Association Between Gut Microbiota and CD4 Recovery in HIV-1 Infected Patients
Composition of the gut microbiota has been linked with human immunedeficiency virus (HIV)-infected patients on antiretroviral therapy (ART). Evidence suggests that ART-treated patients with poor CD4 T-cell recovery have higher levels of microbial translocation and immune activation. However, the ass...
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Published in | Frontiers in microbiology Vol. 9; p. 1451 |
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Main Authors | , , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
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Frontiers Media S.A
02.07.2018
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Abstract | Composition of the gut microbiota has been linked with human immunedeficiency virus (HIV)-infected patients on antiretroviral therapy (ART). Evidence suggests that ART-treated patients with poor CD4
T-cell recovery have higher levels of microbial translocation and immune activation. However, the association of the gut microbiota and immune recovery remains unclear. We performed a cross-sectional study on 30 healthy controls (HC) and 61 HIV-infected individuals, including 15 immunological ART responders (IRs), 20 immunological ART non-responders (INRs) and 26 untreated individuals (VU). IR and INR groups were classified by CD4
T-cell counts of ≥350 cells/mm
and <350 cells/mm
after 2 years of ART, respectively. Each subject's gut microbiota composition was analyzed by metagenomics sequencing. Levels of CD4
T cells, CD8
HLA-DR
T cells and CD8
CD38
T cells were measured by flow cytometry. We identified more
and fewer
in HIV-infected individuals than in HC. Patients in INR group were enriched with
, unclassified
and
when compared with those in IR group.
and unclassified
were overrepresented in individuals in VU group with CD4
T-cell counts <350 cells/mm
. Moreover, we found that the relative abundance of unclassified
and
were positively correlated with CD8
HLA-DR
T-cell count and CD8
HLA-DR
/CD8
percentage. Our study has shown that gut microbiota changes were associated with CD4
T-cell counts and immune activation in HIV-infected subjects. Interventions to reverse gut dysbiosis and inhibit immune activation could be a new strategy for improving immune reconstitution of HIV-1-infected individuals. |
---|---|
AbstractList | Composition of the gut microbiota has been linked with human immunedeficiency virus (HIV)-infected patients on antiretroviral therapy (ART). Evidence suggests that ART-treated patients with poor CD4+ T-cell recovery have higher levels of microbial translocation and immune activation. However, the association of the gut microbiota and immune recovery remains unclear. We performed a cross-sectional study on 30 healthy controls (HC) and 61 HIV-infected individuals, including 15 immunological ART responders (IRs), 20 immunological ART non-responders (INRs) and 26 untreated individuals (VU). IR and INR groups were classified by CD4+ T-cell counts of ≥350 cells/mm3 and <350 cells/mm3 after 2 years of ART, respectively. Each subject's gut microbiota composition was analyzed by metagenomics sequencing. Levels of CD4+ T cells, CD8+HLA-DR+ T cells and CD8+CD38+ T cells were measured by flow cytometry. We identified more Prevotella and fewer Bacteroides in HIV-infected individuals than in HC. Patients in INR group were enriched with Faecalibacterium prausnitzii, unclassified Subdoligranulum sp. and Coprococcus comes when compared with those in IR group. F. prausnitzii and unclassified Subdoligranulum sp. were overrepresented in individuals in VU group with CD4+ T-cell counts <350 cells/mm3. Moreover, we found that the relative abundance of unclassified Subdoligranulum sp. and C. comes were positively correlated with CD8+HLA-DR+ T-cell count and CD8+HLA-DR+/CD8+ percentage. Our study has shown that gut microbiota changes were associated with CD4+ T-cell counts and immune activation in HIV-infected subjects. Interventions to reverse gut dysbiosis and inhibit immune activation could be a new strategy for improving immune reconstitution of HIV-1-infected individuals.Composition of the gut microbiota has been linked with human immunedeficiency virus (HIV)-infected patients on antiretroviral therapy (ART). Evidence suggests that ART-treated patients with poor CD4+ T-cell recovery have higher levels of microbial translocation and immune activation. However, the association of the gut microbiota and immune recovery remains unclear. We performed a cross-sectional study on 30 healthy controls (HC) and 61 HIV-infected individuals, including 15 immunological ART responders (IRs), 20 immunological ART non-responders (INRs) and 26 untreated individuals (VU). IR and INR groups were classified by CD4+ T-cell counts of ≥350 cells/mm3 and <350 cells/mm3 after 2 years of ART, respectively. Each subject's gut microbiota composition was analyzed by metagenomics sequencing. Levels of CD4+ T cells, CD8+HLA-DR+ T cells and CD8+CD38+ T cells were measured by flow cytometry. We identified more Prevotella and fewer Bacteroides in HIV-infected individuals than in HC. Patients in INR group were enriched with Faecalibacterium prausnitzii, unclassified Subdoligranulum sp. and Coprococcus comes when compared with those in IR group. F. prausnitzii and unclassified Subdoligranulum sp. were overrepresented in individuals in VU group with CD4+ T-cell counts <350 cells/mm3. Moreover, we found that the relative abundance of unclassified Subdoligranulum sp. and C. comes were positively correlated with CD8+HLA-DR+ T-cell count and CD8+HLA-DR+/CD8+ percentage. Our study has shown that gut microbiota changes were associated with CD4+ T-cell counts and immune activation in HIV-infected subjects. Interventions to reverse gut dysbiosis and inhibit immune activation could be a new strategy for improving immune reconstitution of HIV-1-infected individuals. Composition of the gut microbiota has been linked with human immunedeficiency virus (HIV)-infected patients on antiretroviral therapy (ART). Evidence suggests that ART-treated patients with poor CD4 T-cell recovery have higher levels of microbial translocation and immune activation. However, the association of the gut microbiota and immune recovery remains unclear. We performed a cross-sectional study on 30 healthy controls (HC) and 61 HIV-infected individuals, including 15 immunological ART responders (IRs), 20 immunological ART non-responders (INRs) and 26 untreated individuals (VU). IR and INR groups were classified by CD4 T-cell counts of ≥350 cells/mm and <350 cells/mm after 2 years of ART, respectively. Each subject's gut microbiota composition was analyzed by metagenomics sequencing. Levels of CD4 T cells, CD8 HLA-DR T cells and CD8 CD38 T cells were measured by flow cytometry. We identified more and fewer in HIV-infected individuals than in HC. Patients in INR group were enriched with , unclassified and when compared with those in IR group. and unclassified were overrepresented in individuals in VU group with CD4 T-cell counts <350 cells/mm . Moreover, we found that the relative abundance of unclassified and were positively correlated with CD8 HLA-DR T-cell count and CD8 HLA-DR /CD8 percentage. Our study has shown that gut microbiota changes were associated with CD4 T-cell counts and immune activation in HIV-infected subjects. Interventions to reverse gut dysbiosis and inhibit immune activation could be a new strategy for improving immune reconstitution of HIV-1-infected individuals. Composition of the gut microbiota has been linked with human immunedeficiency virus (HIV)-infected patients on antiretroviral therapy (ART). Evidence suggests that ART-treated patients with poor CD4 + T-cell recovery have higher levels of microbial translocation and immune activation. However, the association of the gut microbiota and immune recovery remains unclear. We performed a cross-sectional study on 30 healthy controls (HC) and 61 HIV-infected individuals, including 15 immunological ART responders (IRs), 20 immunological ART non-responders (INRs) and 26 untreated individuals (VU). IR and INR groups were classified by CD4 + T-cell counts of ≥350 cells/mm 3 and <350 cells/mm 3 after 2 years of ART, respectively. Each subject’s gut microbiota composition was analyzed by metagenomics sequencing. Levels of CD4 + T cells, CD8 + HLA-DR + T cells and CD8 + CD38 + T cells were measured by flow cytometry. We identified more Prevotella and fewer Bacteroides in HIV-infected individuals than in HC. Patients in INR group were enriched with Faecalibacterium prausnitzii , unclassified Subdoligranulum sp. and Coprococcus comes when compared with those in IR group. F. prausnitzii and unclassified Subdoligranulum sp. were overrepresented in individuals in VU group with CD4 + T-cell counts <350 cells/mm 3 . Moreover, we found that the relative abundance of unclassified Subdoligranulum sp. and C. comes were positively correlated with CD8 + HLA-DR + T-cell count and CD8 + HLA-DR + /CD8 + percentage. Our study has shown that gut microbiota changes were associated with CD4 + T-cell counts and immune activation in HIV-infected subjects. Interventions to reverse gut dysbiosis and inhibit immune activation could be a new strategy for improving immune reconstitution of HIV-1-infected individuals. Composition of the gut microbiota has been linked with human immunedeficiency virus (HIV)-infected patients on antiretroviral therapy (ART). Evidence suggests that ART-treated patients with poor CD4+ T-cell recovery have higher levels of microbial translocation and immune activation. However, the association of the gut microbiota and immune recovery remains unclear. We performed a cross-sectional study on 30 healthy controls (HC) and 61 HIV-infected individuals, including 15 immunological ART responders (IRs), 20 immunological ART non-responders (INRs) and 26 untreated individuals (VU). IR and INR groups were classified by CD4+ T-cell counts of ≥350 cells/mm3 and <350 cells/mm3 after 2 years of ART, respectively. Each subject’s gut microbiota composition was analyzed by metagenomics sequencing. Levels of CD4+ T cells, CD8+HLA-DR+ T cells and CD8+CD38+ T cells were measured by flow cytometry. We identified more Prevotella and fewer Bacteroides in HIV-infected individuals than in HC. Patients in INR group were enriched with Faecalibacterium prausnitzii, unclassified Subdoligranulum sp. and Coprococcus comes when compared with those in IR group. F. prausnitzii and unclassified Subdoligranulum sp. were overrepresented in individuals in VU group with CD4+ T-cell counts <350 cells/mm3. Moreover, we found that the relative abundance of unclassified Subdoligranulum sp. and C. comes were positively correlated with CD8+HLA-DR+ T-cell count and CD8+HLA-DR+/CD8+ percentage. Our study has shown that gut microbiota changes were associated with CD4+ T-cell counts and immune activation in HIV-infected subjects. Interventions to reverse gut dysbiosis and inhibit immune activation could be a new strategy for improving immune reconstitution of HIV-1-infected individuals. |
Author | Lu, Wei Jing, Fanhui Routy, Bertrand Song, Xiaojing Han, Yang Li, Jing Zhu, Ting Xie, Jing Routy, Jean-Pierre Liu, Fei Lyu, Na Li, Taisheng Zhu, Baoli Feng, Yuqing Qiu, Zhifeng |
AuthorAffiliation | 5 Beijing Key Laboratory of Microbial Drug Resistance and Resistome , Beijing , China 2 Center for AIDS Research, Chinese Academy of Medical Sciences and Peking Union Medical College , Beijing , China 3 CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences , Beijing , China 7 Centre de Recherche du Centre Hospitalier de l’Université de Montréal (CRCHUM) , Montreal, QC , Canada 4 Savaid School of Medicine, University of Chinese Academy of Sciences , Beijing , China 10 Department of Pathogenic Biology, School of Basic Medical Sciences, Southwest Medical University , Luzhou , China 9 Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, College of Medicine, Zhejiang University , Hangzhou , China 1 Department of Infectious Disease, Peking Union Medical College Hospital , Beijing , China 8 Chronic Viral Illnesses Service Research Institute and Division of Hematology, McGill Un |
AuthorAffiliation_xml | – name: 1 Department of Infectious Disease, Peking Union Medical College Hospital , Beijing , China – name: 10 Department of Pathogenic Biology, School of Basic Medical Sciences, Southwest Medical University , Luzhou , China – name: 2 Center for AIDS Research, Chinese Academy of Medical Sciences and Peking Union Medical College , Beijing , China – name: 7 Centre de Recherche du Centre Hospitalier de l’Université de Montréal (CRCHUM) , Montreal, QC , Canada – name: 8 Chronic Viral Illnesses Service Research Institute and Division of Hematology, McGill University Health Centre , Montreal, QC , Canada – name: 6 Division of Hematology and Oncology Division, Department of Medicine, Centre Hospitalier de l’Université de Montréal (CHUM), Montreal , QC , Canada – name: 5 Beijing Key Laboratory of Microbial Drug Resistance and Resistome , Beijing , China – name: 4 Savaid School of Medicine, University of Chinese Academy of Sciences , Beijing , China – name: 3 CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences , Beijing , China – name: 9 Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, College of Medicine, Zhejiang University , Hangzhou , China |
Author_xml | – sequence: 1 givenname: Wei surname: Lu fullname: Lu, Wei – sequence: 2 givenname: Yuqing surname: Feng fullname: Feng, Yuqing – sequence: 3 givenname: Fanhui surname: Jing fullname: Jing, Fanhui – sequence: 4 givenname: Yang surname: Han fullname: Han, Yang – sequence: 5 givenname: Na surname: Lyu fullname: Lyu, Na – sequence: 6 givenname: Fei surname: Liu fullname: Liu, Fei – sequence: 7 givenname: Jing surname: Li fullname: Li, Jing – sequence: 8 givenname: Xiaojing surname: Song fullname: Song, Xiaojing – sequence: 9 givenname: Jing surname: Xie fullname: Xie, Jing – sequence: 10 givenname: Zhifeng surname: Qiu fullname: Qiu, Zhifeng – sequence: 11 givenname: Ting surname: Zhu fullname: Zhu, Ting – sequence: 12 givenname: Bertrand surname: Routy fullname: Routy, Bertrand – sequence: 13 givenname: Jean-Pierre surname: Routy fullname: Routy, Jean-Pierre – sequence: 14 givenname: Taisheng surname: Li fullname: Li, Taisheng – sequence: 15 givenname: Baoli surname: Zhu fullname: Zhu, Baoli |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/30034377$$D View this record in MEDLINE/PubMed |
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ContentType | Journal Article |
Copyright | Copyright © 2018 Lu, Feng, Jing, Han, Lyu, Liu, Li, Song, Xie, Qiu, Zhu, Routy, Routy, Li and Zhu. 2018 Lu, Feng, Jing, Han, Lyu, Liu, Li, Song, Xie, Qiu, Zhu, Routy, Routy, Li and Zhu |
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Keywords | metagenomics sequencing HIV-infected individuals butyrate-producing bacteria gut microbiota CD4 recovery |
Language | English |
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Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Reviewed by: Bin Su, Capital Medical University, China; Xiaoming Sun, Ragon Institute of MGH, MIT and Harvard, United States Edited by: Tao Dong, University of Oxford, United Kingdom This article was submitted to Infectious Diseases, a section of the journal Frontiers in Microbiology These authors have contributed equally to this work. |
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SubjectTerms | butyrate-producing bacteria CD4 recovery gut microbiota HIV-infected individuals metagenomics sequencing Microbiology |
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Title | Association Between Gut Microbiota and CD4 Recovery in HIV-1 Infected Patients |
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