Human Endogenous Retrovirus Expression Is Inversely Associated with Chronic Immune Activation in HIV-1 Infection

Human endogenous retroviruses (HERV) are remnants of ancestral retroviral infections integrated into the germ line, and constitute approximately 8% of the genome. Several autoimmune disorders, malignancies, and infectious diseases such as HIV-1 are associated with higher HERV expression. The degree...

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Published inPloS one Vol. 7; no. 8; p. e41021
Main Authors Ormsby, Christopher E., SenGupta, Devi, Tandon, Ravi, Deeks, Steven G., Martin, Jeffrey N., Jones, R. Brad, Ostrowski, Mario A., Garrison, Keith E., Vázquez-Pérez, Joel A., Reyes-Terán, Gustavo, Nixon, Douglas F.
Format Journal Article
LanguageEnglish
Published United States Public Library of Science 07.08.2012
Public Library of Science (PLoS)
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Online AccessGet full text
ISSN1932-6203
1932-6203
DOI10.1371/journal.pone.0041021

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Abstract Human endogenous retroviruses (HERV) are remnants of ancestral retroviral infections integrated into the germ line, and constitute approximately 8% of the genome. Several autoimmune disorders, malignancies, and infectious diseases such as HIV-1 are associated with higher HERV expression. The degree to which HERV expression in vivo results in persistent inflammation is not known. We studied the association of immune activation and HERV-K expression in 20 subjects with chronic, untreated progressive HIV-1 infection and 10 HIV-1 negative controls. The mean HERV-K gag and env RNA expression level in the HIV-1 infected cohort was higher than in the control group (p = 0.0003), and was negatively correlated with the frequency of activated CD38+HLA-DR+CD4+ T cells (Rho = -0.61; p = 0.01) and activated CD38+HLA-DR+CD8+ T cells (Rho = -0.51; p = 0.03). Although HIV-infected persons had higher levels of HERV-K RNA expression (as expected), the level of RNA expression was negatively associated with level of T cell activation. The mechanism for this unexpected association remains to be defined.
AbstractList Human endogenous retroviruses (HERV) are remnants of ancestral retroviral infections integrated into the germ line, and constitute approximately 8% of the genome. Several autoimmune disorders, malignancies, and infectious diseases such as HIV-1 are associated with higher HERV expression. The degree to which HERV expression in vivo results in persistent inflammation is not known. We studied the association of immune activation and HERV-K expression in 20 subjects with chronic, untreated progressive HIV-1 infection and 10 HIV-1 negative controls. The mean HERV-K gag and env RNA expression level in the HIV-1 infected cohort was higher than in the control group (p = 0.0003), and was negatively correlated with the frequency of activated CD38+HLA-DR+CD4+ T cells (Rho = −0.61; p = 0.01) and activated CD38+HLA-DR+CD8+ T cells (Rho  = −0.51; p = 0.03). Although HIV-infected persons had higher levels of HERV-K RNA expression (as expected), the level of RNA expression was negatively associated with level of T cell activation. The mechanism for this unexpected association remains to be defined.
Human endogenous retroviruses (HERV) are remnants of ancestral retroviral infections integrated into the germ line, and constitute approximately 8% of the genome. Several autoimmune disorders, malignancies, and infectious diseases such as HIV-1 are associated with higher HERV expression. The degree to which HERV expression in vivo results in persistent inflammation is not known. We studied the association of immune activation and HERV-K expression in 20 subjects with chronic, untreated progressive HIV-1 infection and 10 HIV-1 negative controls. The mean HERV-K gag and env RNA expression level in the HIV-1 infected cohort was higher than in the control group (p = 0.0003), and was negatively correlated with the frequency of activated CD38+HLA-DR+CD4+ T cells (Rho = -0.61; p = 0.01) and activated CD38+HLA-DR+CD8+ T cells (Rho = -0.51; p = 0.03). Although HIV-infected persons had higher levels of HERV-K RNA expression (as expected), the level of RNA expression was negatively associated with level of T cell activation. The mechanism for this unexpected association remains to be defined.
Human endogenous retroviruses (HERV) are remnants of ancestral retroviral infections integrated into the germ line, and constitute approximately 8% of the genome. Several autoimmune disorders, malignancies, and infectious diseases such as HIV-1 are associated with higher HERV expression. The degree to which HERV expression in vivo results in persistent inflammation is not known. We studied the association of immune activation and HERV-K expression in 20 subjects with chronic, untreated progressive HIV-1 infection and 10 HIV-1 negative controls. The mean HERV-K gag and env RNA expression level in the HIV-1 infected cohort was higher than in the control group (p = 0.0003), and was negatively correlated with the frequency of activated CD38+HLA-DR+CD4+ T cells (Rho = -0.61; p = 0.01) and activated CD38+HLA-DR+CD8+ T cells (Rho = -0.51; p = 0.03). Although HIV-infected persons had higher levels of HERV-K RNA expression (as expected), the level of RNA expression was negatively associated with level of T cell activation. The mechanism for this unexpected association remains to be defined.Human endogenous retroviruses (HERV) are remnants of ancestral retroviral infections integrated into the germ line, and constitute approximately 8% of the genome. Several autoimmune disorders, malignancies, and infectious diseases such as HIV-1 are associated with higher HERV expression. The degree to which HERV expression in vivo results in persistent inflammation is not known. We studied the association of immune activation and HERV-K expression in 20 subjects with chronic, untreated progressive HIV-1 infection and 10 HIV-1 negative controls. The mean HERV-K gag and env RNA expression level in the HIV-1 infected cohort was higher than in the control group (p = 0.0003), and was negatively correlated with the frequency of activated CD38+HLA-DR+CD4+ T cells (Rho = -0.61; p = 0.01) and activated CD38+HLA-DR+CD8+ T cells (Rho = -0.51; p = 0.03). Although HIV-infected persons had higher levels of HERV-K RNA expression (as expected), the level of RNA expression was negatively associated with level of T cell activation. The mechanism for this unexpected association remains to be defined.
Human endogenous retroviruses (HERV) are remnants of ancestral retroviral infections integrated into the germ line, and constitute approximately 8% of the genome. Several autoimmune disorders, malignancies, and infectious diseases such as HIV-1 are associated with higher HERV expression. The degree to which HERV expression in vivo results in persistent inflammation is not known. We studied the association of immune activation and HERV-K expression in 20 subjects with chronic, untreated progressive HIV-1 infection and 10 HIV-1 negative controls. The mean HERV-K gag and env RNA expression level in the HIV-1 infected cohort was higher than in the control group (p = 0.0003), and was negatively correlated with the frequency of activated CD38+HLA-DR+CD4+ T cells (Rho = −0.61; p = 0.01) and activated CD38+HLA-DR+CD8+ T cells (Rho  = −0.51; p = 0.03). Although HIV-infected persons had higher levels of HERV-K RNA expression (as expected), the level of RNA expression was negatively associated with level of T cell activation. The mechanism for this unexpected association remains to be defined.
Audience Academic
Author SenGupta, Devi
Nixon, Douglas F.
Tandon, Ravi
Ostrowski, Mario A.
Deeks, Steven G.
Vázquez-Pérez, Joel A.
Reyes-Terán, Gustavo
Ormsby, Christopher E.
Martin, Jeffrey N.
Garrison, Keith E.
Jones, R. Brad
AuthorAffiliation Imperial College London, United Kingdom
1 Center for Research in Infectious Diseases, National Institute of Respiratory Diseases, Mexico City, Federal District, Mexico
3 Positive Health Program, San Francisco General Hospital, San Francisco, California, United States of America
4 Department of Epidemiology and Biostatistics, University of California San Francisco, San Francisco, California, United States of America
2 Division of Experimental Medicine, Department of Medicine, University of California San Francisco, San Francisco, California, United States of America
5 Department of Immunology, University of Toronto, Toronto, Ontario, Canada
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/22879884$$D View this record in MEDLINE/PubMed
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2012 Ormsby et al 2012 Ormsby et al
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Conceived and designed the experiments: CEO DS RT DFN. Performed the experiments: CEO DS RT. Analyzed the data: CEO DS RT JVP. Contributed reagents/materials/analysis tools: SGD JNM RBJ MAO KEG. Wrote the paper: CEO DS RT JVP GRT DFN.
Competing Interests: The authors have declared that no competing interests exist.
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PublicationDecade 2010
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PublicationTitle PloS one
PublicationTitleAlternate PLoS One
PublicationYear 2012
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Snippet Human endogenous retroviruses (HERV) are remnants of ancestral retroviral infections integrated into the germ line, and constitute approximately 8% of the...
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SubjectTerms Adult
Antiretroviral drugs
Apoptosis
Autoimmune diseases
Biology
Breast cancer
Case-Control Studies
CD38 antigen
CD4 antigen
CD4-Positive T-Lymphocytes - immunology
CD4-Positive T-Lymphocytes - virology
CD8 antigen
CD8-Positive T-Lymphocytes - immunology
CD8-Positive T-Lymphocytes - virology
Cell activation
Chronic infection
Communicable diseases
Control
Cytomegalovirus
Cytotoxicity
Demography
Drug therapy
Endogenous retroviruses
Endogenous Retroviruses - genetics
Endogenous Retroviruses - immunology
Female
Gene expression
Gene Expression Regulation, Viral
Genomes
Genomics
Health aspects
Histocompatibility antigen HLA
HIV
HIV Infections - immunology
HIV Infections - virology
HIV-1 - immunology
Human immunodeficiency virus
Humans
Immunity - immunology
Immunology
Infections
Infectious diseases
Inflammation
Lymphocytes
Lymphocytes T
Male
Medicine
Middle Aged
Respiratory diseases
Ribonucleic acid
RNA
RNA, Viral - genetics
RNA, Viral - metabolism
T cell receptors
T cells
Viral infections
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Title Human Endogenous Retrovirus Expression Is Inversely Associated with Chronic Immune Activation in HIV-1 Infection
URI https://www.ncbi.nlm.nih.gov/pubmed/22879884
https://www.proquest.com/docview/1326511993
https://www.proquest.com/docview/1033159002
https://pubmed.ncbi.nlm.nih.gov/PMC3413683
https://doaj.org/article/d69162197cad401db23a89d82c0653ab
http://dx.doi.org/10.1371/journal.pone.0041021
Volume 7
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