Aa
HEP B Virus
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?
i confused with the email of another member, if you PM me your email i will send you all sstudies i have
i have sent you an email with all the studies i have
of course hbvdna is the most close test we have to measure circulating virions but it is not an exact test to reflect infection or what happens in the liver, it is like a picture taken far from the liver
it is helpful to refer to a couple of scientists about studies made in the last two years, no t to all, many studies are not well done
one of the best scientists on hbv is from my hospital, maurizia brunetto, she has made the caraterization of the hbe negative mutants and the role of hbsag quantification
she has made a conference in pisa with all the biggest scientists only in 2009, i understood most of hbv from their posters, i will send you an email with a rar file of all the studies i have from her and the most advanced scientists on hbv, they take time but it is good to know hbv so you can choose the best strategy togehter with the doctors
I think this link is pretty helpful in understanding the life cycle of virus.
http://biology.kenyon.edu/slonc/bio38/scuderi/parti.html
I don't claim to understand it entirely but I think it is pretty clear that the hbv dna test directly measures the number of virons in the blood. Because, according to this only three types of particle are released by the infected cells, two composed entirely of s antigen proteins and the viron itself which contains the virus dna. If the virus is replicating at a high rate there are lots of virons containing dna, If it is not there are few or perhaps none. Another source that says clearly that this is the case (the hbv dna test quantifies circulating virons) can be seen here.
http://www.labtestsonline.org/understanding/analytes/hepatitis_b/test.html
I don't think it's correct that the s antigen is suppressing the immune system either, but it may be that the large quantities of non infective s antigen in the blood act as decoys and bind up the hbvsab allowing the virons to circulate and infect new cells. That is suggested as a possibility in the first source. In fact (again according to the first source above) purified s-antigen proteins are what the hbv vaccine is made up of and they stimulate the immune system. At least if it works.
I don't mean to be nit picky on these details but I would like to get as many details as possible straight in my own head. Exchanging these comments with you is very helpful. thank you.
http://biology.kenyon.edu/slonc/bio38/scuderi/parti.html
I don't claim to understand it entirely but I think it is pretty clear that the hbv dna test directly measures the number of virons in the blood. Because, according to this only three types of particle are released by the infected cells, two composed entirely of s antigen proteins and the viron itself which contains the virus dna. If the virus is replicating at a high rate there are lots of virons containing dna, If it is not there are few or perhaps none. Another source that says clearly that this is the case (the hbv dna test quantifies circulating virons) can be seen here.
http://www.labtestsonline.org/understanding/analytes/hepatitis_b/test.html
I don't think it's correct that the s antigen is suppressing the immune system either, but it may be that the large quantities of non infective s antigen in the blood act as decoys and bind up the hbvsab allowing the virons to circulate and infect new cells. That is suggested as a possibility in the first source. In fact (again according to the first source above) purified s-antigen proteins are what the hbv vaccine is made up of and they stimulate the immune system. At least if it works.
I don't mean to be nit picky on these details but I would like to get as many details as possible straight in my own head. Exchanging these comments with you is very helpful. thank you.
both hbsag and hbeag are produced to suppress immune system, the most potent is hbsag, hbeg is not needed by the virus and is the only antigen that can go through placenta so it is thought it is a mean of immune tollerance and infection to a baby, which is the main source of hbv infections since babies have more than 90% chances to get cronic hbv and not adults.but there are many many other ways hbv escape immune response and even suppressing hbvdna is good for immune system.
in any case the main antigen blocking immune system is hbsag since hbv can be cleared even without hbeab antibodies
To the extent that it is quantitative the hbvdna directly represents the number of circulating infectious virons doesn't it?
no it has nothing to do with the virions, i don t know exact terms but i think the dna is released when a cell is infected but that cell produces many many virions and many immune suppressing antigens not just one virion, there is no direct correlation between virions and hbvdna just an idea.
all the tests that you can make in the blood gives only an idea of the infection but the only mean to really measure with high sensitivity and precision is hbv biopsy and measuring virus and antigenes directly in the liver cells
It seems like the hbvsag couldn't go undetectable while....
i m sorry i cannot understand this question but the main consideration is hbsab antibody blocks virus entrance in liver cells so you can understand the meaning of this for the virus.hbvdna can be still positive even if hbsag is undetactable but at very low levels because the virus cannot replicate since all liver cells are closed for him and ,unless like in your case there is mutation, the virus will have a very short life and hbvdna slowly und since hbv has no way to replicate
some cccdna will be left in your liver anyway but until hbsab is present the infection will never be able to start again, this is a danger only in case of transplant or chemiotherapy but both entecavir or tenofovir can block infection if started before transplant/chemiotherapy
in any case the main antigen blocking immune system is hbsag since hbv can be cleared even without hbeab antibodies
To the extent that it is quantitative the hbvdna directly represents the number of circulating infectious virons doesn't it?
no it has nothing to do with the virions, i don t know exact terms but i think the dna is released when a cell is infected but that cell produces many many virions and many immune suppressing antigens not just one virion, there is no direct correlation between virions and hbvdna just an idea.
all the tests that you can make in the blood gives only an idea of the infection but the only mean to really measure with high sensitivity and precision is hbv biopsy and measuring virus and antigenes directly in the liver cells
It seems like the hbvsag couldn't go undetectable while....
i m sorry i cannot understand this question but the main consideration is hbsab antibody blocks virus entrance in liver cells so you can understand the meaning of this for the virus.hbvdna can be still positive even if hbsag is undetactable but at very low levels because the virus cannot replicate since all liver cells are closed for him and ,unless like in your case there is mutation, the virus will have a very short life and hbvdna slowly und since hbv has no way to replicate
some cccdna will be left in your liver anyway but until hbsab is present the infection will never be able to start again, this is a danger only in case of transplant or chemiotherapy but both entecavir or tenofovir can block infection if started before transplant/chemiotherapy
Thank you. I hadn't understood that in addition to reproducing "itself" (infectious viron particles) the virus also produces a lot of non infectious surplus protein particles and that these are what are referred to as hbvsag. (wikipedia life cycle of hbv) The same proteins (s antigens) also appear in the infectious particles but the infectious particles may only make up around 1% of the total hbvsag in circulation (http://biology.kenyon.edu/slonc/bio38/scuderi/parti.html). This same source says the hbveag is thought to reside on the core protein which (I think) means it is only present on the infectious viron particles, do you know if that's correct?
You say that hbvdna reflects the virus replication but not the virons number, but that doesn't sound right to me. To the extent that it is quantitative the hbvdna directly represents the number of circulating infectious virons doesn't it? It seems like the hbvsag couldn't go undetectable while the hbvdna remained high unless I had what amounts to a false negative, i.e. the hbvsag test missed the hbvsag, possibly due to mutations of the s antigen. likewise, it doesn't seem like the hbvdna could go undetectable (indicating very low viral replication) while the hbvsag (surplus proteins reproduced during replication) remained high. what am i missing here?
i think i see your larger point though, that a major goal of treatment is that my immune system succeed in clearing the hbvsag. In my case I guess this would mean that I developed an additional antibody that was able to bind the s antigen variant that is seemingly not recognized by the hbvsab that I already have in abundance.
I really appreciate your willingness to entertain these questions and respond to them. I think i am slowly getting a better understanding of the disease and what kind of treatment options make sense to try in my case.
You say that hbvdna reflects the virus replication but not the virons number, but that doesn't sound right to me. To the extent that it is quantitative the hbvdna directly represents the number of circulating infectious virons doesn't it? It seems like the hbvsag couldn't go undetectable while the hbvdna remained high unless I had what amounts to a false negative, i.e. the hbvsag test missed the hbvsag, possibly due to mutations of the s antigen. likewise, it doesn't seem like the hbvdna could go undetectable (indicating very low viral replication) while the hbvsag (surplus proteins reproduced during replication) remained high. what am i missing here?
i think i see your larger point though, that a major goal of treatment is that my immune system succeed in clearing the hbvsag. In my case I guess this would mean that I developed an additional antibody that was able to bind the s antigen variant that is seemingly not recognized by the hbvsab that I already have in abundance.
I really appreciate your willingness to entertain these questions and respond to them. I think i am slowly getting a better understanding of the disease and what kind of treatment options make sense to try in my case.
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
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
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
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
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.
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.
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
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
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
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
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)
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)
as for therapy consider and find as much info as possible on interferon and nitazoxanide and avoid antivirals that work on hbvdna
there is a new interferon which is a little more potent and with less sides by the combo of these drugs you might have chances to eradicate hbv, both drugs are active on hbsag wild type or mutated, they don t make mutations or resistance, and can be stopped.i guess only having two genotypes mixed (i mean the a,b,c,d genotypes) might be a different situation from the reports of trials in lowering hbsag
i have also read, but i don t know if this is your case, that patients with hbsag mutations have lower levels and this makes eradication by alinia (nitazoxanide) and interferon much easier and faster.ask for hbsag, hbcag and cccdna/intraepatic hbvdna quantification by biopsies, this is a test which can be easily made in any hbv research university/hospital and do save your biopsies so that when more tests are available you don t need to remake them
thanks stefano, good to know. my fiance will see his doctor in a couple of weeks (he just had a biopsy done today - mine was couple of weeks ago) and see if we can get the genotype identified through a test-lab his doctor can refer us to, hoping near by. We are in Idaho. If that results in more questions, and we need to have tested further for mutations, I will ask you then for names you know. I really appreciate your help, you are a huge source of info, and this is sooo confusing to me...so I am a little scared, but hopeful, too, that there are some possibilities out there.
thanks again, I will stay online and read, and learn what I can for the time being.
thanks again, I will stay online and read, and learn what I can for the time being.
there is competition for liver cells between hbv and hcv, hcv is able to suppress hbv, this might be the reason
in boston conference i read a study on this the found the hcv substance which suppress hbv
in boston conference i read a study on this the found the hcv substance which suppress hbv
And I forgot to add that I had my vaccination against B virus only around 15 years ago.-April.
Hello, I've been reading this thread about virus B transmission between HBV carriers and I have one related question. Maybe someone will be able to help me out. Is there a scientific explanation why there is a low risk of transmission in long term relationships? It's seem rather peculiar,don't you think? My partner of 30 years (my husband) and I have had unprotected sex for many years. His infection is one with moderate hbvdna level ( 350 000 IU/ml). I'm very happy I didn't get HBV from him. On the same note he didn't get my HCV. None of our 2 children didn't get our viruses. I'm very,very happy. Don't get me wrong but I would like to know why? I can't be just a lucky coincidence. Is there a scientific explanation of this? Thank you kindly for your answers.
stevenNY suggested me harvard in boston or if you are close to LA maybe trying to get in touch with HR, if you are interested in one of these locations i can PM doctors names
thanks..I see...hmmm...I guess we are looking research center in the US to find out our genotype, since that is where we live. So far, it doesn't seem so simple to find one here...
if there is no water treatment like in swimming pool you might get many other diseases like fungus and bacteria (the types you get at swimming pools)
as to hbv if you have cuts it is possible but very unlikly, dentists have still high percentages of hbv/hcv since it is not possible to lower it to zero despite hygenization.I've read that in US also healthcare settings are a very big source because of wrong procedures since hospitals try to save money on anything, the other main sources are sex and mothers at birth but there is also a high percentage where the way of infection is unkown
the mutants are present in all genotypes, as for the tests i go to the main research centers which are normal hospitals for our healthcare system, you just book and go there free of charge for any blood test, ultrasound/fibroscan.
visits are made by the team of doctors/researchers, not the main researcher director brunetto.we have many researchers on hbv in italy but the best are brunetto in pisa and lampertico in milan.so in those settings you have the most updated tests, machines and drugs on trial
as to hbv if you have cuts it is possible but very unlikly, dentists have still high percentages of hbv/hcv since it is not possible to lower it to zero despite hygenization.I've read that in US also healthcare settings are a very big source because of wrong procedures since hospitals try to save money on anything, the other main sources are sex and mothers at birth but there is also a high percentage where the way of infection is unkown
the mutants are present in all genotypes, as for the tests i go to the main research centers which are normal hospitals for our healthcare system, you just book and go there free of charge for any blood test, ultrasound/fibroscan.
visits are made by the team of doctors/researchers, not the main researcher director brunetto.we have many researchers on hbv in italy but the best are brunetto in pisa and lampertico in milan.so in those settings you have the most updated tests, machines and drugs on trial
I was just reading something about how HBV can survive extreme temperatures.
Do you think it is possible to get infected I HOT SPRINGS? Me and my fiance often visit Hot Springs...wondering if that is maybe how we got the virus about 3 years ago....Also, can we possibly infect others by going to Hot Springs? (say we have a cut, bleeding type of circumstances)
Do you think it is possible to get infected I HOT SPRINGS? Me and my fiance often visit Hot Springs...wondering if that is maybe how we got the virus about 3 years ago....Also, can we possibly infect others by going to Hot Springs? (say we have a cut, bleeding type of circumstances)
thanks for all these VERY valuable information.
You said you got yours tested in Italy. Was that done by mail?
The cancer marker mutants you listed are "A" genotype?
You said you got yours tested in Italy. Was that done by mail?
The cancer marker mutants you listed are "A" genotype?
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