Assessment Of Nutritional Status Among Patients Suffering From HCV Visiting Public Hospitals Of Lahore

2020 ◽  
pp. 54-60
Author(s):  
OJS Admin
Keyword(s):  
Hepatitis C Virus ◽  
Liver Disease ◽  
Hepatitis C ◽  
Liver Fibrosis ◽  
Nutritional Status ◽  
Liver Diseases ◽  
Public Hospitals ◽  
Early Stages

Hepatitis C virus is an infectious liver disease. The infection is generally asymptomatic commonly in its early stages but when it's confirmed, it can lead to advanced liver diseases such as liver fibrosis and thencirrhosis.

Progression of liver fibrosis in HIV/hepatitis C virus-coinfected individuals on antiretroviral therapy with early stages of liver fibrosis at baseline

HIV Medicine ◽  
2013 ◽  
Vol 15 (4) ◽  
pp. 203-212 ◽  
Author(s):  
R Sanmartín ◽  
J Tor ◽  
A Sanvisens ◽  
JJ López ◽  
A Jou ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Antiretroviral Therapy ◽  
Liver Fibrosis ◽  
Early Stages

scholarly journals Relationship between skeletal muscle mass and liver fibrosis markers for patients with hepatitis C virus related liver disease

Medicine ◽  
2017 ◽  
Vol 96 (48) ◽  
pp. e8761
Author(s):  
Ryo Takata ◽  
Hiroki Nishikawa ◽  
Hirayuki Enomoto ◽  
Yoshinori Iwata ◽  
Akio Ishii ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Hepatitis C Virus ◽  
Liver Disease ◽  
Hepatitis C ◽  
Liver Fibrosis ◽  
Muscle Mass ◽  
Skeletal Muscle Mass ◽  
Related Liver Disease

scholarly journals Exosome-Mediated Intercellular Communication between Hepatitis C Virus-Infected Hepatocytes and Hepatic Stellate Cells

2017 ◽  
Vol 91 (6) ◽  
Author(s):  
Pradip B. Devhare ◽  
Reina Sasaki ◽  
Shubham Shrivastava ◽  
Adrian M. Di Bisceglie ◽  
Ranjit Ray ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Liver Disease ◽  
Hepatitis C ◽  
Liver Fibrosis ◽  
Intercellular Communication ◽  
Hepatic Stellate Cells ◽  
Molecular Mechanisms ◽  
Stellate Cells ◽  
Hcv Infection ◽  
Marker Genes

ABSTRACT Fibrogenic pathways in the liver are principally regulated by activation of hepatic stellate cells (HSC). Fibrosis is associated with chronic hepatitis C virus (HCV) infection, although the mechanism is poorly understood. HSC comprise the major population of nonparenchymal cells in the liver. Since HCV does not replicate in HSC, we hypothesized that exosomes secreted from HCV-infected hepatocytes activate HSC. Primary or immortalized human hepatic stellate (LX2) cells were exposed to exosomes derived from HCV-infected hepatocytes (HCV-exo), and the expression of fibrosis-related genes was examined. Our results demonstrated that HCV-exo internalized to HSC and increased the expression of profibrotic markers. Further analysis suggested that HCV-exo carry miR-19a and target SOCS3 in HSC, which in turn activates the STAT3-mediated transforming growth factor β (TGF-β) signaling pathway and enhances fibrosis marker genes. The higher expression of miR-19a in exosomes was also observed from HCV-infected hepatocytes and in sera of chronic HCV patients with fibrosis compared to healthy volunteers and non-HCV-related liver disease patients with fibrosis. Together, our results demonstrated that miR-19a carried through the exosomes from HCV-infected hepatocytes activates HSC by modulating the SOCS-STAT3 axis. Our results implicated a novel mechanism of exosome-mediated intercellular communication in the activation of HSC for liver fibrosis in HCV infection. IMPORTANCE HCV-associated liver fibrosis is a critical step for end-stage liver disease progression. However, the molecular mechanisms for hepatic stellate-cell activation by HCV-infected hepatocytes are underexplored. Here, we provide a role for miR-19a carried through the exosomes in intercellular communication between HCV-infected hepatocytes and HSC in fibrogenic activation. Furthermore, we demonstrate the role of exosomal miR-19a in activation of the STAT3–TGF-β pathway in HSC. This study contributes to the understanding of intercellular communication in the pathogenesis of liver disease during HCV infection.

Serum Hyaluronan as a Marker of Liver Fibrosis in Hemophiliacs with Hepatitis C Virus-Associated Chronic Liver Disease

1998 ◽  
Vol 99 (4) ◽  
pp. 212-216 ◽  
Author(s):  
Masahiko Yamada ◽  
Yoshihide Fukuda ◽  
Isao Nakano ◽  
Yoshiaki Katano ◽  
Junki Takamatsu ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Liver Disease ◽  
Hepatitis C ◽  
Liver Fibrosis ◽  
Chronic Liver Disease ◽  
Chronic Liver ◽  
Serum Hyaluronan

scholarly journals M2 Macrophages Play Critical Roles in Progression of Inflammatory Liver Disease in Hepatitis C Virus Transgenic Mice

2015 ◽  
Vol 90 (1) ◽  
pp. 300-307 ◽  
Author(s):  
Takahiro Ohtsuki ◽  
Kiminori Kimura ◽  
Yuko Tokunaga ◽  
Kyoko Tsukiyama-Kohara ◽  
Chise Tateno ◽  
...  
Keyword(s):  
Chronic Hepatitis ◽  
Hepatitis C Virus ◽  
Liver Disease ◽  
Hepatitis C ◽  
Transgenic Mice ◽  
Liver Tissue ◽  
Liver Diseases ◽  
Chronic Liver ◽  
M2 Macrophages ◽  
Tnf Α

ABSTRACT Macrophages in liver tissue are widely defined as important inflammatory cells in chronic viral hepatitis due to their proinflammatory activity. We reported previously that interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) play significant roles in causing chronic hepatitis in hepatitis C virus (HCV) transgenic mice (S. Sekiguchi et al., PLoS One 7: e51656, 2012, http://dx.doi.org/10.1371/journal.pone.0051656 ). In addition, we showed that recombinant vaccinia viruses expressing an HCV nonstructural protein (rVV-N25) could protect against the progression of chronic hepatitis by suppression of macrophage activation. Here, we focus on the role of macrophages in liver disease progression in HCV transgenic mice and examine characteristic features of macrophages following rVV-N25 treatment. The number of CD11b + F4/80 + CD11c − CD206 + (M2) macrophages in the liver of HCV transgenic mice was notably increased compared to that of age-matched control mice. These M2 macrophages in the liver produced elevated levels of IL-6 and TNF-α. rVV-N25 infection suppressed the number and activation of M2 macrophages in liver tissue. These results suggested that inflammatory cytokines produced by M2-like macrophages contribute to the induction of chronic liver inflammation in HCV transgenic mice. Moreover, the therapeutic effect of rVV-N25 might be induced by the suppression of the number and activation of hepatic macrophages. IMPORTANCE HCV causes persistent infections that can lead to chronic liver diseases, liver fibrosis, and hepatocellular carcinoma; the search for an HCV curative is the focus of ongoing research. Recently, effective anti-HCV drugs have been developed; however, vaccine development still is required for the prevention and therapy of infection by this virus. We demonstrate here that M2 macrophages are important for the pathogenesis of HCV-caused liver diseases and additionally show that M2 macrophages contribute to the therapeutic mechanism observed following rVV-N25 treatment.

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