the only thing i know about these variants is they are weaker, i asked a researcher in pisa what if i get this by etv and he said it is very very rare on etv since too potent for virus to mutate like that and even if so the virus is weaker immune modulator treatments
in the trials they had a patient with hbsag mutant after lam treatment and they treated him with interferon eradicating hbv
so probably the best therapies to try first are:
peginterferon or interferon lambda better if you can get it and alinia (nitazoxanide), i'd try or add entecavir only after failure of immune modulators
Stefano, thank you that's very interesting. I had the second article by Lada et al already. In my read of it, the authors are mainly concerned with the possibility of "us" (chronic HBV carriers with the "a" variant virus that enable the virus to escape our immune responses) being infectious to vaccinated individuals and possibly able to contaminate blood supplies because the screening tests used may miss some of the "a" variants. The article is neutral as far as the relative risks of being a chronic carrier of the variant vs being a chronic carrier of the wild type virus. Do you see something else here?
This one came up as related
http://www.ncbi.nlm.nih.gov/pubmed/17573090?ordinalpos=1&itool=PPMCLayout.PPMCAppController.PPMCArticlePage.PPMCPubmedRA&linkpos=3
and i got a paper copy of that too. It mentions an increased possibility of resistance to lamivudine and adv anti virals and notes several of the hbvsAb+ patients also had advanced fibrosis. Since the same patients were older and the length of infection was unknown and were also immune suppressed, it was not clear if the fibrosis resulted from the "a" variant virus or not.
here's the article
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1395421/