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Untitled

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The following section was removed as it showed no relevance with HLA-A

Further reading

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  • Geyer M, Fackler OT, Peterlin BM (2001). "Structure--function relationships in HIV-1 Nef". EMBO Rep. 2 (7): 580–5. doi:10.1093/embo-reports/kve141. PMID 11463741.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  • Greenway AL, Holloway G, McPhee DA; et al. (2004). "HIV-1 Nef control of cell signalling molecules: multiple strategies to promote virus replication". J. Biosci. 28 (3): 323–35. PMID 12734410. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  • Scolari F (2003). "Inherited forms of IgA nephropathy". J. Nephrol. 16 (2): 317–20. PMID 12768083.
  • Bénichou S, Benmerah A (2003). "[The HIV nef and the Kaposi-sarcoma-associated virus K3/K5 proteins: "parasites"of the endocytosis pathway]". Med Sci (Paris). 19 (1): 100–6. PMID 12836198.
  • Leavitt SA, SchOn A, Klein JC; et al. (2004). "Interactions of HIV-1 proteins gp120 and Nef with cellular partners define a novel allosteric paradigm". Curr. Protein Pept. Sci. 5 (1): 1–8. PMID 14965316. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  • Tolstrup M, Ostergaard L, Laursen AL; et al. (2004). "HIV/SIV escape from immune surveillance: focus on Nef". Curr. HIV Res. 2 (2): 141–51. PMID 15078178. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  • Joseph AM, Kumar M, Mitra D (2005). "Nef: "necessary and enforcing factor" in HIV infection". Curr. HIV Res. 3 (1): 87–94. PMID 15638726.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  • Anderson JL, Hope TJ (2005). "HIV accessory proteins and surviving the host cell". Current HIV/AIDS reports. 1 (1): 47–53. PMID 16091223.
  • Li L, Li HS, Pauza CD; et al. (2006). "Roles of HIV-1 auxiliary proteins in viral pathogenesis and host-pathogen interactions". Cell Res. 15 (11–12): 923–34. doi:10.1038/sj.cr.7290370. PMID 16354571. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  • Stove V, Verhasselt B (2006). "Modelling thymic HIV-1 Nef effects". Curr. HIV Res. 4 (1): 57–64. PMID 16454711.

Major rewrite

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I understand this article was due for a clean-up. I have restructured the article and cleaned-up.

  • Restructured the protein-box, created a new protein box that handles heterodimers _cleanly_
  • Created a new section for the HLA-A gene.
  • Reworked tables so they are compact and fit between text.
  • Moved historical guide to new page.
  • Cleaned up the HLA-A gene infobox will move structures to pertinent HLA-Ax pages when I have time.
    • The New protein boxes are non-compact, I believe this is due to transludation which often introduces unneccesary spaces, I see alot of problems in the boxes for HLA, there should be a separate instance of the box used for HLA genes.

PB666 yap 14:06, 15 August 2008 (UTC)[reply]

Archaic Hominid Introgression

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From "Origin and plasticity of MHC I-associated self peptides" Nov 12, 2011 (Accessible link)

  • The TCR of classic adaptive CD8 T cells recognizes MHC I-associated peptides (MIPs). MHC I genes are polygenic, extremely polymorphic and represent the most conserved MHC genes. In most modern human populations, the majority of MHC I alleles have been acquired by introgression from archaic humans (Neanderthals and Denisovans)

From "The Shaping of Modern Human Immune Systems by Multiregional Admixture with Archaic Humans" August 25 2011 (Accessible link)

  • From the combined frequencies of these six alleles, we estimate the putative archaic HLA-A ancestry to be >50% in Europe, >70% in Asia, and >95% in parts of PNG (Fig. 4, C and D). These estimates for HLA class I arc much higher than the genome-wide estimates of introgression (1-6%), showing how limited interbreeding with archaic humans has, in combination with natural selection, significantly shaped the HLA system in modern human populations outside of Africa. Our results demonstrate how highly polymorphic HLA genes can be sensitive probes of introgression, and we predict the same will apply to other polymorphic immunesystem genes, for example the killer-cell immunoglobulin-like receptors (KIR) of NK cells. Present in the Denisovan genome (11), a candidate KIR for introgression is KIR3DS1 *013 (Fig. 4E), rare in sub-Saharan Africans, but the most common KIR3DL1/S1 allele outside Africa (24).

From "Virus-hunter gatherers" October 2011 (Accessible link)

  • And could this have been a dangerous liaison? Human HLA alleles that are associated with autoimmune diseases were present in Denisovans. Study co-author Paul Norman proposes that when we acquired those genes "we weren't kind of prepared for them, we hadn't grown up with them ... they can start to attack us as well as the viruses" (Today Online, 27 Aug 2011).

Slartibartfastibast (talk) 02:10, 17 November 2011 (UTC)[reply]