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000288506 1001_ $$00000-0003-2956-1410$$aZimmermann, Cosima$$b0
000288506 245__ $$aDiverse cytomegalovirus US11 antagonism and MHC-A evasion strategies reveal a tit-for-tat coevolutionary arms race in hominids.
000288506 260__ $$aWashington, DC$$bNational Acad. of Sciences$$c2024
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000288506 520__ $$aRecurrent, ancient arms races between viruses and hosts have shaped both host immunological defense strategies as well as viral countermeasures. One such battle is waged by the glycoprotein US11 encoded by the persisting human cytomegalovirus. US11 mediates degradation of major histocompatibility class I (MHC-I) molecules to prevent CD8+ T-cell activation. Here, we studied the consequences of the arms race between US11 and primate MHC-A proteins, leading us to uncover a tit-for-tat coevolution and its impact on MHC-A diversification. We found that US11 spurred MHC-A adaptation to evade viral antagonism: In an ancestor of great apes, the MHC-A A2 lineage acquired a Pro184Ala mutation, which confers resistance against the ancestral US11 targeting strategy. In response, US11 deployed a unique low-complexity region (LCR), which exploits the MHC-I peptide loading complex to target the MHC-A2 peptide-binding groove. In addition, the global spread of the human HLA-A*02 allelic family prompted US11 to employ a superior LCR strategy with an optimally fitting peptide mimetic that specifically antagonizes HLA-A*02. Thus, despite cytomegaloviruses low pathogenic potential, the increasing commitment of US11 to MHC-A has significantly promoted diversification of MHC-A in hominids.
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000288506 650_7 $$2Other$$aHLA-A
000288506 650_7 $$2Other$$aMHC class I
000288506 650_7 $$2Other$$acoevolution
000288506 650_7 $$2Other$$acytomegalovirus
000288506 650_7 $$2Other$$atapasin
000288506 7001_ $$aWatson, Gabrielle M$$b1
000288506 7001_ $$aBauersfeld, Liane$$b2
000288506 7001_ $$00000-0001-7043-0469$$aBerry, Richard$$b3
000288506 7001_ $$aCiblis, Barbara$$b4
000288506 7001_ $$00009-0004-4790-2498$$aLan, Huan$$b5
000288506 7001_ $$aGerke, Carolin$$b6
000288506 7001_ $$aOberhardt, Valerie$$b7
000288506 7001_ $$00000-0003-1974-212X$$aFuchs, Jonas$$b8
000288506 7001_ $$00000-0001-8410-8833$$aHofmann, Maike$$b9
000288506 7001_ $$00000-0001-7416-8226$$aFreund, Christian$$b10
000288506 7001_ $$00000-0002-2020-7522$$aRossjohn, Jamie$$b11
000288506 7001_ $$0P:(DE-He78)b2290261145f21c46f2d42783c69d104$$aMomburg, Frank$$b12$$udkfz
000288506 7001_ $$00000-0002-3482-816X$$aHengel, Hartmut$$b13
000288506 7001_ $$00000-0001-6335-1017$$aHalenius, Anne$$b14
000288506 773__ $$0PERI:(DE-600)1461794-8$$a10.1073/pnas.2315985121$$gVol. 121, no. 9, p. e2315985121$$n9$$pe2315985121$$tProceedings of the National Academy of Sciences of the United States of America$$v121$$x0027-8424$$y2024
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