HEP B Virus

[Bee55]

if both partners have HEP B and no antibody, and/or one have antibody AND mutated HEP B, can unprotected sex increase viral count in both, and does that increase damage to the liver?

[stef2011]

i mean:
hbsag quantification importance is now well known around the world but antvirals have no effect on it except interferon and alinia

the key to eradication will be the combos of interferon lambda and entecavir or tenofovir if lambda makes mild sides

[stef2011]

they reflect 2 different things:
hbsag, number of infected cells in the body and if decreasing immune system taking hold of more cells and eradicating virus from them.
hbv virus has a template (cccdna) inside liver cells that makes hbsag in a huge number to neautrilize the immunety antibody hbsab, this is the way it persists.in your case we can see only hbsag quantity not the antibody because there is no test at the moment but if you see hbsag down and hbvdna down you are eradicating.
cccdna maes also the complete virions and the other antigens

hbvdna reflects the virus relication but not the virions number, if it decreases there is less replication and this might reflect less virions around.hbsag/hbvdna ratio gives an idea of the number of virions produced

making only hbvdna is useless because you might have hbvdna almost zero but the liver full of cells infected by cccdna and blood full of hbsag, in any case with a very low hbsag it is not possible to have a lot of hbvdna and virions, when hbsag is zero the neutralizing antibody takes hold of virus

so you need both but hbsag is more important to know if drugs are working in terms of eradicating infection.

hbsag quantification is from 2008/9 studies made by the researchers in my hospital, doctor brunetto (a she), known well known around the world but all antivirals have almost no effect on it, only interferon and alinia

[goofygoatboy]

We do intend to get our genotype.  Luckily we both have insurance now.  That doesn't make it free but it means we can probably afford it.  

Is there an advantage to first using hbsag quantification and only then switching to hbvdna quantification?  I mean as opposed to just using hbvdna quantification as the primary measure.

[stef2011]

Does it sound reasonable to you?
yes perfectly.i'd just make the genotype because that's a simple routine test here, but i understand US might be different everything is free here so maybe we have a different approch on tests we just make them all if there is disease activity.
genotype is important to know interferon response, if you have a double mix of genotypes hbsag clearance rates cannot be applied.generally speaking:
peginterferon (not lambda) has 11-30% hbsag negative by 5 years
alinia (ntz) from small preclinical trials 25% hbsag eradication in one year monotherapy in hbe negative

about interferon use combo with nitazoxanide, not alone, and if possible lambda and if hbsag decreases go on with this therapy 2-3 years until hbsag gets negative.it is all off label but many doctors have done that already with normal interferon too

of course to make this therapy you need absolutely hbsag quantification, once hbsag is eradicated you must check hbvdna pcr ultraquant (sensibility 0.19iu/ml) for occult hbv which is very frequent on s variants

[goofygoatboy]

Bee55 and i have no reason to believe we have two genotypes.  I was acute (symptomatic and IgM c Ab positive) about 2.5 years ago when we had been together about 6 months.  She was checked at that time and found to s Ag positive and IgM c Ab negative.  I then went on to develop the high titer of s Ab that I currently have but failed to clear the virus.  My doctors interpretation of the results (which seems correct to me) is that I caught the virus from Bee55.  We don't know whether I got the immune escape variant from her directly or if I developed it on my own when my immune system kicked in and produced the s Ab.  I guess the second may be more likely since I'm not sure why I would produce the s Ab if i was initially infected with a virus with the s Ag mutation.  

Either way, we have had plenty of exposure to each other since then and assume that whatever we have we both have the same thing.  I understand that some mutations are less replication competent and die out in the presence of wild type, but in my understanding the common s Ag mutations are roughly equally competent so I am assuming bee55 can have both.  Of course I don't know this for a fact.  Does it sound reasonable to you?

I found some papers suggesting that success (sustained off treatment viral clearance) with peg interferon treatment is considerably more likely with A or B genotype (around 45%) than with C or D (around 15%) which is why I want to know my genotype.   If success is defined as e Ag sero conversion then the numbers are closer I think.  Plus, it may be worth trying it anyway because even 15% is much higher than the chance of sustained off treatment viral clearance with the antivirals which i think is only 1 or 2 %.
Do these numbers match your understanding?  Have you gone through the interferon treatment yourself?  Also, i'm not aware of how adding alina changes the response rates, do you know?

thanks

[stef2011]

both drugs are on trial for hcv but work on all viruses since immune modulators:
interferon lambda and alinia (nitazoxanide)

the first is on trail so difficult to have but nitazoxanide is already on market for other illnesses from as early as 2000-2004 so easy to have especially as a generic from mexico or indian producers (US alinia is way too expensive)