Personalized therapy in chronic viral hepatitis

Brunetto, Maurizia Rossana; Colombatto, P.; Bonino, Ferruccio

doi:10.1016/j.mam.2007.09.015

Cited by 5 publications

(4 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…1). The HBV DNA decline flattens in a significant portion of the patients after 4–5 weeks of antiviral treatment; this effect might be caused by reduction of the clearance rate of the infected cells over time [33]. This phenomenon was described as “negative feedback” by Colombatto et al; the progressive reduction of the infected cell clearance rate which is proportionate to the decline of the infected cells during treatment.…”

Section: Discussionmentioning

confidence: 99%

“…[33] We modified the model proposed by Neumann et al [6] with introducing immune-mediated clearance of infected cells by cytolytic as well as noncytolytic activities of immune effector cells; these are reflected by serum ALT level and serum HBsAg titer, respectively. In our model equations, the activities of immune effectors were designated as directly cytolytic activity (parameter “α”) and noncytolytic activity (parameter “f”).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Mathematical Modeling of Triphasic Viral Dynamics in Patients with HBeAg-Positive Chronic Hepatitis B Showing Response to 24-Week Clevudine Therapy

et al. 2012

View full text Add to dashboard Cite

BackgroundModeling of short-term viral dynamics of hepatitis B with traditional biphasic model might be insufficient to explain long-term viral dynamics. The aim was to develop a novel method of mathematical modeling to shed light on the dissociation between early and long-term dynamics in previous studies.MethodsWe investigated the viral decay pattern in 50 patients from the phase III clinical trial of 24-week clevudine therapy, who showed virological response and HBsAg decline. Immune effectors were added as a new compartment in the model equations. We determined some parameter values in the model using the non-linear least square minimization method.ResultsMedian baseline viral load was 8.526 Log10copies/mL, and on-treatment viral load decline was 5.683 Log10copies/mL. The median half-life of free virus was 24.89 hours. The median half-life of infected hepatocytes was 7.39 days. The viral decay patterns were visualized as triphasic curves with decreasing slopes over time: fastest decay in the first phase; slowest in the third phase; the second phase in between.ConclusionsIn the present study, mathematical modeling of hepatitis B in patients with virological response and HBsAg decline during 24-week antiviral therapy showed triphasic viral dynamics with direct introduction of immune effectors as a new compartment, which was thought to reflect the reduction of clearance rate of infected cells over time. This modeling method seems more appropriate to describe long-term viral dynamics compared to the biphasic model, and needs further validation.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Mathematical Modeling of Triphasic Viral Dynamics in Patients with HBeAg-Positive Chronic Hepatitis B Showing Response to 24-Week Clevudine Therapy

et al. 2012

View full text Add to dashboard Cite

show abstract

“…When mutated, the viruses are no longer able to express HBeAg, which leads to a significantly lower replication rate and a lack of HBeAg in the blood of the patients [12]. Nevertheless, chronic hepatitis B can occur in both HBeAg-positive and HBeAg-negative infected people [20]. In the second immune clearance phase, the immune system gains control over the virus and the concentration of HBV DNA in the blood begins to decrease.…”

Section: Hepatitis B (Hbv)mentioning

confidence: 99%

“…Recently, mutations in the surface gene encoding HBsAg resulted in infections of already-vaccinated children in Southeast Asia [6]. Additionally, the genotype can also be an important influencing factor in antiviral therapy [20].…”

Section: Hepatitis B (Hbv)mentioning

confidence: 99%

The Translational Bridge between Inflammation and Hepatocarcinogenesis

Gufler

Seeboeck

Schatz

et al. 2022

Cells

View full text Add to dashboard Cite

Viral infections or persistent alcohol or drug abuse, together with intrinsic factors, lead to hepatitis, which often ends in the development of liver cirrhosis or hepatocellular carcinoma (HCC). With this review, we describe inflammatory liver diseases, such as acute liver failure, virus-induced hepatitis, alcoholic- and non-alcoholic steatohepatitis, and autoimmune hepatitis, and highlight their driving mechanisms. These include external factors such as alcohol misuse, viral infection and supernutrition, as well as intrinsic parameters such as genetic disposition and failure, in immune tolerance. Additionally, we describe what is known about the translational machinery within all these diseases. Distinct eukaryotic translation initiation factors (eIFs) with specific functional roles and aberrant expression in HCC are reported. Many alterations to the translational machinery are already triggered in the precancerous lesions described in this review, highlighting mTOR pathway proteins and eIFs to emphasize their putative clinical relevance. Here, we identified a lack of knowledge regarding the roles of single eIF proteins. A closer investigation will help to understand and treat HCC as well as the antecedent diseases.

show abstract

Viral interference: A potential therapeutic method for chronic viral hepatitis?

Bang-song

Wang

et al. 2008

Bioscience Hypotheses

View full text Add to dashboard Cite

Personalized therapy in chronic viral hepatitis

Cited by 5 publications

References 40 publications

Mathematical Modeling of Triphasic Viral Dynamics in Patients with HBeAg-Positive Chronic Hepatitis B Showing Response to 24-Week Clevudine Therapy

Mathematical Modeling of Triphasic Viral Dynamics in Patients with HBeAg-Positive Chronic Hepatitis B Showing Response to 24-Week Clevudine Therapy

The Translational Bridge between Inflammation and Hepatocarcinogenesis

Viral interference: A potential therapeutic method for chronic viral hepatitis?

Contact Info

Product

Resources

About