Avian influenza: Difference between revisions

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==Characteristics of the symbiont/pathogen==
==Characteristics of the symbiont/pathogen==
Avian influenza is part of the Orthomyxoviridae group, which are single-stranded RNA viruses. There are two different classifications of avian influenza, highly pathogenic avian influenza (HPAI) and mildly or non-pathogenic avian influenza (MPAI). The replication process of the virus varies in HPAI and MPAI. In HPAI, the HA proteins start in most of the cells in the body of the host, while in MPIA, the HA proteins start in the respiratory and enteric tracts of the host (4). There is a viral envelope that encases the surface proteins: Hemagglutinin (HA), which has 1,775 base pairs (bp) and Neuraminidase (NA), 1,413bp and Matrix 2 (M2), when paired with Matrix 1 has 1,027bp (4,7). There are 16 HA subtypes that are the virus receptor-binding site and also allow the viral RNA to be released into the host cell (1). The HA protein has to grow into the HA1 and HA2 subunits to be infectious (4). There are nine NA subtypes that are enzymatically active proteins that allow the virus to be released from the cell surface (4). The M2 proteins are an ion channel that activate the HA proteins to release the virus (4). Inside these surface proteins, there are six internal proteins that make up the viral genome and transcribe the virus (4). These proteins include: polymerase proteins PB1 with 2,341bp, PB2 with 2,341bp and PA with 2,233bp, the nucleoprotein (NP) with 1,565bp, Matrix 1 (M1), and nonstructural protein 1 and 2 (NS1 and NS2 with 890bp)(7). NS1 is the only protein not located inside the virion (4,7).
Avian influenza was first discovered in free living ducks in 1972. Avian influenza is part of the [[Orthomyxoviridae]] group, which is single-stranded RNA virus. There are two different classifications of avian influenza, the highly pathogenic avian influenza (HPAI) and the mildly or non-pathogenic avian influenza (MPAI). The replication process of the virus varies in HPAI and MPAI. The cleavage of Hemagglutinin (HA) proteins is different in HPAI and MPAI viruses. In HPAI virus, the HA proteins are cleaved by endogenous protease which occurs in most of the cells in the body of the host, while the HA proteins of the MPIA virus is cleaved by trypsin-like protease, which is present in the respiratory and enteric tracts of the host (4). There is a viral envelope that encases the surface proteins: HA, which encodes a gene with 1,775 base pairs (bp) and Neuraminidase (NA), encodes a gene with 1,413 bp, and Matrix 2 (M2), when paired with Matrix 1 encodes a gene with 1,027 bp (4,7). There are 16 HA subtypes which are the virus receptor-binding site and allow the viral RNA to be released into the host cell (1). The HA protein needs to be cleaved by enzymes into the HA1 and HA2 subunits to be infectious (4). There are nine NA subtypes that are enzymatically active proteins that allow the virus to be released from the cell surface (4). The M2 proteins act as ion channels that activate the HA proteins to release the virus (4). Inside these surface proteins, there are six internal proteins that make up the viral genome and transcribe the virus (4). These proteins include: polymerase proteins PB1 with a gene encoding 2,341bp, PB2 with a gene encoding 2,341bp, PA with a gene encoding 2,233bp, the nucleoprotein (NP) with a gene encoding 1,565bp, Matrix 1 (M1), and nonstructural protein 1 and 2 (NS1 and NS2 with a gene encoding 890bp) (7). NS1 is the only protein not located inside the virion (4,7).  
 
[[File:Poultry.jpg|thumb|left| Chicken]]
[[File:Poultry.jpg|thumb|left| Chicken]]


==Characteristics of the host==
==Characteristics of the host==
Avian influenza affects a variety of species. There are three types of the virus, type A, type B, and type C. Type A affects a range of animals including, but not limited to wild birds, including ducks, gulls, and seabirds, domesticated birds, such as chicken and turkey,  mammals, such as horses, pigs, and humans (4). At least 88 species of wild birds have been found to have type A avian inflenza (3). Types B and C only affect humans (4).
Avian influenza affects a variety of species. There are three types of avian influenza viruses: type A, type B, and type C. Type A influenza affects a range of animals, including wild birds, ducks, gulls, seabirds, mammals (horses, pigs, humans), and domesticated birds, such as chicken and turkey (4). At least 88 species of wild birds have been found to have type A avian influenza (3). Types B and C influenzas only affect humans (4).  
Avian Influenza is spread through the fecal-oral transmission, thus water birds and surface feeders are more susceptible to contract the influenza than birds that forage. The influenza virus becomes highly pathogenic during the spread between wild birds and domesticated birds (5).


Avian Influenza is spread through the fecal-oral transmission, this makes water birds and surface feeders more suseptible to contract it than birds that forage. The virus spreads from the wild birds to domesticated birds, where it becomes highly pathogenic and then returns to the wild birds again (5).
H5N1, a subtype of avian influenza virus, had spread to fifteen different countries in 2009. The two prevalent areas are Southeast Asia and the Middle East. The domestic birds as well as the migrating birds could be the potential carriers of H5N1 virus (8).  


Avian influenza is different from the human influenza in which avian influenza affects people of all age groups, not just the young and the elderly individuals. Avian influenza has high mortality rate even in healthy people. Avian influenza causes fast progressive pneumonitis, and the incubation period is in the range of two to nine days (6).
Avian influenza is different from the human influenza, in that avian influenza affects people of all age groups, not just the young and the elderly individuals. Avian influenza has high mortality rates even in healthy people (6).
[[File:H1N1 navbox.jpg|thumb| Avian Influenza, [http://en.wikipedia.org/wiki/File:H1N1_navbox.jpg CDC]]]
[[File:H1N1 navbox.jpg|thumb| Avian Influenza, [http://en.wikipedia.org/wiki/File:H1N1_navbox.jpg CDC]]]


==Host-Symbiont Interaction ==
==Host-Symbiont Interaction ==
Migratory waterfowl are the primary source of infection in poultry and mammals. Mammals are infected regularly, but since they are not the starting place for the virus, some of the subtypes have become extinct. Examples of this are the H2N2 subtype becoming extinct in humans and H7N7 becoming extinct in horses. Because the subtypes become extinct, more fit subtypes are developed (4).
Migratory waterfowl are the primary source of infection in poultry and mammals. Mammals are infected regularly, but since they are not the sites of replication for the viruses, some of the subtypes have become extinct. Examples of this are the H2N2 subtype becoming extinct in humans and H7N7 becoming extinct in horses. Because the subtypes become extinct, more fit subtypes for infecting humans are developed (4).  


Most birds suffering from avian influenza have mild respiratory problems and decreased egg production. Chicken and turkey that have HPAI typically show a decrease in their vocalization, food and water consumption. They also have signs of depression and apathy. Birds that have avian influenza can develop significant physical problems, such as head tremors, wing paralysis, and a lack of coordination (2).
Most birds suffering from avian influenza have mild respiratory problems and decreased egg production. Chicken and turkey that have HPAI typically show a decrease in their vocalization, food, and water consumption. They also have signs of depression and apathy. Birds that have avian influenza can develop significant physical problems, such as head tremors, wing paralysis, and a lack of coordination (2).


==Molecular Insights into the Symbiosis==
==Molecular Insights into the Symbiosis==
One way to determine if the strain of the virus is HPAI or MPAI is to place the strain into fluid from embryonated eggs that are specific pathogen free (SPF) chickens. If six out of eight of the chickens die within 10 days the strain is determined to be highly pathogenic. If fewer than six die within 10 days, it is classified as mildly pathogenic or non-pathogenic (4).
One way to determine if the strain of the virus is HPAI or MPAI is to place the strain into fluids from embryonated eggs that are specific pathogen free (SPF) chickens. If six out of eight of the chickens die within 10 days, the strain is determined to be highly pathogenic. If fewer than six chickens die within 10 days, it is classified as mildly pathogenic or non-pathogenic (4).  
[[File:MallardDuck.jpg|thumb|Mallard Duck, [http://animals.nationalgeographic.com/animals/birds/mallard-duck//wiki/File:MallardDuck.jpg National Geographic]]]
[[File:MallardDuck.jpg|thumb|Mallard Duck, [http://animals.nationalgeographic.com/animals/birds/mallard-duck//wiki/File:MallardDuck.jpg National Geographic]]]


==Ecological and Evolutionary Aspects ==
==Ecological and Evolutionary Aspects ==
Avian influenza was first discovered in free living ducks in 1972. Mallard ducks were found to have the most HA and NA subtypes; however, not all of the HA subtypes were found in abundance. This means that these ducks are probably not the starting place for all of the HA subtypes.  
Mallard ducks were found to have the most HA and NA subtypes; however, not all of the HA subtypes were found in abundance. This means that these ducks are probably not the first vectors for all of the HA subtypes. HPAI was one of the first viral diseases found in poultry. The virus was found to have a rapid rate of evolution in mammals and domesticated birds, whereas, there is a low rate of evolution in wild birds. This is evident that mammals are not the primary hosts, but wild birds are. It is hard to know the full evolutionary history of how avian influenza has developed and evolved due to the viral interactions with many types of wild birds (4).
HPAI was one of the first viral diseases found in poultry.  
The virus was found to have a rapid rate of evolution in mammals and domesticated birds, whereas, there is a low rate of evolution in wild birds. This is evidence that mammals are not primary hosts, but wild birds are.  
It is hard to know the full evolutionary history of how avian influenza has developed and evolved due to the viral interaction with many types of wild birds (4).


==References==
==References==
[http://www.sciencedirect.com.ezproxy2.rmc.edu/science/article/pii/S0147957108000052] Boyce, W.M, Sandrock, C., Kreuder-Johnson, C., Kelly, T., and Cardona, C. 2008. Avian influenza viruses in wild birds: a moving target. "Comparative Immunology, Microbiology and Infectious Diseases." 32:275-286.
[http://www.sciencedirect.com.ezproxy2.rmc.edu/science/article/pii/S0147957108000052] Boyce, W.M, Sandrock, C., Kreuder-Johnson, C., Kelly, T., and Cardona, C. 2008. Avian influenza viruses in wild birds: a moving target. "Comparative Immunology, Microbiology and Infectious Diseases" 32:275-286.


[http://www.sciencedirect.com.ezproxy2.rmc.edu/science/article/pii/S1573521406800217] Koch, G. and Elbers, A.R.W. 2006. Outdoor ranging of poultry: a major risk factor for the introduction and development of high-pathogenicity avian influenza. "Wageningen Journal of Life Sciences." 54:179-194.
[http://www.sciencedirect.com.ezproxy2.rmc.edu/science/article/pii/S1573521406800217] Koch, G. and Elbers, A.R.W. 2006. Outdoor ranging of poultry: a major risk factor for the introduction and development of high-pathogenicity avian influenza. "Wageningen Journal of Life Sciences" 54:179-194.


[http://www.springerlink.com/content/j7233073mr440631/] Stallknecht, D.E. and Shane, S.M. 1988. Host range of avian influenza virus in free-living birds. "Veterinary Research Communications" 12:125-141.
[http://www.springerlink.com/content/j7233073mr440631/] Stallknecht, D.E. and Shane, S.M. 1988. Host range of avian influenza virus in free-living birds. "Veterinary Research Communications" 12:125-141.


[http://www.sciencedirect.com.ezproxy2.rmc.edu/science/article/pii/S0145305X99000786#sec3] Suarez, D. L. and Schultz-Cherry, S. 2000. Immunology of avian influenza virus: a review. "Developmental and Comparative Immunology." 24:269-283.
[http://www.sciencedirect.com.ezproxy2.rmc.edu/science/article/pii/S0145305X99000786#sec3] Suarez, D. L. and Schultz-Cherry, S. 2000. Immunology of avian influenza virus: a review. "Developmental and Comparative Immunology" 24:269-283.


[http://web.ebscohost.com/ehost/pdfviewer/pdfviewer?vid=6&hid=119&sid=acd51844-b612-4202-beec-2ffd70e1c882%40sessionmgr113] Takekawa, J. Y., Prosser, D. J.,Newman, S.H., Muzaffar, S.B., Hill, N.J., Yan, B., Xiao, X., Lei, F., Li, T., Schwarzbach, S.C., Howell, J.A. 2010. Victims and vectors: highly pathogenic avian influenza H5N1 and the ecology of wild birds. "Avian Biology Research" 51-73.
[http://web.ebscohost.com/ehost/pdfviewer/pdfviewer?vid=6&hid=119&sid=acd51844-b612-4202-beec-2ffd70e1c882%40sessionmgr113] Takekawa, J. Y., Prosser, D. J.,Newman, S.H., Muzaffar, S.B., Hill, N.J., Yan, B., Xiao, X., Lei, F., Li, T., Schwarzbach, S.C., Howell, J.A. 2010. Victims and vectors: highly pathogenic avian influenza H5N1 and the ecology of wild birds. "Avian Biology Research" 51-73.
[http://www.ncbi.nlm.nih.gov/pubmed/20188299] Taylor, W. R. J., Burhan, E., Wertheim, H., Soepandi, P.Z., Horby, P., Fox, A., Benamore, R., Simone, L., Hien, T.T., and Chappuis, F. 2010. Avian influenza- A review for doctors in travel medicine. "Travel Medicine and Infectious Disease" 8: 1-12.


[http://www.sciencedirect.com.ezproxy2.rmc.edu/science/article/pii/S1286457911000438] Tsai, K-N. and Chen, G-W. 2011. Influenza genome diversity and evolution. "Microbes and Infection" 13:479-488.
[http://www.sciencedirect.com.ezproxy2.rmc.edu/science/article/pii/S1286457911000438] Tsai, K-N. and Chen, G-W. 2011. Influenza genome diversity and evolution. "Microbes and Infection" 13:479-488.
[http://www.ncbi.nlm.nih.gov/pubmed/20633908] Tseng, W. C., Li, H. A., Huang, W. C., and Liang, L. H. 2010. Potential number of human cases of H5N1 avian influenza in Egypt. "Public Health" 124: 452-459.


Edited by Jane Oh, students of [mailto:glim@rmc.edu Grace Lim-Fong]
Edited by Jane Oh, students of [mailto:glim@rmc.edu Grace Lim-Fong]


<!--Do not edit or remove this line.-->[[Category:Pages edited by students of Grace Lim-Fong at Randolph-Macon College]]
<!--Do not edit or remove this line.-->[[Category:Pages edited by students of Grace Lim-Fong at Randolph-Macon College]]

Latest revision as of 19:13, 2 December 2012

Characteristics of the symbiont/pathogen

Avian influenza was first discovered in free living ducks in 1972. Avian influenza is part of the Orthomyxoviridae group, which is single-stranded RNA virus. There are two different classifications of avian influenza, the highly pathogenic avian influenza (HPAI) and the mildly or non-pathogenic avian influenza (MPAI). The replication process of the virus varies in HPAI and MPAI. The cleavage of Hemagglutinin (HA) proteins is different in HPAI and MPAI viruses. In HPAI virus, the HA proteins are cleaved by endogenous protease which occurs in most of the cells in the body of the host, while the HA proteins of the MPIA virus is cleaved by trypsin-like protease, which is present in the respiratory and enteric tracts of the host (4). There is a viral envelope that encases the surface proteins: HA, which encodes a gene with 1,775 base pairs (bp) and Neuraminidase (NA), encodes a gene with 1,413 bp, and Matrix 2 (M2), when paired with Matrix 1 encodes a gene with 1,027 bp (4,7). There are 16 HA subtypes which are the virus receptor-binding site and allow the viral RNA to be released into the host cell (1). The HA protein needs to be cleaved by enzymes into the HA1 and HA2 subunits to be infectious (4). There are nine NA subtypes that are enzymatically active proteins that allow the virus to be released from the cell surface (4). The M2 proteins act as ion channels that activate the HA proteins to release the virus (4). Inside these surface proteins, there are six internal proteins that make up the viral genome and transcribe the virus (4). These proteins include: polymerase proteins PB1 with a gene encoding 2,341bp, PB2 with a gene encoding 2,341bp, PA with a gene encoding 2,233bp, the nucleoprotein (NP) with a gene encoding 1,565bp, Matrix 1 (M1), and nonstructural protein 1 and 2 (NS1 and NS2 with a gene encoding 890bp) (7). NS1 is the only protein not located inside the virion (4,7).

Chicken

Characteristics of the host

Avian influenza affects a variety of species. There are three types of avian influenza viruses: type A, type B, and type C. Type A influenza affects a range of animals, including wild birds, ducks, gulls, seabirds, mammals (horses, pigs, humans), and domesticated birds, such as chicken and turkey (4). At least 88 species of wild birds have been found to have type A avian influenza (3). Types B and C influenzas only affect humans (4). Avian Influenza is spread through the fecal-oral transmission, thus water birds and surface feeders are more susceptible to contract the influenza than birds that forage. The influenza virus becomes highly pathogenic during the spread between wild birds and domesticated birds (5).

H5N1, a subtype of avian influenza virus, had spread to fifteen different countries in 2009. The two prevalent areas are Southeast Asia and the Middle East. The domestic birds as well as the migrating birds could be the potential carriers of H5N1 virus (8).

Avian influenza is different from the human influenza, in that avian influenza affects people of all age groups, not just the young and the elderly individuals. Avian influenza has high mortality rates even in healthy people (6).

Avian Influenza, CDC

Host-Symbiont Interaction

Migratory waterfowl are the primary source of infection in poultry and mammals. Mammals are infected regularly, but since they are not the sites of replication for the viruses, some of the subtypes have become extinct. Examples of this are the H2N2 subtype becoming extinct in humans and H7N7 becoming extinct in horses. Because the subtypes become extinct, more fit subtypes for infecting humans are developed (4).

Most birds suffering from avian influenza have mild respiratory problems and decreased egg production. Chicken and turkey that have HPAI typically show a decrease in their vocalization, food, and water consumption. They also have signs of depression and apathy. Birds that have avian influenza can develop significant physical problems, such as head tremors, wing paralysis, and a lack of coordination (2).

Molecular Insights into the Symbiosis

One way to determine if the strain of the virus is HPAI or MPAI is to place the strain into fluids from embryonated eggs that are specific pathogen free (SPF) chickens. If six out of eight of the chickens die within 10 days, the strain is determined to be highly pathogenic. If fewer than six chickens die within 10 days, it is classified as mildly pathogenic or non-pathogenic (4).

Mallard Duck, National Geographic

Ecological and Evolutionary Aspects

Mallard ducks were found to have the most HA and NA subtypes; however, not all of the HA subtypes were found in abundance. This means that these ducks are probably not the first vectors for all of the HA subtypes. HPAI was one of the first viral diseases found in poultry. The virus was found to have a rapid rate of evolution in mammals and domesticated birds, whereas, there is a low rate of evolution in wild birds. This is evident that mammals are not the primary hosts, but wild birds are. It is hard to know the full evolutionary history of how avian influenza has developed and evolved due to the viral interactions with many types of wild birds (4).

References

[1] Boyce, W.M, Sandrock, C., Kreuder-Johnson, C., Kelly, T., and Cardona, C. 2008. Avian influenza viruses in wild birds: a moving target. "Comparative Immunology, Microbiology and Infectious Diseases" 32:275-286.

[2] Koch, G. and Elbers, A.R.W. 2006. Outdoor ranging of poultry: a major risk factor for the introduction and development of high-pathogenicity avian influenza. "Wageningen Journal of Life Sciences" 54:179-194.

[3] Stallknecht, D.E. and Shane, S.M. 1988. Host range of avian influenza virus in free-living birds. "Veterinary Research Communications" 12:125-141.

[4] Suarez, D. L. and Schultz-Cherry, S. 2000. Immunology of avian influenza virus: a review. "Developmental and Comparative Immunology" 24:269-283.

[5] Takekawa, J. Y., Prosser, D. J.,Newman, S.H., Muzaffar, S.B., Hill, N.J., Yan, B., Xiao, X., Lei, F., Li, T., Schwarzbach, S.C., Howell, J.A. 2010. Victims and vectors: highly pathogenic avian influenza H5N1 and the ecology of wild birds. "Avian Biology Research" 51-73.

[6] Taylor, W. R. J., Burhan, E., Wertheim, H., Soepandi, P.Z., Horby, P., Fox, A., Benamore, R., Simone, L., Hien, T.T., and Chappuis, F. 2010. Avian influenza- A review for doctors in travel medicine. "Travel Medicine and Infectious Disease" 8: 1-12.

[7] Tsai, K-N. and Chen, G-W. 2011. Influenza genome diversity and evolution. "Microbes and Infection" 13:479-488.

[8] Tseng, W. C., Li, H. A., Huang, W. C., and Liang, L. H. 2010. Potential number of human cases of H5N1 avian influenza in Egypt. "Public Health" 124: 452-459.

Edited by Jane Oh, students of Grace Lim-Fong