1tx1: Difference between revisions
New page: '''Theoretical Model''' The entry 1TX1 is a Theoretical Model titled 'Model structure of influenza B virus HA1'. Category:Theoretical Model ''Page seeded by [http://oca.weizmann.ac... |
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{{Theoretical_model}} | |||
The | ==MODEL STRUCTURE OF INFLUENZA B VIRUS HA1== | ||
<StructureSection load='1tx1' size='340' side='right'caption='[[1tx1]]' scene=''> | |||
== Structural highlights == | |||
<table><tr><td colspan='2'>For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1TX1 FirstGlance]. <br> | |||
</td></tr><tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=1tx1 FirstGlance], [https://www.ebi.ac.uk/pdbsum/1tx1 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1tx1 ProSAT]</span></td></tr> | |||
</table> | |||
<div style="background-color:#fffaf0;"> | |||
== Publication Abstract from PubMed == | |||
Influenza B virus is one of two types of influenza virus that cause substantial morbidity and mortality in humans, the other being influenza A virus. The inability to provide lasting protection to humans against influenza B virus infection is due, in part, to antigenic drift of the viral surface glycoprotein, haemagglutinin (HA). Studies of the antigenicity of the HA of influenza B virus have been hampered by lack of knowledge of its structure. To address this gap, two possible models have been inferred for this structure, based on two known structures of the homologous HA of the influenza A virus (subtypes H3 and H9). Statistical, structural and functional analyses of these models suggested that they matched important details of experimental observations and did not differ from each other in any substantive way. These models were used to investigate two HA sites at which viral variants appeared to carry a selective advantage. It was found that each of these sites coevolved with nearby sites to compensate for either size or charge changes. | |||
Homology model of the structure of influenza B virus HA1.,Tung CS, Goodman JL, Lu H, Macken CA J Gen Virol. 2004 Nov;85(Pt 11):3249-59. PMID:15483238<ref>PMID:15483238</ref> | |||
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br> | |||
</div> | |||
<div class="pdbe-citations 1tx1" style="background-color:#fffaf0;"></div> | |||
== References == | |||
<references/> | |||
__TOC__ | |||
</StructureSection> | |||
[[Category: Theoretical Model]] | |||
[[Category: Large Structures]] | |||
[[Category: Goodman, J L]] | |||
[[Category: Lu, H]] | |||
[[Category: Macken, C A]] | |||
[[Category: Tung, C S]] | |||
Latest revision as of 12:33, 29 September 2021
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MODEL STRUCTURE OF INFLUENZA B VIRUS HA1MODEL STRUCTURE OF INFLUENZA B VIRUS HA1
Structural highlights
Publication Abstract from PubMedInfluenza B virus is one of two types of influenza virus that cause substantial morbidity and mortality in humans, the other being influenza A virus. The inability to provide lasting protection to humans against influenza B virus infection is due, in part, to antigenic drift of the viral surface glycoprotein, haemagglutinin (HA). Studies of the antigenicity of the HA of influenza B virus have been hampered by lack of knowledge of its structure. To address this gap, two possible models have been inferred for this structure, based on two known structures of the homologous HA of the influenza A virus (subtypes H3 and H9). Statistical, structural and functional analyses of these models suggested that they matched important details of experimental observations and did not differ from each other in any substantive way. These models were used to investigate two HA sites at which viral variants appeared to carry a selective advantage. It was found that each of these sites coevolved with nearby sites to compensate for either size or charge changes. Homology model of the structure of influenza B virus HA1.,Tung CS, Goodman JL, Lu H, Macken CA J Gen Virol. 2004 Nov;85(Pt 11):3249-59. PMID:15483238[1] From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine. References
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