Effect of sustained virological response after direct-acting antivirals on liver fibrosis in patients with chronic HCV infection

Agwa, Ramy Hassan; Elgazzar, Mohamed H.; El-Zayyadi, Islam Abd El-Hamid; Saed, Ahmed M; Ghannam, Mayada A.; Saleh, Ahmed

doi:10.1186/s43162-022-00111-1

Cited by 7 publications

(4 citation statements)

References 23 publications

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“…In consistent with the current study, Reddy et al (13) concluded that the recent antiviral agents were found to improve hepatic functions during short term follow up in particular increase in serum albumin. Such observations have been made during short-term follow-up in many studies as well (14)(15)(16)(17) .…”

Section: Discussionmentioning

confidence: 87%

Assessment of Changes in Liver Fibrosis and Stiffness, Lipid Profile and Insulin Resistance in Patients with Chronic Hepatitis C Viral Infection Who Received Direct Acting Antiviral Therapy

Abdelmohsen¹,

Abotaleb²,

Zohne

et al. 2022

The Egyptian Journal of Hospital Medicine

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Background: With introduction of direct acting antivirals (DAAs) in the management of chronic hepatitis C viral (HCV) infection, this leads to high frequency of sustained viral response (SVR). Effect of these agents on liver stiffness and lipid isn't well studied. Objective: We tried to assess changes in liver stiffness, insulin resistance (IR) and lipid profile after achievement of SVR with DAAs. Patients and methods: A total of 80 patients with chronic HCV infection were recruited in the study. All patients received dual therapy of sofosbuvir and daclatasvir either without ribavirin (in case of chronic hepatitis) or with ribavirin (in case of liver cirrhosis). Liver stiffness, lipid profile and IR were assessed at baseline and at the end of therapy. Results: All patients achieved SVR. Majority (58.8%) of patients were males. There was significant improvement in liver transaminases after therapy. There was significant reduction in frequency of IR after therapy (42.5% vs. 68.7%; p= 0.04) with percentage of decrease was 16.11%. Also, there was significant decrease in degree of fibrosis as assessed by fibroScan with percentage of decrease was 48.2%. Predictors for persistence IR after DAAs therapy were only body mass index and advanced fibrosis. Cholesterol, low density lipoproteins and triglycerides showed significant increase after therapy. Conclusion: Sofosbuvir and daclatasvir with or without ribavirin are effective and tolerable agents in management of chronic HCV infection. Degree of liver fibrosis and insulin resistance would be reduced after DAAs therapy. Future multi centers are warranted to confirm these findings.

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Section: Discussionmentioning

confidence: 87%

Assessment of Changes in Liver Fibrosis and Stiffness, Lipid Profile and Insulin Resistance in Patients with Chronic Hepatitis C Viral Infection Who Received Direct Acting Antiviral Therapy

Abdelmohsen¹,

Abotaleb²,

Zohne

et al. 2022

The Egyptian Journal of Hospital Medicine

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“…Recent advances in direct acting antiviral development have revolutionized the therapy of HCV infection. However, a sustained virological response in a significant proportion of patients does not reverse liver pathology [45,46]. Pathological mechanisms in liver fibrosis and cirrhosis in HCV patients [47,48], and in vivo models [49], have mainly highlighted the deregulation of inflammatory and metabolic processes.…”

Section: Discussionmentioning

confidence: 99%

Hepatitis C Core Protein Induces a Genotype-Specific Susceptibility of Hepatocytes to TNF-Induced Death In Vitro and In Vivo

Moustafa

Kassela

Bampali

et al. 2022

Viruses

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Hepatitis C virus (HCV) core protein is a multifunctional protein that is involved in the proliferation, inflammation, and apoptosis mechanism of hepatocytes. HCV core protein genetic variability has been implicated in various outcomes of HCV pathology and treatment. In the present study, we aimed to analyze the role of the HCV core protein in tumor necrosis factor α (TNFα)-induced death under the viewpoint of HCV genetic variability. Immortalized hepatocytes (IHH), and not the Huh 7.5 hepatoma cell line, stably expressing HCV subtype 4a and HCV subtype 4f core proteins showed that only the HCV 4a core protein could increase sensitivity to TNFα-induced death. Development of two transgenic mice expressing the two different core proteins under the liver-specific promoter of transthyretin (TTR) allowed for the in vivo assessment of the role of the core in TNFα-induced death. Using the TNFα-dependent model of lipopolysaccharide/D-galactosamine (LPS/Dgal), we were able to recapitulate the in vitro results in IHH cells in vivo. Transgenic mice expressing the HCV 4a core protein were more susceptible to the LPS/Dgal model, while mice expressing the HCV 4f core protein had the same susceptibility as their littermate controls. Transcriptome analysis in liver biopsies from these transgenic mice gave insights into HCV core molecular pathogenesis while linking HCV core protein genetic variability to differential pathology in vivo.

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“…Recent advances in direct acting antiviral development have revolutionized the therapy of HCV infection. However, a sustained virological response in a significant proportion of patients does not reverse liver pathology [46,47]. Pathological mechanisms in liver fibrosis and cirrhosis in HCV patients [48,49] and in vivo models [50] have mainly highlighted the deregulation of inflammatory and metabolic processes.…”

Section: Discussionmentioning

confidence: 99%

Hepatitis C Core Protein Induces a Genotype-specific Susceptibility of Hepatocytes to TNF-induced Death in vitro and in vivo

Moustafa¹,

Kassela²,

Bampali³

et al. 2022

Preprint

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Hepatitis C virus (HCV) core protein is a multifunctional protein that is involved in proliferation, inflammation and apoptosis mechanism of hepatocytes. HCV core protein genetic variability has been implicated in various outcomes of HCV pathology and treatment. In the present study, we aimed to analyze the role of HCV core protein in tumor necrosis factor α (TNFα)-induced death under the viewpoint of HCV genetic variability. Immortalized hepatocytes (IHH), and not the Huh7.5 hepatoma cell line, stably expressing HCV subtype 4a and HCV subtype 4f core proteins showed that only HCV 4a core protein could increase sensitivity to TNFα-induced death. Development of two transgenic mice expressing the two different core proteins under the liver-specific promoter of transthyretin (TTR) allowed for the in vivo assessment of the role of core in TNFα-induced death. Using the TNFα-dependent model of lipopolysaccharide/D-galactosamine (LPS/Dgal) we were able to recapitulate the in vitro results in IHH cells in vivo. Transgenic mice expressing HCV 4a core protein were more susceptible to the LPS/Dgal model while mice expressing HCV 4f core protein had the same susceptibility as their littermate controls. Transcriptome analysis in liver biopsies from these transgenic mice gave insights into HCV core molecular pathogenesis, while linking HCV core protein genetic variability to differential pathology in vivo.

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Effect of sustained virological response after direct-acting antivirals on liver fibrosis in patients with chronic HCV infection

Cited by 7 publications

References 23 publications

Assessment of Changes in Liver Fibrosis and Stiffness, Lipid Profile and Insulin Resistance in Patients with Chronic Hepatitis C Viral Infection Who Received Direct Acting Antiviral Therapy

Assessment of Changes in Liver Fibrosis and Stiffness, Lipid Profile and Insulin Resistance in Patients with Chronic Hepatitis C Viral Infection Who Received Direct Acting Antiviral Therapy

Hepatitis C Core Protein Induces a Genotype-Specific Susceptibility of Hepatocytes to TNF-Induced Death In Vitro and In Vivo

Hepatitis C Core Protein Induces a Genotype-specific Susceptibility of Hepatocytes to TNF-induced Death <em>in </em><em>vitro</em> and <em>in vivo</em>

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