HIV infection and cardiovascular disease have both shared and distinct monocyte gene expression features: Women’s Interagency HIV study
Persistent inflammation contributes to the development of cardiovascular disease (CVD) as an HIV-associated comorbidity. Innate immune cells such as monocytes are major drivers of inflammation in men and women with HIV. The study objectives are to examine the contribution of circulating non-classica...
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| Published in | PloS one Vol. 18; no. 5; p. e0285926 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Public Library of Science
19.05.2023
Public Library of Science (PLoS) |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1932-6203 1932-6203 |
| DOI | 10.1371/journal.pone.0285926 |
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| Abstract | Persistent inflammation contributes to the development of cardiovascular disease (CVD) as an HIV-associated comorbidity. Innate immune cells such as monocytes are major drivers of inflammation in men and women with HIV. The study objectives are to examine the contribution of circulating non-classical monocytes (NCM, CD14
dim
CD16
+
) and intermediate monocytes (IM, CD14
+
CD16
+
) to the host response to long-term HIV infection and HIV-associated CVD. Women with and without chronic HIV infection (H) were studied. Subclinical CVD (C) was detected as plaques imaged by B-mode carotid artery ultrasound. The study included H-C-, H+C-, H-C+, and H+C+ participants (23 of each, matched on race/ethnicity, age and smoking status), selected from among enrollees in the Women’s Interagency HIV Study. We assessed transcriptomic features associated with HIV or CVD alone or comorbid HIV/CVD comparing to healthy (H-C-) participants in IM and NCM isolated from peripheral blood mononuclear cells. IM gene expression was little affected by HIV alone or CVD alone. In IM, coexisting HIV and CVD produced a measurable gene transcription signature, which was abolished by lipid-lowering treatment. In NCM, versus non-HIV controls, women with HIV had altered gene expression, irrespective of whether or not they had comorbid CVD. The largest set of differentially expressed genes was found in NCM among women with both HIV and CVD. Genes upregulated in association with HIV included several potential targets of drug therapies, including LAG3 (CD223). In conclusion, circulating monocytes from patients with well controlled HIV infection demonstrate an extensive gene expression signature which may be consistent with the ability of these cells to serve as potential viral reservoirs. Gene transcriptional changes in HIV patients were further magnified in the presence of subclinical CVD. |
|---|---|
| AbstractList | Persistent inflammation contributes to the development of cardiovascular disease (CVD) as an HIV-associated comorbidity. Innate immune cells such as monocytes are major drivers of inflammation in men and women with HIV. The study objectives are to examine the contribution of circulating non-classical monocytes (NCM, CD14dimCD16+) and intermediate monocytes (IM, CD14+CD16+) to the host response to long-term HIV infection and HIV-associated CVD. Women with and without chronic HIV infection (H) were studied. Subclinical CVD (C) was detected as plaques imaged by B-mode carotid artery ultrasound. The study included H-C-, H+C-, H-C+, and H+C+ participants (23 of each, matched on race/ethnicity, age and smoking status), selected from among enrollees in the Women's Interagency HIV Study. We assessed transcriptomic features associated with HIV or CVD alone or comorbid HIV/CVD comparing to healthy (H-C-) participants in IM and NCM isolated from peripheral blood mononuclear cells. IM gene expression was little affected by HIV alone or CVD alone. In IM, coexisting HIV and CVD produced a measurable gene transcription signature, which was abolished by lipid-lowering treatment. In NCM, versus non-HIV controls, women with HIV had altered gene expression, irrespective of whether or not they had comorbid CVD. The largest set of differentially expressed genes was found in NCM among women with both HIV and CVD. Genes upregulated in association with HIV included several potential targets of drug therapies, including LAG3 (CD223). In conclusion, circulating monocytes from patients with well controlled HIV infection demonstrate an extensive gene expression signature which may be consistent with the ability of these cells to serve as potential viral reservoirs. Gene transcriptional changes in HIV patients were further magnified in the presence of subclinical CVD. Persistent inflammation contributes to the development of cardiovascular disease (CVD) as an HIV-associated comorbidity. Innate immune cells such as monocytes are major drivers of inflammation in men and women with HIV. The study objectives are to examine the contribution of circulating non-classical monocytes (NCM, CD14 dim CD16 + ) and intermediate monocytes (IM, CD14 + CD16 + ) to the host response to long-term HIV infection and HIV-associated CVD. Women with and without chronic HIV infection (H) were studied. Subclinical CVD (C) was detected as plaques imaged by B-mode carotid artery ultrasound. The study included H-C-, H+C-, H-C+, and H+C+ participants (23 of each, matched on race/ethnicity, age and smoking status), selected from among enrollees in the Women’s Interagency HIV Study. We assessed transcriptomic features associated with HIV or CVD alone or comorbid HIV/CVD comparing to healthy (H-C-) participants in IM and NCM isolated from peripheral blood mononuclear cells. IM gene expression was little affected by HIV alone or CVD alone. In IM, coexisting HIV and CVD produced a measurable gene transcription signature, which was abolished by lipid-lowering treatment. In NCM, versus non-HIV controls, women with HIV had altered gene expression, irrespective of whether or not they had comorbid CVD. The largest set of differentially expressed genes was found in NCM among women with both HIV and CVD. Genes upregulated in association with HIV included several potential targets of drug therapies, including LAG3 (CD223). In conclusion, circulating monocytes from patients with well controlled HIV infection demonstrate an extensive gene expression signature which may be consistent with the ability of these cells to serve as potential viral reservoirs. Gene transcriptional changes in HIV patients were further magnified in the presence of subclinical CVD. Persistent inflammation contributes to the development of cardiovascular disease (CVD) as an HIV-associated comorbidity. Innate immune cells such as monocytes are major drivers of inflammation in men and women with HIV. The study objectives are to examine the contribution of circulating non-classical monocytes (NCM, CD14.sup.dim CD16.sup.+) and intermediate monocytes (IM, CD14.sup.+ CD16.sup.+) to the host response to long-term HIV infection and HIV-associated CVD. Women with and without chronic HIV infection (H) were studied. Subclinical CVD (C) was detected as plaques imaged by B-mode carotid artery ultrasound. The study included H-C-, H+C-, H-C+, and H+C+ participants (23 of each, matched on race/ethnicity, age and smoking status), selected from among enrollees in the Women's Interagency HIV Study. We assessed transcriptomic features associated with HIV or CVD alone or comorbid HIV/CVD comparing to healthy (H-C-) participants in IM and NCM isolated from peripheral blood mononuclear cells. IM gene expression was little affected by HIV alone or CVD alone. In IM, coexisting HIV and CVD produced a measurable gene transcription signature, which was abolished by lipid-lowering treatment. In NCM, versus non-HIV controls, women with HIV had altered gene expression, irrespective of whether or not they had comorbid CVD. The largest set of differentially expressed genes was found in NCM among women with both HIV and CVD. Genes upregulated in association with HIV included several potential targets of drug therapies, including LAG3 (CD223). In conclusion, circulating monocytes from patients with well controlled HIV infection demonstrate an extensive gene expression signature which may be consistent with the ability of these cells to serve as potential viral reservoirs. Gene transcriptional changes in HIV patients were further magnified in the presence of subclinical CVD. Persistent inflammation contributes to the development of cardiovascular disease (CVD) as an HIV-associated comorbidity. Innate immune cells such as monocytes are major drivers of inflammation in men and women with HIV. The study objectives are to examine the contribution of circulating non-classical monocytes (NCM, CD14 dim CD16 + ) and intermediate monocytes (IM, CD14 + CD16 + ) to the host response to long-term HIV infection and HIV-associated CVD. Women with and without chronic HIV infection (H) were studied. Subclinical CVD (C) was detected as plaques imaged by B-mode carotid artery ultrasound. The study included H-C-, H+C-, H-C+, and H+C+ participants (23 of each, matched on race/ethnicity, age and smoking status), selected from among enrollees in the Women’s Interagency HIV Study. We assessed transcriptomic features associated with HIV or CVD alone or comorbid HIV/CVD comparing to healthy (H-C-) participants in IM and NCM isolated from peripheral blood mononuclear cells. IM gene expression was little affected by HIV alone or CVD alone. In IM, coexisting HIV and CVD produced a measurable gene transcription signature, which was abolished by lipid-lowering treatment. In NCM, versus non-HIV controls, women with HIV had altered gene expression, irrespective of whether or not they had comorbid CVD. The largest set of differentially expressed genes was found in NCM among women with both HIV and CVD. Genes upregulated in association with HIV included several potential targets of drug therapies, including LAG3 (CD223). In conclusion, circulating monocytes from patients with well controlled HIV infection demonstrate an extensive gene expression signature which may be consistent with the ability of these cells to serve as potential viral reservoirs. Gene transcriptional changes in HIV patients were further magnified in the presence of subclinical CVD. Persistent inflammation contributes to the development of cardiovascular disease (CVD) as an HIV-associated comorbidity. Innate immune cells such as monocytes are major drivers of inflammation in men and women with HIV. The study objectives are to examine the contribution of circulating non-classical monocytes (NCM, CD14dimCD16+) and intermediate monocytes (IM, CD14+CD16+) to the host response to long-term HIV infection and HIV-associated CVD. Women with and without chronic HIV infection (H) were studied. Subclinical CVD (C) was detected as plaques imaged by B-mode carotid artery ultrasound. The study included H-C-, H+C-, H-C+, and H+C+ participants (23 of each, matched on race/ethnicity, age and smoking status), selected from among enrollees in the Women's Interagency HIV Study. We assessed transcriptomic features associated with HIV or CVD alone or comorbid HIV/CVD comparing to healthy (H-C-) participants in IM and NCM isolated from peripheral blood mononuclear cells. IM gene expression was little affected by HIV alone or CVD alone. In IM, coexisting HIV and CVD produced a measurable gene transcription signature, which was abolished by lipid-lowering treatment. In NCM, versus non-HIV controls, women with HIV had altered gene expression, irrespective of whether or not they had comorbid CVD. The largest set of differentially expressed genes was found in NCM among women with both HIV and CVD. Genes upregulated in association with HIV included several potential targets of drug therapies, including LAG3 (CD223). In conclusion, circulating monocytes from patients with well controlled HIV infection demonstrate an extensive gene expression signature which may be consistent with the ability of these cells to serve as potential viral reservoirs. Gene transcriptional changes in HIV patients were further magnified in the presence of subclinical CVD.Persistent inflammation contributes to the development of cardiovascular disease (CVD) as an HIV-associated comorbidity. Innate immune cells such as monocytes are major drivers of inflammation in men and women with HIV. The study objectives are to examine the contribution of circulating non-classical monocytes (NCM, CD14dimCD16+) and intermediate monocytes (IM, CD14+CD16+) to the host response to long-term HIV infection and HIV-associated CVD. Women with and without chronic HIV infection (H) were studied. Subclinical CVD (C) was detected as plaques imaged by B-mode carotid artery ultrasound. The study included H-C-, H+C-, H-C+, and H+C+ participants (23 of each, matched on race/ethnicity, age and smoking status), selected from among enrollees in the Women's Interagency HIV Study. We assessed transcriptomic features associated with HIV or CVD alone or comorbid HIV/CVD comparing to healthy (H-C-) participants in IM and NCM isolated from peripheral blood mononuclear cells. IM gene expression was little affected by HIV alone or CVD alone. In IM, coexisting HIV and CVD produced a measurable gene transcription signature, which was abolished by lipid-lowering treatment. In NCM, versus non-HIV controls, women with HIV had altered gene expression, irrespective of whether or not they had comorbid CVD. The largest set of differentially expressed genes was found in NCM among women with both HIV and CVD. Genes upregulated in association with HIV included several potential targets of drug therapies, including LAG3 (CD223). In conclusion, circulating monocytes from patients with well controlled HIV infection demonstrate an extensive gene expression signature which may be consistent with the ability of these cells to serve as potential viral reservoirs. Gene transcriptional changes in HIV patients were further magnified in the presence of subclinical CVD. |
| Audience | Academic |
| Author | Gange, Stephen Anastos, Kathryn Lazar, Jason M. Kaplan, Robert C. Mack, Wendy J. Heath, Sonya L. Mueller, Karin Ghosheh, Yanal Hanna, David B. Liu, Chenglong Lin, Juan Wang, Tao Berman, Joan W. Tien, Phyllis C. Tracy, Russell P. Cohen, Mardge H. Qi, Qibin Ley, Klaus Hodis, Howard N. Ehinger, Erik Ofotokun, Igho Landay, Alan L. |
| AuthorAffiliation | 3 Department of Cardiology, Eberhard Karls University, Tuebingen University Hospital, Tuebingen, Germany 1 Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, NY, United States of America 13 Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, United States of America 11 Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD, United States of America 9 Department of Medicine, John Stroger Hospital and Rush University, Chicago, IL, United States of America 16 Department of Internal Medicine, Rush University Medical Center, Chicago, IL, United States of America Medizinische Universitat Graz, AUSTRIA 7 Department of Medicine, and Department of Veterans Affairs, Medical Center, University of California, San Francisco, San Francisco, CA, United States of America 10 Department of Medicine, Infectious Disease Division and Grady Health Care System, Emory University School of Medicine, Atlanta, GA, United States of Am |
| AuthorAffiliation_xml | – name: 7 Department of Medicine, and Department of Veterans Affairs, Medical Center, University of California, San Francisco, San Francisco, CA, United States of America – name: 9 Department of Medicine, John Stroger Hospital and Rush University, Chicago, IL, United States of America – name: 14 Department of Pathology & Laboratory Medicine and Biochemistry, University of Vermont Larner College of Medicine, Colchester, VT, United States of America – name: Medizinische Universitat Graz, AUSTRIA – name: 16 Department of Internal Medicine, Rush University Medical Center, Chicago, IL, United States of America – name: 1 Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, NY, United States of America – name: 6 Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA, United States of America – name: 4 Department of Medicine, Albert Einstein College of Medicine, Bronx, NY, United States of America – name: 12 Department of Medicine, Georgetown University Medical Center, Washington, DC, United States of America – name: 3 Department of Cardiology, Eberhard Karls University, Tuebingen University Hospital, Tuebingen, Germany – name: 10 Department of Medicine, Infectious Disease Division and Grady Health Care System, Emory University School of Medicine, Atlanta, GA, United States of America – name: 17 Department of Bioengineering, University of California San Diego, San Diego, CA, United States of America – name: 13 Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, United States of America – name: 18 Fred Hutchinson Cancer Research Center, Division of Public Health Sciences, Seattle, WA, United States of America – name: 15 Department of Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA, United States of America – name: 5 Department of Medicine, Downstate Medical Center, State University of New York, Brooklyn, NY, United States of America – name: 8 Department of Pathology, Albert Einstein College of Medicine, Bronx, NY, United States of America – name: 11 Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD, United States of America – name: 2 Department of Inflammation Biology, La Jolla Institute for Allergy and Immunology, La Jolla, CA, United States of America |
| Author_xml | – sequence: 1 givenname: Juan orcidid: 0000-0001-5143-8158 surname: Lin fullname: Lin, Juan – sequence: 2 givenname: Erik surname: Ehinger fullname: Ehinger, Erik – sequence: 3 givenname: David B. surname: Hanna fullname: Hanna, David B. – sequence: 4 givenname: Qibin surname: Qi fullname: Qi, Qibin – sequence: 5 givenname: Tao surname: Wang fullname: Wang, Tao – sequence: 6 givenname: Yanal surname: Ghosheh fullname: Ghosheh, Yanal – sequence: 7 givenname: Karin surname: Mueller fullname: Mueller, Karin – sequence: 8 givenname: Kathryn surname: Anastos fullname: Anastos, Kathryn – sequence: 9 givenname: Jason M. surname: Lazar fullname: Lazar, Jason M. – sequence: 10 givenname: Wendy J. surname: Mack fullname: Mack, Wendy J. – sequence: 11 givenname: Phyllis C. surname: Tien fullname: Tien, Phyllis C. – sequence: 12 givenname: Joan W. surname: Berman fullname: Berman, Joan W. – sequence: 13 givenname: Mardge H. surname: Cohen fullname: Cohen, Mardge H. – sequence: 14 givenname: Igho surname: Ofotokun fullname: Ofotokun, Igho – sequence: 15 givenname: Stephen surname: Gange fullname: Gange, Stephen – sequence: 16 givenname: Chenglong surname: Liu fullname: Liu, Chenglong – sequence: 17 givenname: Sonya L. orcidid: 0000-0002-3826-0954 surname: Heath fullname: Heath, Sonya L. – sequence: 18 givenname: Russell P. surname: Tracy fullname: Tracy, Russell P. – sequence: 19 givenname: Howard N. surname: Hodis fullname: Hodis, Howard N. – sequence: 20 givenname: Alan L. surname: Landay fullname: Landay, Alan L. – sequence: 21 givenname: Klaus surname: Ley fullname: Ley, Klaus – sequence: 22 givenname: Robert C. orcidid: 0000-0003-3271-801X surname: Kaplan fullname: Kaplan, Robert C. |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/37205656$$D View this record in MEDLINE/PubMed |
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| CitedBy_id | crossref_primary_10_1007_s12012_023_09815_4 crossref_primary_10_3390_pathogens12070925 crossref_primary_10_3390_v15071612 |
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| Copyright | Copyright: © 2023 Lin et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. COPYRIGHT 2023 Public Library of Science 2023 Lin et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. 2023 Lin et al 2023 Lin et al 2023 Lin et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
| Copyright_xml | – notice: Copyright: © 2023 Lin et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. – notice: COPYRIGHT 2023 Public Library of Science – notice: 2023 Lin et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. – notice: 2023 Lin et al 2023 Lin et al – notice: 2023 Lin et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
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| DOI | 10.1371/journal.pone.0285926 |
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| SubjectTerms | Biology and Life Sciences Biomarkers Cardiovascular disease Cardiovascular diseases Cardiovascular Diseases - complications Carotid arteries Carotid artery CD14 antigen CD16 antigen CD223 antigen Chronic infection Comorbidity Development and progression Female Gene Expression Genes Genetic aspects Genetic transcription Health aspects Heart diseases HIV HIV (Viruses) HIV infection HIV Infections - complications HIV Infections - drug therapy HIV Infections - genetics HIV patients Human immunodeficiency virus Humans Hydrogen Immune system Infections Inflammation Inflammation - metabolism Leukocytes, Mononuclear Lipids Male Medical research Medicine and Health Sciences Medicine, Experimental Minority & ethnic groups Monocytes Monocytes - metabolism Peripheral blood mononuclear cells Proteins Research and analysis methods Risk factors Transcriptomics Veins & arteries Women patients |
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| Title | HIV infection and cardiovascular disease have both shared and distinct monocyte gene expression features: Women’s Interagency HIV study |
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