cccdna level and not alt related to liver damage/hcc development on hbe neg
Elevated cccDNA Levels in HBeAg-Negative Patients Indicates Active Liver Disease
HBV’s covalently closed circular DNA (cccDNA) contributes to high rates of viral replication, and is also believed to contribute to development of liver cancer. Chinese researchers investigated the role cccDNA plays in HBeAg-negative disease progression.
They monitored 33 HBeAg-negative patients, with and without active liver disease—which was defined as ALT rates of less than 40 IU/L and HBV DNA levels less than 10,000 copies/mL. They found a “significant” correlation between elevated HBV DNA and cccDNA levels—which resulted in active liver disease. They found no significant correlation between HBsAg and cccDNA.
“The HBV replicative efficiency, defined as the ratio of HBV DNA to cccDNA, was approximately 20% higher in patients with active disease,” they wrote in the September 2010 issue of the Journal of Medical Virology. “In conclusion, serum HBV DNA, but not HBsAg, reflects the amount of cccDNA and the replication efficiency of HBV in patients with HBeAg-negative chronic hepatitis B.”
Very interesting article never knew HBV DNA reflect the amount of cccDNA so in a nut shell low level ofHBV DNA equal *maybe* less cccDNA and low cccDNA reflect the quantity of HBsag ? Am l correct pls ?
well all these studies are not very relevant since sometimes there is a poor correlation and sometimes not.hbvdna und is not equal to cccdna und in the liver nor is intraepatic hbvdna but they both get lower when hbvdna in the blood is und
i hope we will have cccdna and intraepatic hbvdna test by mononuclear cell in the blood since the sensitivity of hbvdna in the blood is very very low
i have found labs in hongkong that measure cccdna in blood and liver by biopsy, cccdna in blood is used to monitor resistance since it gets detectable again before hbvdna and alt rise, it is the most sensitive tool to prevent resistance
i posted this article also because a low level of alt is not important alone to reflect disease activity, they are both needed together with liver fibrosis to know what is happening in the liver
What do you think about this information?
Study Finds Interferon Ineffective Against HBeAg-Negative Hepatitis B
Researchers, writing in the August 2010 issue of the American Journal of Gastroenterolgy, reported disappointing results in a recent randomized trial that tested the effectiveness of pegylated interferon (Pegasys) in people infected with hepatitis B “e” antigen (HBeAg)-negative hepatitis B.
An accompanying editorial questioned the effectiveness of the interferon in this patient group based on the study results.
Pegylated interferon, delivered in a weekly injection, had been recently recommended as a first-choice treatment for HBeAg-negative patients based on results from a single randomized trial, which used a control group.
But results from a second randomized controlled trial, involving 138 HBeAg-negative patients, were disappointing. Only 7.5% of the study’s participants achieved undetectable hepatitis B virus (HBV) DNA (less than 400 copies/mL) at 24 weeks over a 48-week course of pegylated interferon. None lost hepatitis B surface antigen (HBsAg), which indicates clearance of the infection.
“This study challenges the value and limits the appeal of pegylated interferon therapy for HBeAg-negative chronic hepatitis B,” the editorial noted.
"chronic infection is maintained by the viral cccDNA pool. short term antiviral therapy cannot completely EXHAUST the viral pool which is relatively stable and constitutes the source of viral production renewal after the cessation of therapy...if the production of virions can be blocked, cccDNA is eliminated rather as a result of of hepatocyte death than through the cccDNA clearance.
Two immune mechanisms have been proposed for the cccDNA clearance from the hepatocyte nucleus:
1. noncytolytic cytokine dependent mechanism
2. cytolytic mechanism cytotoxic T lymphocyte dependent, by which the infected cells are eliminated and replaced with non-infected cells."
basically, is the new investigational treatment, the REPLICOR, under the first mechanism of noncytolytic cytokine dependent approach since it does not cause elevated LFT?
no replicor block hbsag production so that it cannot neautralize the antibody hbsab which is able to block viral entry this way the same thing made by antivirals is made by hbsab antibody
cccdna is always there and will be cleared slowly by liver cells deaths, the same thing happens in those who clear acute hbv, cccdna is never eliminated fast and in some it might persist forever but as long as hbsab can block viral entry and hbvdna cccdna is not a problem
just thinking radically with some absurd idea.. please don't laugh. what if i have a monthly blood extraction amounting to around 300 cc of blood. at least not enough to kill me or cause any medical problems since the total amount of blood in our body amounts to 6000 cc. would this approach be able to lower my circulating HBsAg in the blood enough for some antiHbs to function properly? since from the researches it seems that the circulating antigens interferes with the cell mediated and humoral immunity of my body..
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