2c7u: Difference between revisions
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|RESOURCES=<span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2c7u FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2c7u OCA], [http://www.ebi.ac.uk/pdbsum/2c7u PDBsum], [http://www.rcsb.org/pdb/explore.do?structureId=2c7u RCSB]</span> | |||
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==Overview== | ==Overview== | ||
Cytotoxic T lymphocytes (CTLs) are critical for the control of human immunodeficiency virus, but containment of virus replication can be undermined by mutations in CTL epitopes that lead to virus escape. We analyzed the evolution in vivo of an immunodominant, HLA-A2-restricted CTL epitope and found two principal, diametrically opposed evolutionary pathways that exclusively affect T cell-receptor contact residues. One pathway was characterized by acquisition of CTL escape mutations and the other by selection for wild-type amino acids. The pattern of CTL responses to epitope variants shaped which variant(s) prevailed in the virus population. The pathways notably influenced the amount of plasma virus, as patients with efficient CTL selection had lower plasma viral loads than did patients without efficient selection. Thus, viral escape from CTL responses does not necessarily correlate with disease progression. | Cytotoxic T lymphocytes (CTLs) are critical for the control of human immunodeficiency virus, but containment of virus replication can be undermined by mutations in CTL epitopes that lead to virus escape. We analyzed the evolution in vivo of an immunodominant, HLA-A2-restricted CTL epitope and found two principal, diametrically opposed evolutionary pathways that exclusively affect T cell-receptor contact residues. One pathway was characterized by acquisition of CTL escape mutations and the other by selection for wild-type amino acids. The pattern of CTL responses to epitope variants shaped which variant(s) prevailed in the virus population. The pathways notably influenced the amount of plasma virus, as patients with efficient CTL selection had lower plasma viral loads than did patients without efficient selection. Thus, viral escape from CTL responses does not necessarily correlate with disease progression. | ||
==About this Structure== | ==About this Structure== | ||
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[[Category: transmembrane]] | [[Category: transmembrane]] | ||
''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on | ''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Mon Mar 31 02:17:40 2008'' | ||
Revision as of 02:17, 31 March 2008
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| Resources: | FirstGlance, OCA, PDBsum, RCSB | ||||||
| Coordinates: | save as pdb, mmCIF, xml | ||||||
CONFLICTING SELECTIVE FORCES AFFECT CD8 T-CELL RECEPTOR CONTACT SITES IN AN HLA-A2 IMMUNODOMINANT HIV EPITOPE.
OverviewOverview
Cytotoxic T lymphocytes (CTLs) are critical for the control of human immunodeficiency virus, but containment of virus replication can be undermined by mutations in CTL epitopes that lead to virus escape. We analyzed the evolution in vivo of an immunodominant, HLA-A2-restricted CTL epitope and found two principal, diametrically opposed evolutionary pathways that exclusively affect T cell-receptor contact residues. One pathway was characterized by acquisition of CTL escape mutations and the other by selection for wild-type amino acids. The pattern of CTL responses to epitope variants shaped which variant(s) prevailed in the virus population. The pathways notably influenced the amount of plasma virus, as patients with efficient CTL selection had lower plasma viral loads than did patients without efficient selection. Thus, viral escape from CTL responses does not necessarily correlate with disease progression.
About this StructureAbout this Structure
2C7U is a Protein complex structure of sequences from Homo sapiens. Full crystallographic information is available from OCA.
ReferenceReference
Conflicting selective forces affect T cell receptor contacts in an immunodominant human immunodeficiency virus epitope., Iversen AK, Stewart-Jones G, Learn GH, Christie N, Sylvester-Hviid C, Armitage AE, Kaul R, Beattie T, Lee JK, Li Y, Chotiyarnwong P, Dong T, Xu X, Luscher MA, MacDonald K, Ullum H, Klarlund-Pedersen B, Skinhoj P, Fugger L, Buus S, Mullins JI, Jones EY, van der Merwe PA, McMichael AJ, Nat Immunol. 2006 Feb;7(2):179-89. Epub 2006 Jan 1. PMID:16388312
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Proteopedia Page Contributors and Editors (what is this?)Proteopedia Page Contributors and Editors (what is this?)
OCA- Pages with broken file links
- Homo sapiens
- Protein complex
- Armitage, A E.
- Beattie, T.
- Buus, S.
- Chotiyarnwong, P.
- Christie, N.
- Dong, T.
- Fugger, J L.
- Iversen, A K.
- Jones, E Y.
- Kaul, R.
- Klarlund-Pedersen, B.
- Learn, G H.
- Lee, J K.
- Li, Y.
- Luscher, M A.
- Macdonald, K.
- Mcmichael, A J.
- Merwe, P A.Van Der.
- Mullins, J I.
- Skinhoj, P.
- Stewart-Jones, G.
- Sylvester-Hviid, C.
- Ullum, H.
- Xu, X.
- Aid
- Glycoprotein
- Glycoprotein/peptide complex
- Hiv
- Hla-a2
- Immune response
- Immunoglobulin domain
- Mhc
- Mhc i
- Polymorphism
- Pyrrolidone carboxylic acid
- Tcr
- Transmembrane