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Printable Handouts
Navigable Slide Index
- Introduction
- HBV- a major public health and clinical problem
- Natural history of chronic hepatitis B
- Pre-therapeutic assessment of liver disease
- The goal of therapy
- Endpoints of therapy
- Prevention of disease progression
- Virologic endpoints
- Antivirals approved for hepatitis B
- Results of main antiviral drugs in clinical trials
- Indications for treatment (1)
- Indications for treatment (2)
- Predictors of response (1)
- Predictors of response (2)
- How to treat (1)
- How to treat (2)
- Choosing a nucleoside analog
- HBV life cycle and antiviral targets
- Development of antiviral drug resistance
- Treatment failure
- Kinetics of antiviral drug resistance
- Incidence of drug resistance over time
- Lamivudine resistance and liver disease
- The position of the resistance mutations
- Cross-resistance data for the main mutants
- Factors associated with the barrier of resistance
- Maximizing the barrier to resistance
- Resistance impact prevention in first line therapy
- Rates of drug resistance among naive patients
- Results of tenofovir administration
- Results of entecavir administration
- Cumulative probability of entecavir resistance (1)
- Cumulative probability of HBsAg loss
- Control of antiviral drug resistance
- Management of treatment failure- tenofovir
- Tenofovir in patients with lamivudine exposure
- Tenofovir in patients with adefovir failure
- Evolution of viral resistance mutations over time
- Viral genome evolution during tenofovir therapy
- Management of treatment failure- entecavir (ETV)
- Cumulative probability of entecavir resistance (2)
- Response to ETV in patients receiving lamivudine
- Response to ETV in patients receiving adefovir
- Management algorithm (1)
- Management algorithm (2)
- Conclusions
- New challenges in HBV resistance
- Emergence of multi-drug resistant mutants
- New targets
- Acknowledgements
Topics Covered
- Hepatitis B virus
- Chronic hepatitis B
- Interferon
- Nucleoside analogs
- Viral resistance
- Treatment management
Links
Series:
Categories:
Therapeutic Areas:
Talk Citation
Zoulim, F. (2011, August 30). Antiviral therapy of chronic hepatitis B virus infections: is resistance still a challenge? [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved October 7, 2024, from https://doi.org/10.69645/GXZY2719.Export Citation (RIS)
Publication History
Financial Disclosures
- Prof. Zoulim consults for the following companies: Aligos, Antios, Arbutus, Assembly, Enochian, Gilead, GSK, Roche Molecular Systems and Zhimeng. He also receives research funding from INSERM to conduct research at Assembly Biosciences, Beam Therapeutics and Viravaxx AG.
Antiviral therapy of chronic hepatitis B virus infections: is resistance still a challenge?
A selection of talks on Clinical Practice
Transcript
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0:00
I am Professor Fabien Zoulim and I am the head of the Liver department at the Civil de Lyon
and Hepatitis Research Laboratory at INSERM U871, located in Lyon.
Today, I will try to give you another view on the antiviral therapy of
chronic hepatitis B virus infection and we will see
with HPV resistance is still a challenge for therapy.
0:29
Chronic Hepatitis B virus infections remain a major public health problem.
Indeed, the World Health Organization estimates that
more than 300 million people are chronic carriers of
that virus despite the availability of an efficient vaccine.
Chronic hepatitis B remains the first cause of primary liver cancer,
also called hepatocellular carcinoma.
In the last decade,
there was major progress in the treatment of
chronic hepatitis B with the development of potent nucleoside and nucleotide analogs.
The goals of antivirals therapy are to obtain viral suppression,
which is a identified by undetectable HPV DNA viral
real-time PCR assays and to achieve remission of liver disease.
However, the treatment of chronic hepatitis B remains
a clinical challenge because viral eradication is not yet possible.
1:38
The natural history of liver damage in
chronic hepatitis B is a result of the interplay between
viral replication in infected parasite and
the host immune response against the infected cells.
It's a measure of phases of natural history of the disease
are depicted on this slide.
The first phase of the chronic hepatitis B infection is the immuno-tolerant phase.
It is characterized by high viral load and identified by the positivity of
HBe antigen and high HPV DNA levels with normal ALT levels in the serum.
This is usually associated with minimal liver disease or minimal chronic hepatitis.
This is followed by the immunoreactive phase,
where the immune system's kicks in and tries to kill infected cells, try to eradicate the infection.
There is an equilibrium between the rate of
cell killing and the rate of viral replication.
Chronic liver lesions can occur.
This is characterized by decreasing HPV DNA in the serum
because of the number of infected cells that are killed by
the immune system which is associated by rising ALT levels.
This defines a chronic hepatitis phase where a
liver biopsy may show moderate to severe chronic hepatitis.
These patients are at risk of developing liver cirrhosis.
In this phase, treatment is indicated when
the immune system can take over or when antiviral treatment is efficient.
This phase is followed by the inactive phase associated with a low replication level.
Usually, HBe antigen and becomes negative, and anti-HIV antibodies seroconversion occurs.
HBV DNA levels are below 2,000 international units per mL and ALT levels become normal.
This is associated with a remission of liver disease and usually,
even the biopsy shows inactive diseases.
Also, the state may occur at a stage of advanced fibrosis or cirrhosis.
Since the virus can persist in the liver then this phase may be followed by
a reactivation phase; whereas the level of HPV DNA may go up again,
as well as ALT levels.
In this phase, we can observe moderate to severe chronic hepatitis,
which may be associated with liver cirrhosis.
Again, in this phase,
treatment is indicated. After prolonged infection,
often after dictates of chronic HPV infection and occult infection may occur where
HBS antigen may become undetectable and HPV DNA may be detected only in the liver.
This occult infection may be associated with severe disease.
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