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Barraclude duration

how long do i have to take barraclude if i am HbeAg -ve, Hbe AB +ve, Hb c AB +ve ??
pls help??
9 Responses
Avatar universal
According to the 2007 guideline, there is no clear point since you are HBeAg negative already.  You may need to take Barralude for life to keep HBV under control.
Avatar universal
What is the significance of HbeAg -ve, Hbe AB +ve?

I thought that eAg supports the virus, in its absense shouldn't virus stay still (inactive).
Avatar universal
HBeAg(-) HBeAB (+) usually is a better status unless there is detectable viral duplication which may indicate mutation.  If Barraclude is used with patients already HBeAg(-) and HBeAB (+), then maybe what is being dealt with is mutated viral replication.
575880 tn?1241889939
My cousin's doctor say some people take a for about a year or so. you doctor should run a blood text for you like once a month, to see how much percentage that has been reduced. I don't think you will be in it for life. just make sure you take your medecine everyday.
Avatar universal
What does "Pre-Core Mutation detetected" means?
Avatar universal
Mutations in the precore region or core promoter region of the HBV genome render the host unable to produce HBeAg; therefore, HBeAg remains undetectable despite ongoing viral replication. Patients who are HBeAg-negative with active disease generally have a less favorable long-term prognosis than patients who are HBeAg-positive.
Avatar universal
Thanks! Also found this:
HBeAg, anti-HBe, and pre-core mutations

Hepatitis B e antigen (HBeAg) and its antibody, anti-HBe, are useful markers to determine the likelihood of spread of the virus (transmissibility) by persons affected with chronic hepatitis B viral infection. Detecting both HBeAg and anti-HBe in the blood is usually mutually exclusive. Accordingly, the presence of HBeAg means ongoing viral activity and the ability to infect others, whereas the presence of anti-HBe signifies a more inactive state of the virus and less risk of transmission.

In some individuals infected with hepatitis B virus, the genetic material for the virus has undergone a particular structural change, called a pre-core mutation. This mutation results in an inability of the hepatitis B virus to produce HBeAg, even though the virus is actively reproducing. This means that even though no HBeAg is detected in the blood of people with the mutation, the hepatitis B virus is still active in these persons and they can infect others.
Avatar universal
Precore mutants:
These variants were the first major immune escape mutants of HBV to be discovered.[1] These HBV variants appear during HBeAg seroconversion and they carry mutations in the precore region that prevent HBeAg synthesis, despite continuing production of infectious virions. The most common of these mutations is a G to A substitution at nucleotide 1896, which prevents the production of HBeAg by introducing a premature stop codon into the open reading frame of the precore region. This truncates the precore/core protein into a 28-amino acid peptide.[3] Because the precore region is not essential for HBV replication nor hepatitis B core antigen (HBcAg) expression, the G1896A variant is replication-competent and is infectious.

The presence of the G1896A mutation is restricted to specific viral genotypes (B, C, D, and E). These HBV genotypes are not uniformly distributed around the world. This mutation is more prevalent in geographic regions where genotypes B, C, and D are predominant, such as Asia and the Mediterranean area, where it can be detected in more than 50% of individuals with chronic hepatitis B. It is significantly less prevalent in North America and Europe, where genotype A is more common.[3]

The presence of precore escape mutants should be considered in individuals who exhibit HBeAg negativity, HBsAg positivity, anti-HBe positivity, HBV DNA positivity, and elevated serum aminotransferase levels. However, the precore variant is not uniformly pathogenic, and thus, co-mutations or host factors presumably explain the more virulent forms of precore mutant-associated disease.

Core promoter mutants:
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Another common HBeAg variant is the core promoter mutant, characterized by point mutations in the promoter for both HBeAg mRNA and core protein mRNA[3] The core promoter mutants express less HBeAg through transcriptional downregulation. The most frequent core promoter mutation is the double A1762T and G1764A nucleotide exchange, which results in a substantial decrease in HBeAg expression but enhanced viral genome replication. The reduction of HBeAg expression is apparently mediated by reduced precore RNA transcription, whereas the mechanism for enhanced replication is unclear. These virologic properties lead to enhanced pathogenicity of core promoter mutants in vivo. The enhanced replication capacity and reduced virion secretion may increase viral load in the liver, which triggers liver damage directly or indirectly through the immune response. Massive liver damage during acute infection leads to fulminant hepatitis. Damage during chronic infection increases hepatocyte turnover, induces fibrosis, and increases the chance of hepatocellular transformation and malignancy.[3]

As opposed to precore variants, core promoter variants can be detected in patients who are either HBeAg-positive or -negative. The prevalence of the core promoter variant is about 40%; it is evenly distributed among the major HBV genotypes. Although fulminant forms of HBV-related hepatitis have been linked to infection with core promoter mutants, case-controlled studies are needed to prove the association. These studies should also take into account other viral mutations and the genetic makeup of the host. The association of core promoter mutants and liver cancer is also controversial; carefully done epidemiologic studies are needed to demonstrate a link between core promoter mutations and hepatocellular carcinogenesis.[3,4]

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Impact on treatment:
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Despite the high prevalence of precore and core promoter mutants as the predominant viral species in HBeAg-negative chronic hepatitis B, treatment of these variants is challenging. At present, options include the use of interferon-alfa-based therapy and nucleos(t)ide analogues, such as lamivudine, entecavir, or adefovir. The response rate for precore mutants to interferon-alfa is low, even with a longer duration of therapy, than that for wild-type strains or re-treatment strategies. Lamivudine, entecavir, and adefovir are regarded as safe and efficacious, but they usually require treatment over several years.

Avatar universal
Thanks for the info.
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