Human herpesvirus diversity is altered in HLA class I binding peptides

Human herpesvirus diversity is altered in HLA class I binding peptides

[Significance] Viruses evolve to evade immune recognition that may otherwise limit transmission. Presentation of virus peptides by human leukocyte antigen (HLA) class I is a necessary step in the recognition of infection by immune cells. Virus adaptation to evade this immune recognition has not been formally tested across the diversity of HLA class I allotypes and virus strains. We analyzed genetic diversity of three human herpesviruses across peptides that bind diverse HLA class I allotypes. We find that adaptation to evade HLA class I recognition may be a general phenomenon shaping human herpesvirus genetic diversity, particularly for those proteins expressed during viral latency. This broad scope, across human and virus diversity, provides a unique comparative perspective of human–herpesvirus coevolution.

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Bibliographic Details
Main Authors: Palmer, William H., Telford, Marco, Navarro, Arcadi, Santpere, Gabriel, Norman, Paul J.
Other Authors: National Institutes of Health (US)
Format: artículo biblioteca
Language:English
Published: National Academy of Sciences (U.S.) 2022-04-29
Subjects:HLA, Herpesvirus, Population genetics, EBV, HCMV,
Online Access:http://hdl.handle.net/10261/272143
http://dx.doi.org/10.13039/501100011033
http://dx.doi.org/10.13039/501100000780
http://dx.doi.org/10.13039/501100004587
http://dx.doi.org/10.13039/501100004837
http://dx.doi.org/10.13039/501100003329
http://dx.doi.org/10.13039/100000002
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id dig-ibe-es-10261-272143
record_format koha
institution IBE ES
collection DSpace
country España
countrycode ES
component Bibliográfico
access En linea
databasecode dig-ibe-es
tag biblioteca
region Europa del Sur
libraryname Biblioteca del IBE España
language English
topic HLA
Herpesvirus
Population genetics
EBV
HCMV
HLA
Herpesvirus
Population genetics
EBV
HCMV
spellingShingle HLA
Herpesvirus
Population genetics
EBV
HCMV
HLA
Herpesvirus
Population genetics
EBV
HCMV
Palmer, William H.
Telford, Marco
Navarro, Arcadi
Santpere, Gabriel
Norman, Paul J.
Human herpesvirus diversity is altered in HLA class I binding peptides
description [Significance] Viruses evolve to evade immune recognition that may otherwise limit transmission. Presentation of virus peptides by human leukocyte antigen (HLA) class I is a necessary step in the recognition of infection by immune cells. Virus adaptation to evade this immune recognition has not been formally tested across the diversity of HLA class I allotypes and virus strains. We analyzed genetic diversity of three human herpesviruses across peptides that bind diverse HLA class I allotypes. We find that adaptation to evade HLA class I recognition may be a general phenomenon shaping human herpesvirus genetic diversity, particularly for those proteins expressed during viral latency. This broad scope, across human and virus diversity, provides a unique comparative perspective of human–herpesvirus coevolution.
author2 National Institutes of Health (US)
author_facet National Institutes of Health (US)
Palmer, William H.
Telford, Marco
Navarro, Arcadi
Santpere, Gabriel
Norman, Paul J.
format artículo
topic_facet HLA
Herpesvirus
Population genetics
EBV
HCMV
author Palmer, William H.
Telford, Marco
Navarro, Arcadi
Santpere, Gabriel
Norman, Paul J.
author_sort Palmer, William H.
title Human herpesvirus diversity is altered in HLA class I binding peptides
title_short Human herpesvirus diversity is altered in HLA class I binding peptides
title_full Human herpesvirus diversity is altered in HLA class I binding peptides
title_fullStr Human herpesvirus diversity is altered in HLA class I binding peptides
title_full_unstemmed Human herpesvirus diversity is altered in HLA class I binding peptides
title_sort human herpesvirus diversity is altered in hla class i binding peptides
publisher National Academy of Sciences (U.S.)
publishDate 2022-04-29
url http://hdl.handle.net/10261/272143
http://dx.doi.org/10.13039/501100011033
http://dx.doi.org/10.13039/501100000780
http://dx.doi.org/10.13039/501100004587
http://dx.doi.org/10.13039/501100004837
http://dx.doi.org/10.13039/501100003329
http://dx.doi.org/10.13039/100000002
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AT navarroarcadi humanherpesvirusdiversityisalteredinhlaclassibindingpeptides
AT santperegabriel humanherpesvirusdiversityisalteredinhlaclassibindingpeptides
AT normanpaulj humanherpesvirusdiversityisalteredinhlaclassibindingpeptides
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spelling dig-ibe-es-10261-2721432022-07-16T02:44:30Z Human herpesvirus diversity is altered in HLA class I binding peptides Palmer, William H. Telford, Marco Navarro, Arcadi Santpere, Gabriel Norman, Paul J. National Institutes of Health (US) Ministerio de Ciencia e Innovación (España) Ministerio de Economía y Competitividad (España) European Commission Instituto de Salud Carlos III Agencia Estatal de Investigación (España) HLA Herpesvirus Population genetics EBV HCMV [Significance] Viruses evolve to evade immune recognition that may otherwise limit transmission. Presentation of virus peptides by human leukocyte antigen (HLA) class I is a necessary step in the recognition of infection by immune cells. Virus adaptation to evade this immune recognition has not been formally tested across the diversity of HLA class I allotypes and virus strains. We analyzed genetic diversity of three human herpesviruses across peptides that bind diverse HLA class I allotypes. We find that adaptation to evade HLA class I recognition may be a general phenomenon shaping human herpesvirus genetic diversity, particularly for those proteins expressed during viral latency. This broad scope, across human and virus diversity, provides a unique comparative perspective of human–herpesvirus coevolution. Herpesviruses are ubiquitous, genetically diverse DNA viruses, with long-term presence in humans associated with infrequent but significant pathology. Human leukocyte antigen (HLA) class I presents intracellularly derived peptide fragments from infected tissue cells to CD8+ T and natural killer cells, thereby directing antiviral immunity. Allotypes of highly polymorphic HLA class I are distinguished by their peptide binding repertoires. Because this HLA class I variation is a major determinant of herpesvirus disease, we examined if sequence diversity of virus proteins reflects evasion of HLA presentation. Using population genomic data from Epstein–Barr virus (EBV), human cytomegalovirus (HCMV), and Varicella–Zoster virus, we tested whether diversity differed between the regions of herpesvirus proteins that can be recognized, or not, by HLA class I. Herpesviruses exhibit lytic and latent infection stages, with the latter better enabling immune evasion. Whereas HLA binding peptides of lytic proteins are conserved, we found that EBV and HCMV proteins expressed during latency have increased peptide sequence diversity. Similarly, latent, but not lytic, herpesvirus proteins have greater population structure in HLA binding than nonbinding peptides. Finally, we found patterns consistent with EBV adaption to the local HLA environment, with less efficient recognition of EBV isolates by high-frequency HLA class I allotypes. Here, the frequency of CD8+ T cell epitopes inversely correlated with the frequency of HLA class I recognition. Previous analyses have shown that pathogen-mediated natural selection maintains exceptional polymorphism in HLA residues that determine peptide recognition. Here, we show that HLA class I peptide recognition impacts diversity of globally widespread pathogens. This work was supported AQ15 by NIH Grants R56AI151549 (to P.J.N) and R01 AI158410 (to P.J.N). W.H.P is supported by NIHGrant F32 AI161790. A.N. is supported by Ministerio de Ciencia e Innovación,Spain Grant PGC2018-101927-B-I00, Ministerio de Economía y Competitividad/Fondo Europeo de Desarrollo Regional, Union Europea and by“Unidad de Exce-lencia María de Maeztu funded by MINECO Grant MDM-2014-0370. G.S. is sup-ported by Instituto de Salud Carlos III (Spain) Grant MS20/00064 and cofundedby European Social Fund Grant PID2019-104700GA-I00 funded by Agencia Estatal de Investigación, Spain and NIH Grant R01HG010898-01. Peer reviewed 2022-06-10T07:14:07Z 2022-06-10T07:14:07Z 2022-04-29 artículo Proceedings of the National Academy of Sciences 119 (18): e2123248119 (2022) 0027-8424 1091-6490 http://hdl.handle.net/10261/272143 10.1073/pnas.212324811 http://dx.doi.org/10.13039/501100011033 http://dx.doi.org/10.13039/501100000780 http://dx.doi.org/10.13039/501100004587 http://dx.doi.org/10.13039/501100004837 http://dx.doi.org/10.13039/501100003329 http://dx.doi.org/10.13039/100000002 en #PLACEHOLDER_PARENT_METADATA_VALUE# #PLACEHOLDER_PARENT_METADATA_VALUE# #PLACEHOLDER_PARENT_METADATA_VALUE# info:eu-repo/grantAgreement/AEI/Plan Estatal de Investigación Científica y Técnica y de Innovación 2017-2020/PGC2018-101927-B-I00/ES/LAS CAUSAS EVOLUTIVAS Y MECANICAS DE LA SENESCENCIA Y SUS FENOTIPOS RELACIONADOS EN VERTEBRADOS: UNA APROXIMACION DE GENOMICA COMPARADA/ info:eu-repo/grantAgreement/MINECO//MDM-2014-0370/ES/DPTO. CIENCIAS EXPERIMENTALES Y DE LA SALUD/ info:eu-repo/grantAgreement/AEI/Plan Estatal de Investigación Científica y Técnica y de Innovación 2017-2020/PID2019-104700GA-I00/ES/TAXONOMIA DE LA UNION DE FACTORES DE TRANSCRIPCION EN EL GENOMA COMPLETO DE PRIMATES PARA EL ESTUDIO DE ESPECIALIZACIONES DEL CEREBRO HUMANO EN SALUD Y EN ENFERMEDAD/ Sí open National Academy of Sciences (U.S.)

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