TY - JOUR
T1 - Immuno-pathomechanism of liver fibrosis
T2 - Targeting chemokine CCL2-mediated HIV: HCV nexus
AU - Ansari, Wahid W.W.
AU - Schmidt, Reinhold E.
AU - Shankar, Esaki M.
AU - Kamarulzaman, Adeeba
N1 - Funding Information:
The authors acknowledge the funding supported by the University of Malaya Research Grant (RG 501-13HTM) of the Health and Translational Medicine Research Cluster to AWA and High Impact Research Grant (HIRGA E000001-20001) of the Ministry of Higher Education (MoHE) Malaysia to AK.
Publisher Copyright:
© Ansari et al.
PY - 2014/12/10
Y1 - 2014/12/10
N2 - 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.
AB - 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.
KW - C-C chemokine ligand-2
KW - Combination anti-retroviral therapy
KW - Hepatic stellate cells
KW - HIV/Hepatitis-C co-infection
KW - Immuno-pathogenesis
KW - Inflammation
KW - Liver fibrosis
KW - Viral cross-talk
UR - http://www.scopus.com/inward/record.url?scp=84924865060&partnerID=8YFLogxK
U2 - 10.1186/s12967-014-0341-8
DO - 10.1186/s12967-014-0341-8
M3 - Review Article
C2 - 25528160
AN - SCOPUS:84924865060
SN - 1479-5876
VL - 12
JO - Journal of Translational Medicine
JF - Journal of Translational Medicine
IS - 1
M1 - 341
ER -
