=Pathology, molecular biology, and pathogenesis of avian influenza A (H5N1) infection in humans. | journal=Am J Pathol | year= 2008 | volume= 172 | issue= 5 | pages= 1155-70 | pmid=18403604 | doi=10.2353/ajpath.2008.070791 | pmc=PMC2329826 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18403604 }} </ref> | *'''Matrix proteins''': M1 and M2. M1 has a role in viral assembly. M2 controls pH in the Golgi body.<ref name="pmid18403604">{{cite journal| author=Korteweg C, Gu J| title=Pathology, molecular biology, and pathogenesis of avian influenza A (H5N1) infection in humans. | journal=Am J Pathol | year= 2008 | volume= 172 | issue= 5 | pages= 1155-70 | pmid=18403604 | doi=10.2353/ajpath.2008.070791 | pmc=PMC2329826 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18403604 }} </ref> | ||
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[[Category:Bird diseases]] | [[Category:Bird diseases]] | ||
[[Category:Avian influenza]] | [[Category:Avian influenza]] | ||
[[Category:Animal virology]] | [[Category:Animal virology]] | ||
[[Category:Microbiology]] | [[Category:Microbiology]] | ||
Latest revision as of 17:04, 18 September 2017
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For more information about seasonal human influenza virus that is not associated with animal exposure, see Influenza
For more details about the avian influenza transmission, replication, and mechanism of infection in humans, click here
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Yazan Daaboul, M.D.
Overview
Avian influenza is caused by influenza A virus. Neither influenza B nor influenza C causes avian influenza. Influenza belongs to the Orthomyxoviridae family. Influenza is an enveloped, pleomorphic (spherical and filamentous forms) virus that contains a linear, segmented (8 segments), negative-sense, single-stranded RNA genome. The genome is composed of 8 segmented genes that encode 11 proteins.
Causes
Avian influenza is caused by influenza A virus. Neither influenza B nor influenza C causes avian influenza.
Family
- The influenza virus belongs to the Orthomyxoviridae family.
Genome
- The influenza A virus contains linear, segmented, negative-sense, single-stranded RNA.
- The RNA genome is segmented into 8 distinct segments.
- The total genomic length is approximately 13,000 nucleotides (range from 12,000 to 15,000).
- The genome is composed of 8 genes that encode 11 proteins.
The genome of influenza A consists of 8 gene segments, which encode 11 proteins[1]:
- Hemagglutinin (HA): Surface protein that acts as a receptor binding site. HA is targeted by host antibodies to neutralize the virus.[1][2][3]
- Neuraminidase (NA): Cleaves progeny virions from host cell receptors.[1]
- Polymerase proteins: PB1, PB2, PA, and PB1-F2. These proteins form the polymerase complex. Together with the NP protein, form the ribonucleoprotein (RNP) complex to induce replication and transcription. Additionally, PB1-F2 has a role in inducing apoptosis.[1][4]
- Nucleoprotein (NP): Together with the polymerase proteins, NP forms the RNP complex to induce replication and transcription.[1]
- Non-structural proteins: NS1 and NS2. NS1 processes mRNA and helps the virus evade the host immune responses. NS2 controls the exporting process of RNP from the host nucleus.[1]
- Matrix proteins: M1 and M2. M1 has a role in viral assembly. M2 controls pH in the Golgi body.[1]
Morphology
- The influenza virus contains an envelope.
- The influenza virus is pleomorphic with spherical and filamentous forms with particles that are approximately 80 nm to 120 nm in diameter.
References
- ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 Korteweg C, Gu J (2008). "Pathology, molecular biology, and pathogenesis of avian influenza A (H5N1) infection in humans". Am J Pathol. 172 (5): 1155–70. doi:10.2353/ajpath.2008.070791. PMC 2329826. PMID 18403604.
- ↑ Zhou J, Law HK, Cheung CY, Ng IH, Peiris JS, Lau YL (2006). "Functional tumor necrosis factor-related apoptosis-inducing ligand production by avian influenza virus-infected macrophages". J Infect Dis. 193 (7): 945–53. doi:10.1086/500954. PMID 16518756.
- ↑ de Jong MD, Tran TT, Truong HK, Vo MH, Smith GJ, Nguyen VC; et al. (2005). "Oseltamivir resistance during treatment of influenza A (H5N1) infection". N Engl J Med. 353 (25): 2667–72. doi:10.1056/NEJMoa054512. PMID 16371632.
- ↑ Hatta M, Gao P, Halfmann P, Kawaoka Y (2001). "Molecular basis for high virulence of Hong Kong H5N1 influenza A viruses". Science. 293 (5536): 1840–2. doi:10.1126/science.1062882. PMID 11546875.