I read long time I think from Middle East or east Europe.
I'm genotype D. Usually genotype D is hard to respond to interfron. They say genotype D have precore mutant. Now since you have BCP this is called basal core promotor which they consider you are at higher risk to HCC however all this are just prediction and after so many readings on genotypes there is lot of contradiction. Many members here are genotype D including myself , stef2011 and many others. Where did you do the BCP test as i never done one
Accumulated evidence shows that HBV carriers with A1762T/G1764A double mutation in the BCP region are significantly associated with HCC. Patients with these mutations die at an earlier age from HCC than those without the mutations.6, 7, 8 and 9 Beyond that, there is ∼70% increased risk of HCC in individuals with these mutations and total HBV plasma level of >10 000 copies/mL.16 The A1762T/G1764A double mutation is not only a predictive biomarker for HCC development, but also a prognostic indicator of life expectancy of the patient with HCC.8 Thus, it is very important to detect these mutations.
Am I #$$#$$# ? ;-(
I'm in similar situation and i saw many articles contradict itself. Don't worry what is meant to happen it will happen some lived for 100 years with hbv and some earlier
Do you also have the A1762T/G1764A double mutation in the BCP region?
The test I got was at Quest Diagnostics test code: 10529
Many articles that contradict itself? For an instance?
I'm not worried, I guess I'm screwed plus genotype d is lousy at reacting to int treatment... I guess I can forget about getting my hbsag levels it's pointless right now... Just gotta wait for my death or hopefully some cure before it's too late...
From your report one can see that you also have the c1858t mutation, a true precore mutation, which means that the production of the e antigen is blocked at this position.
While the basic core promotor mutation is an immune escape mutation against the immune pressure that the virus faces due to the high number of cytosolic e antigen proteins, which in turn translate into a high proteasome processing and MHC class 1 presentation of the e and core antigen class I epitopes,
that reduces expression and presentation in the infected hepatocytes, thus escaping detection and elimination by cd8 CTL T cells,
the precore mutation further reduces this immune pressure on the virus by completely switching off the e antigen production.
Both mutations are quite common in e antigen negative patients.
Genotype A typically does not develop the precore stop mutation, since a double nucleotide switch would be necessary. Genotype D does not have this limitation.
what does that all mean?
Is having c1858t mutation considered good or bad for HCC?
Am I considered a dead man?
It means that seroconversion is likely harder to achieve. The precore mutation is worse than the BCP mutation for the reasons explained.
The higher HCC rate is however a result of a more inflammatory, cytotoxic and carcinogenic type of immunity and cytokine profile than in patients with intact e antigen production.
Effective antiviral treatment will however reduce the ongoing inflammation and reduce the remaining risk to one similar to non mutated patients.
Do you think I'm a good candidate for treatment based on these mutations alone? If so, what treatment would you recommend? I don't think many doctors are even aware of this... I wonder what they gonna say if I tell them I have these mutations and a link to one of these studies above, I doubt their guidelines tell them do anything about it...
so is it possible to be HBeAg- and HBeAB+ with genotype A or rather uncommon ?
is G1899A also a true precore mutation in regards of reduced hbsag loss on pegintf?
I might go to this lab and run same test however it will just add to my worry :( do you need a doctor order to take this test?