title: The Role of HIV-1 in Affecting the Proliferation Ability of HPCs Derived From BM.
abstract: HIV-1 causes chronic infection characterized by the depletion of CD4+ T lymphocytes and the development of AIDS. Current antiretroviral drugs inhibit viral spread, but they do not lead to a full immune recovery. Hematopoietic stem cells (HSCs) and multipotent hematopoietic progenitor cells (HPCs) give rise to all blood and immune cells, and in HIV infection, hematological abnormalities frequently occur in patients. Here, we used bone marrow samples from HIV-1-infected people to study the relationship between the proliferation ability of HSCs/HPCs and peripheral CD4+ T lymphocytes. Three indexes were used to reflect the proliferation ability of HSCs and HPCs: (1) colony-forming units of bone marrow mononuclear cells (BMMCs), (2) amplification of CD34+ cells purified from bone marrow mononuclear cells, (3) expression of HOXB4 and HOXA9 in CD34+ cells. We observed a direct correlation between peripheral number of CD4+ T lymphocytes and the HSCs/HPCs proliferation ability in our study. We also compared HIV-infected patients with or without antiretroviral therapy (ART). Our results demonstrated that after antiretroviral therapy, CD4+ T-cell recovery and HPCs proliferation ability are correlated. Our findings have implications in understanding whether bone marrow-derived HPCs can supplement for the loss of CD4+ T lymphocytes during HIV-1 infection.
authors.affiliation: *Key Laboratory of AIDS Immunology of National Health and Family Planning Commission, Department of Laboratory Medicine, The First Affiliated Hospital, China Medical University, Shenyang, China;†Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Hangzhou, China;‡Department of Hematology, The First Affiliated Hospital, China Medical University, Shenyang, China; and§Department of Clinical Laboratory, Dongying People's Hospital, Dongying, China.
authors.forename: Xiaolin
authors.initials: X
authors.lastname: Guo
authors.forename: Sijia
authors.initials: S
authors.lastname: He
authors.forename: Xiaoyi
authors.initials: X
authors.lastname: Lv
authors.forename: Haibo
authors.initials: H
authors.lastname: Ding
authors.forename: Sha
authors.initials: S
authors.lastname: Li
authors.forename: Jing
authors.initials: J
authors.lastname: Kang
authors.forename: Jing
authors.initials: J
authors.lastname: Liu
authors.forename: Chaolong
authors.initials: C
authors.lastname: Qin
authors.forename: Wenqing
authors.initials: W
authors.lastname: Geng
authors.forename: Yongjun
authors.initials: Y
authors.lastname: Jiang
authors.forename: Hong
authors.initials: H
authors.lastname: Shang
mesh_terms: D000328:Adult; D000368:Aged; D018952:Antigens, CD34 / Q000276:immunology / Q000378:metabolism; D018791:CD4 Lymphocyte Count; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology / Q000502:physiology / Q000821:virology; D049109:Cell Proliferation / Q000502:physiology*; D002478:Cells, Cultured; D003114:Colony-Forming Units Assay; D005260:Female; D015658:HIV Infections / Q000188:drug therapy / Q000276:immunology / Q000821:virology*; D015497:HIV-1 / Q000276:immunology / Q000502:physiology*; D006412:Hematopoietic Stem Cells / Q000502:physiology* / Q000821:virology; D018398:Homeodomain Proteins / Q000378:metabolism; D006801:Humans; D008297:Male; D008875:Middle Aged; D039902:Multipotent Stem Cells / Q000502:physiology* / Q000821:virology; D014157:Transcription Factors / Q000378:metabolism
chemical_list: D018952:Antigens, CD34; C090460:HOXB4 protein, human; D018398:Homeodomain Proteins; D014157:Transcription Factors; C097899:homeobox protein HOXA9