HIV-1 replicates in human osteoclasts and enhances their differentiation in vitro

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• 作者：Jin Gohda (1) (2)
  Yijing Ma (1)
  Ying Huang (1)
  Yu Zhang (1)
  Lijun Gu (1) (2)
  Yang Han (3)
  Taisheng Li (3)
  Bin Gao (4)
  George Fu Gao (4)
  Jun-ichiro Inoue (5)
  Aikichi Iwamoto (2) (6)
  Takaomi Ishida (1) (2)
  
  1. China-Japan Joint Laboratory of Molecular Immunology & Microbiology ; Institute of Microbiology ; Chinese Academy of Sciences ; Beijing ; P.R.China
  2. Research Center for Asian Infectious Diseases ; The Institute of Medical Science ; The University of Tokyo ; Tokyo ; Japan
  3. Department of Infectious Diseases ; Peking Union Medical College Hospital ; Chinese Academy of Medical Sciences ; Beijing ; P.R.China
  4. CAS Key Laboratory of Pathogenic Microbiology and Immunology ; Institute of Microbiology ; Chinese Academy of Sciences ; Beijing ; P.R.China
  5. Division of Cellular and Molecular Biology ; The Institute of Medical Science ; The University of Tokyo ; Tokyo ; Japan
  6. Division of Infectious Diseases ; Advanced Clinical Research Center ; The Institute of Medical Science ; The University of Tokyo ; Tokyo ; Japan
  
• 关键词：HIV ; 1 ; Iinfection ; Bone disease ; Osteoclasts ; Macrophages
• 刊名：Retrovirology
• 出版年：2015
• 出版时间：December 2015
• 年：2015
• 卷：12
• 期：1
• 全文大小：1,963 KB
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• 刊物主题：Virology; Infectious Diseases; Cancer Research;
• 出版者：BioMed Central
• ISSN：1742-4690

文摘

Background HIV-1 infected patients frequently have osteolytic bone disease, which is caused by the dysregulation of the bone remodeling system that involves the interaction between osteoblasts and osteoclasts, but the relationship between osteolytic disease and HIV-1 infection remains unclear. In this study we tested whether HIV-1 infection of osteoclasts affects their differentiation. Results We prepared human osteoclasts from CD14+ monocytes and examined them for their susceptibility to HIV-1. Furthermore, we investigated the effect of HIV-1 infection on osteoclast differentiation. CD14-derived osteoclasts were shown to express CD4, CCR5, and CXCR4 each at the similar level to that shown with macrophages. R5-tropic HIV-1 and X4-tropic HIV-1 were found to infect CD14-derived osteoclasts and replicate in them. Furthermore, HIV-1 infection induced formation of larger osteoclastst, enhanced the expression of mRNAs for three osteoclast specific marker molecules (tartrate-resistant acid phosphatase, cathepsin K, and the calcitonin receptor), and up-regulated osteoclast bone resorption activity. Conclusions Our results suggest that osteoclasts serve as a novel target for HIV-1 infection, which may enhance the osteoclast differentiation contributing to the development of osteolytic disease in HIV-1-infected patients.