Thanks for the info.
If there is no mutation, can there be better prognosis for HBeAg -ve patients ?
I will share my viral load after 3 months on viral treatment. Before treatment counts were 90000 copies/ml and 30000 IU/ml. Usualy IU vs count will be 1 to 5 times.
It is kind of interesting to see HBeAb +ve, yet there is active replication.
HBeAg -ve people typically would have low viral replication -- in many cases, low enough to require no further treatment. If the DNA VL is high for Ag -ve people, it means that they have active viral replication despite their Ag -ve. Hence the treatment.
In general Ag +ve people fare worse than Ag -ve people, but keep in mind that this *by itself* is not a criterion for a prognosis or for starting treatment.
On one hand the goal for treating HBeAg + patients is to get sero conversion (then stop treatment), the other HBeAg -ve it is open ended.
It is some what confusing to read HBeAg -ve/HBeAg anti-bodies +ve patients have low viral replication, but still require treatment. Where as HBeAg +ve patients treatment stops with sero conversion.
Is this because with treatment HBeAg +ve patients are converted to HBeAg -ve sooner and have better liver health, thus do not require treatment ?
Genotype: it could influence a decision to start treating with peginterferon. A and B are relatively more easily brought under control than C and D. The genotype also gives an indication as to how severe the disease is going to be.
precore/BCP: the jury still seems to be out.
What conclusions can be drawn from the "core/precore mutation tests" ?
Anyone know about this and the significance of GenoType ?
Is the test I had mentioned at the beginning a confirmation that there is no pre-core/core mutations ?
Or this test is not that useful ?
Any comment is appreciated.