Immuno-pathomechanism of liver fibrosis: targeting chemokine CCL2-mediated HIV:HCV nexus

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• 作者：AW Wahid Ansari (1) (2)
  Reinhold E Schmidt (3)
  Esaki M Shankar (4) (5)
  Adeeba Kamarulzaman (1) (2)
  
  1. Centre of Excellence for Research in AIDS ; Faculty of Medicine ; University of Malaya ; Lambah Pantai ; 50603 ; Kuala Lumpur ; Malaysia
  2. Department of Medicine ; Faculty of Medicine ; University of Malaya ; Lambah Pantai ; 50603 ; Kuala Lumpur ; Malaysia
  3. Department of Clinical Immunology and Rheumatology ; Hannover Medical School ; Carl-Neuberger Str.1 ; D-30625 ; Hannover ; Germany
  4. Department of Medical Microbiology ; Faculty of Medicine ; University of Malaya ; Lambah Pantai ; 50603 ; Kuala Lumpur ; Malaysia
  5. Tropical Infectious Diseases Research and Education Centre ; Faculty of Medicine ; University of Malaya ; Lambah Pantai ; 50603 ; Kuala Lumpur ; Malaysia
  
• 关键词：HIV/Hepatitis ; C co ; infection ; Immuno ; pathogenesis ; Liver fibrosis ; C ; C chemokine ligand ; 2 ; Inflammation ; Combination anti ; retroviral therapy ; Hepatic stellate cells ; Viral cross ; talk
• 刊名：Journal of Translational Medicine
• 出版年：2014
• 出版时间：December 2014
• 年：2014
• 卷：12
• 期：1
• 全文大小：693 KB
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• 刊物主题：Biomedicine general; Medicine/Public Health, general;
• 出版者：BioMed Central
• ISSN：1479-5876

文摘

Even in the era of successful combination antiretroviral therapy (cART), co-infection of Hepatitis C virus (HCV) remains one of the leading causes of non-AIDS-related mortality and morbidity among HIV-positive individuals as a consequence of accelerated liver fibrosis and end-stage liver disease (ESLD). The perturbed liver microenvironment and induction of host pro-inflammatory mediators in response to HIV and HCV infections, play a pivotal role in orchestrating the disease pathogenesis and clinical outcomes. How these viruses communicate each other via chemokine CCL2 and exploit the liver specific cellular environment to exacerbate liver fibrosis in HIV/HCV co-infection setting is a topic of intense discussion. Herein, we provide recent views and insights on potential mechanisms of CCL2 mediated immuno-pathogenesis, and HIV-HCV cross-talk in driving liver inflammation. We believe CCL2 may potentially serve an attractive target of anti-fibrotic intervention against HIV/HCV co-infection associated co-morbidities.