Association of HLA Genotype With T-Cell Activation in Human Immunodeficiency Virus (HIV) and HIV/Hepatitis C Virus–Coinfected Women

Abstract Background Global immune activation and HLA alleles are each associated with the pathogenesis of human immunodeficiency virus (HIV) and hepatitis C virus . Methods We evaluated the relationship between 44 HLA class I and 28 class II alleles and percentages of activated CD8 (CD8+CD38+DR+) an...

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Published inThe Journal of infectious diseases Vol. 221; no. 7; pp. 1156 - 1166
Main Authors Kovacs, Andrea A Z, Kono, Naoko, Wang, Chia-Hao, Wang, Daidong, Frederick, Toni, Operskalski, Eva, Tien, Phyllis C, French, Audrey L, Minkoff, Howard, Kassaye, Seble, T. Golub, Elizabeth, Aouizerat, Bradley E, Kuniholm, Mark H, Millstein, Joshua
Format Journal Article
LanguageEnglish
Published US Oxford University Press 16.03.2020
Subjects
Adolescent
Adult
Aged
Alleles
Antiretroviral drugs
Antiretroviral Therapy, Highly Active
CD38 antigen
CD4 antigen
CD8 antigen
Cell activation
Cohort Studies
Coinfection - complications
Coinfection - epidemiology
Coinfection - genetics
Coinfection - immunology
DQA1 protein
Drb1 protein
Female
Genotype
Genotypes
Hepatitis
Hepatitis C
Hepatitis C - complications
Hepatitis C - epidemiology
Hepatitis C - genetics
Hepatitis C - immunology
Highly active antiretroviral therapy
Histocompatibility antigen HLA
HIV
HIV Infections - complications
HIV Infections - epidemiology
HIV Infections - genetics
HIV Infections - immunology
HLA Antigens - genetics
Human immunodeficiency virus
Humans
Lymphocyte Activation - genetics
Lymphocytes
Lymphocytes T
Major and Brief Reports
Middle Aged
Pathogenesis
Regression analysis
Womens health
Young Adult
HCV
HIV
HLA
immune activation
T-cell activation
Online AccessGet full text

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Abstract Abstract Background Global immune activation and HLA alleles are each associated with the pathogenesis of human immunodeficiency virus (HIV) and hepatitis C virus . Methods We evaluated the relationship between 44 HLA class I and 28 class II alleles and percentages of activated CD8 (CD8+CD38+DR+) and CD4 (CD4+CD38+DR+) T cells in 586 women who were naive to highly active antiretroviral therapy. We used linear generalized estimating equation regression models, adjusting for race/ethnicity, age, HIV load, and hepatitis C virus infection and controlling for multiplicity using a false discovery rate threshold of 0.10. Results Ten HLA alleles were associated with CD8 and/or CD4 T-cell activation. Lower percentages of activated CD8 and/or CD4 T cells were associated with protective alleles B*57:03 (CD8 T cells, −6.6% [P = .002]; CD4 T cells, −2.7% [P = .007]), C*18:01 (CD8 T cells, −6.6%; P < .0008) and DRB1*13:01 (CD4 T cells, −2.7%; P < .0004), and higher percentages were found with B*18:01 (CD8 T cells, 6.2%; P < .0003), a detrimental allele. Other alleles/allele groups associated with activation included C*12:03, group DQA1*01:00, DQB1*03:01, DQB1*03:02, DQB1*06:02, and DQB1*06:03. Conclusion These findings suggest that a person’s HLA type may play a role in modulating T-cell activation independent of viral load and sheds light on the relationship between HLA, T-cell activation, immune control, and HIV pathogenesis. We found that specific HLA alleles predict CD8 and CD4 T-cell activation, independent of HLA associations with viral load. These findings suggest that host genetic variation could affect risk for end-organ diseases through an immune activation mechanism.
AbstractList Global immune activation and HLA alleles are each associated with the pathogenesis of human immunodeficiency virus (HIV) and hepatitis C virus .BACKGROUNDGlobal immune activation and HLA alleles are each associated with the pathogenesis of human immunodeficiency virus (HIV) and hepatitis C virus .We evaluated the relationship between 44 HLA class I and 28 class II alleles and percentages of activated CD8 (CD8+CD38+DR+) and CD4 (CD4+CD38+DR+) T cells in 586 women who were naive to highly active antiretroviral therapy. We used linear generalized estimating equation regression models, adjusting for race/ethnicity, age, HIV load, and hepatitis C virus infection and controlling for multiplicity using a false discovery rate threshold of 0.10.METHODSWe evaluated the relationship between 44 HLA class I and 28 class II alleles and percentages of activated CD8 (CD8+CD38+DR+) and CD4 (CD4+CD38+DR+) T cells in 586 women who were naive to highly active antiretroviral therapy. We used linear generalized estimating equation regression models, adjusting for race/ethnicity, age, HIV load, and hepatitis C virus infection and controlling for multiplicity using a false discovery rate threshold of 0.10.Ten HLA alleles were associated with CD8 and/or CD4 T-cell activation. Lower percentages of activated CD8 and/or CD4 T cells were associated with protective alleles B*57:03 (CD8 T cells, -6.6% [P = .002]; CD4 T cells, -2.7% [P = .007]), C*18:01 (CD8 T cells, -6.6%; P < .0008) and DRB1*13:01 (CD4 T cells, -2.7%; P < .0004), and higher percentages were found with B*18:01 (CD8 T cells, 6.2%; P < .0003), a detrimental allele. Other alleles/allele groups associated with activation included C*12:03, group DQA1*01:00, DQB1*03:01, DQB1*03:02, DQB1*06:02, and DQB1*06:03.RESULTSTen HLA alleles were associated with CD8 and/or CD4 T-cell activation. Lower percentages of activated CD8 and/or CD4 T cells were associated with protective alleles B*57:03 (CD8 T cells, -6.6% [P = .002]; CD4 T cells, -2.7% [P = .007]), C*18:01 (CD8 T cells, -6.6%; P < .0008) and DRB1*13:01 (CD4 T cells, -2.7%; P < .0004), and higher percentages were found with B*18:01 (CD8 T cells, 6.2%; P < .0003), a detrimental allele. Other alleles/allele groups associated with activation included C*12:03, group DQA1*01:00, DQB1*03:01, DQB1*03:02, DQB1*06:02, and DQB1*06:03.These findings suggest that a person's HLA type may play a role in modulating T-cell activation independent of viral load and sheds light on the relationship between HLA, T-cell activation, immune control, and HIV pathogenesis.CONCLUSIONThese findings suggest that a person's HLA type may play a role in modulating T-cell activation independent of viral load and sheds light on the relationship between HLA, T-cell activation, immune control, and HIV pathogenesis.
Global immune activation and HLA alleles are each associated with the pathogenesis of human immunodeficiency virus (HIV) and hepatitis C virus . We evaluated the relationship between 44 HLA class I and 28 class II alleles and percentages of activated CD8 (CD8+CD38+DR+) and CD4 (CD4+CD38+DR+) T cells in 586 women who were naive to highly active antiretroviral therapy. We used linear generalized estimating equation regression models, adjusting for race/ethnicity, age, HIV load, and hepatitis C virus infection and controlling for multiplicity using a false discovery rate threshold of 0.10. Ten HLA alleles were associated with CD8 and/or CD4 T-cell activation. Lower percentages of activated CD8 and/or CD4 T cells were associated with protective alleles B*57:03 (CD8 T cells, -6.6% [P = .002]; CD4 T cells, -2.7% [P = .007]), C*18:01 (CD8 T cells, -6.6%; P < .0008) and DRB1*13:01 (CD4 T cells, -2.7%; P < .0004), and higher percentages were found with B*18:01 (CD8 T cells, 6.2%; P < .0003), a detrimental allele. Other alleles/allele groups associated with activation included C*12:03, group DQA1*01:00, DQB1*03:01, DQB1*03:02, DQB1*06:02, and DQB1*06:03. These findings suggest that a person's HLA type may play a role in modulating T-cell activation independent of viral load and sheds light on the relationship between HLA, T-cell activation, immune control, and HIV pathogenesis.
Background Global immune activation and HLA alleles are each associated with the pathogenesis of human immunodeficiency virus (HIV) and hepatitis C virus . Methods We evaluated the relationship between 44 HLA class I and 28 class II alleles and percentages of activated CD8 (CD8+CD38+DR+) and CD4 (CD4+CD38+DR+) T cells in 586 women who were naive to highly active antiretroviral therapy. We used linear generalized estimating equation regression models, adjusting for race/ethnicity, age, HIV load, and hepatitis C virus infection and controlling for multiplicity using a false discovery rate threshold of 0.10. Results Ten HLA alleles were associated with CD8 and/or CD4 T-cell activation. Lower percentages of activated CD8 and/or CD4 T cells were associated with protective alleles B*57:03 (CD8 T cells, −6.6% [P = .002]; CD4 T cells, −2.7% [P = .007]), C*18:01 (CD8 T cells, −6.6%; P < .0008) and DRB1*13:01 (CD4 T cells, −2.7%; P < .0004), and higher percentages were found with B*18:01 (CD8 T cells, 6.2%; P < .0003), a detrimental allele. Other alleles/allele groups associated with activation included C*12:03, group DQA1*01:00, DQB1*03:01, DQB1*03:02, DQB1*06:02, and DQB1*06:03. Conclusion These findings suggest that a person’s HLA type may play a role in modulating T-cell activation independent of viral load and sheds light on the relationship between HLA, T-cell activation, immune control, and HIV pathogenesis.
Abstract Background Global immune activation and HLA alleles are each associated with the pathogenesis of human immunodeficiency virus (HIV) and hepatitis C virus . Methods We evaluated the relationship between 44 HLA class I and 28 class II alleles and percentages of activated CD8 (CD8+CD38+DR+) and CD4 (CD4+CD38+DR+) T cells in 586 women who were naive to highly active antiretroviral therapy. We used linear generalized estimating equation regression models, adjusting for race/ethnicity, age, HIV load, and hepatitis C virus infection and controlling for multiplicity using a false discovery rate threshold of 0.10. Results Ten HLA alleles were associated with CD8 and/or CD4 T-cell activation. Lower percentages of activated CD8 and/or CD4 T cells were associated with protective alleles B*57:03 (CD8 T cells, −6.6% [P = .002]; CD4 T cells, −2.7% [P = .007]), C*18:01 (CD8 T cells, −6.6%; P < .0008) and DRB1*13:01 (CD4 T cells, −2.7%; P < .0004), and higher percentages were found with B*18:01 (CD8 T cells, 6.2%; P < .0003), a detrimental allele. Other alleles/allele groups associated with activation included C*12:03, group DQA1*01:00, DQB1*03:01, DQB1*03:02, DQB1*06:02, and DQB1*06:03. Conclusion These findings suggest that a person’s HLA type may play a role in modulating T-cell activation independent of viral load and sheds light on the relationship between HLA, T-cell activation, immune control, and HIV pathogenesis. We found that specific HLA alleles predict CD8 and CD4 T-cell activation, independent of HLA associations with viral load. These findings suggest that host genetic variation could affect risk for end-organ diseases through an immune activation mechanism.
We found that specific HLA alleles predict CD8 and CD4 T-cell activation, independent of HLA associations with viral load. These findings suggest that host genetic variation could affect risk for end-organ diseases through an immune activation mechanism.
Author Operskalski, Eva
Kassaye, Seble
Wang, Chia-Hao
Kovacs, Andrea A Z
Frederick, Toni
Tien, Phyllis C
Wang, Daidong
Minkoff, Howard
Kono, Naoko
Aouizerat, Bradley E
T. Golub, Elizabeth
Kuniholm, Mark H
Millstein, Joshua
French, Audrey L
AuthorAffiliation 4 Department of Medicine, University of California, San Francisco and Department of Veterans Affairs , San Francisco, California
2 Department of Preventive Medicine, Keck School of Medicine, University of Southern California , Los Angeles, California
1 Department of Pediatrics, Maternal, Child and Adolescent Center for Infectious Diseases and Virology, Keck School of Medicine, University of Southern California , Los Angeles, California
9 Bluestone Center for Clinical Research, New York University , New York, New York
7 Department of Medicine, Georgetown University School of Medicine , Washington, DC
6 Departments of Obstetrics and Gynecology Maimonides Medical Center and SUNY Downstate , Brooklyn, New York
8 Johns Hopkins Bloomberg School of Public Health, Department of Epidemiology , Baltimore, Maryland
11 Department of Epidemiology and Biostatistics, University at Albany, State University of New York , Rensselaer, New York
3 City of Hope National Medical Center , Duarte, California
10 Departm
AuthorAffiliation_xml – name: 1 Department of Pediatrics, Maternal, Child and Adolescent Center for Infectious Diseases and Virology, Keck School of Medicine, University of Southern California , Los Angeles, California
– name: 4 Department of Medicine, University of California, San Francisco and Department of Veterans Affairs , San Francisco, California
– name: 7 Department of Medicine, Georgetown University School of Medicine , Washington, DC
– name: 6 Departments of Obstetrics and Gynecology Maimonides Medical Center and SUNY Downstate , Brooklyn, New York
– name: 10 Department of Oral and Maxillofacial Surgery, New York University , New York, New York
– name: 3 City of Hope National Medical Center , Duarte, California
– name: 8 Johns Hopkins Bloomberg School of Public Health, Department of Epidemiology , Baltimore, Maryland
– name: 2 Department of Preventive Medicine, Keck School of Medicine, University of Southern California , Los Angeles, California
– name: 9 Bluestone Center for Clinical Research, New York University , New York, New York
– name: 11 Department of Epidemiology and Biostatistics, University at Albany, State University of New York , Rensselaer, New York
– name: 5 Department of Medicine, Stroger Hospital of Cook County/CORE Center, Rush Medical School , Chicago, Illinois
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  surname: Wang
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  organization: Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, California
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ContentType Journal Article
Copyright The Author(s) 2019. Published by Oxford University Press for the Infectious Diseases Society of America. All rights reserved. For permissions, e-mail: journals.permissions@oup.com. 2019
The Author(s) 2019. Published by Oxford University Press for the Infectious Diseases Society of America. All rights reserved. For permissions, e-mail: journals.permissions@oup.com.
Copyright_xml – notice: The Author(s) 2019. Published by Oxford University Press for the Infectious Diseases Society of America. All rights reserved. For permissions, e-mail: journals.permissions@oup.com. 2019
– notice: The Author(s) 2019. Published by Oxford University Press for the Infectious Diseases Society of America. All rights reserved. For permissions, e-mail: journals.permissions@oup.com.
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1537-6613
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Issue 7
Keywords HCV
HIV
HLA
immune activation
T-cell activation
Language English
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M. H. K. and J. M. contributed equally to the manuscript.
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PMID 31802115
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Snippet Abstract Background Global immune activation and HLA alleles are each associated with the pathogenesis of human immunodeficiency virus (HIV) and hepatitis C...
Global immune activation and HLA alleles are each associated with the pathogenesis of human immunodeficiency virus (HIV) and hepatitis C virus . We evaluated...
Background Global immune activation and HLA alleles are each associated with the pathogenesis of human immunodeficiency virus (HIV) and hepatitis C virus ....
Global immune activation and HLA alleles are each associated with the pathogenesis of human immunodeficiency virus (HIV) and hepatitis C virus...
We found that specific HLA alleles predict CD8 and CD4 T-cell activation, independent of HLA associations with viral load. These findings suggest that host...
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SubjectTerms Adolescent
Adult
Aged
Alleles
Antiretroviral drugs
Antiretroviral Therapy, Highly Active
CD38 antigen
CD4 antigen
CD8 antigen
Cell activation
Cohort Studies
Coinfection - complications
Coinfection - epidemiology
Coinfection - genetics
Coinfection - immunology
DQA1 protein
Drb1 protein
Female
Genotype
Genotypes
Hepatitis
Hepatitis C
Hepatitis C - complications
Hepatitis C - epidemiology
Hepatitis C - genetics
Hepatitis C - immunology
Highly active antiretroviral therapy
Histocompatibility antigen HLA
HIV
HIV Infections - complications
HIV Infections - epidemiology
HIV Infections - genetics
HIV Infections - immunology
HLA Antigens - genetics
Human immunodeficiency virus
Humans
Lymphocyte Activation - genetics
Lymphocytes
Lymphocytes T
Major and Brief Reports
Middle Aged
Pathogenesis
Regression analysis
Womens health
Young Adult
Title Association of HLA Genotype With T-Cell Activation in Human Immunodeficiency Virus (HIV) and HIV/Hepatitis C Virus–Coinfected Women
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Volume 221
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