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Already infected, can you catch another genotype?
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Already infected, can you catch another genotype?

If someone is infected with a certain genotype, can they get infected with another genotype?  If on antivirals, will that reduce the chances of getting infected by the new genotype?
15 Comments Post a Comment
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Avatar_m_tn
I always wondered the same thing. I sort of read a study where some people had strains from mixed genotypes but I would have to go back and look.

Bigger question is Hepatitis C seems to be 80% curable/treatable, so why not Hepatitis B? My knowledge is extremely limited. Maybe if I create a separate thread StudyForHope can shed some light.
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Avatar_m_tn
Since the spread of virions is not blocked inside the liver for your current genotype, there is no reason that a new genotype that you aquire cannot get a hold in the liver and slowly spread until an equilibrium is reached.
Yes, superinfection is possible.

The reason that hepatitis C can be much more easily eradicated lies on the fact that it does not have a stored form of hard to destruct genetic material, like cccDNA  of hepatitis B. When you completely block its dynamic life cycle, it will die of.

If the HBV antivirals would block replication 100%, HBV could not continue to slowly spread while at the same time some infected cells die of or loose the cccDNA noncytopathically. But they only block about 99.6%, thus new virions are still slowly formed and infect neighboring cells. These virions never make it into the blood stream, therefore the undetectable status is a bit misleading and the number of infected cells and the total cccDNA and the proportionally produced surface antigen does not decrease.
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Avatar_m_tn
Then if we have more than 1 genotype, how to detect it? Also, this is the first time i've seen an opinion stating Hep C is better than Hep B. Is this really true?
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Avatar_m_tn
I believe HCV RNA reside in the cytoplasm of infected liver cells. Scientists are predicting a complete cure for HCV within the next 5 years.
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Avatar_m_tn
Depending on the percentage of the respective genotype, the innolipa genotype assay will show a second positive line. If there is however a substantial fitness difference, given enough time the fitter strain will prevail.

HCV  has as stephen pointed out a more instable RNA genome residing in the cytoplasm. Its continued existence depends on ongoing replication.
Furthermore there are several independent targets that can be blocked by antivirals, leading to a true synergistic blockage, once sufficiently low toxicity antivirals with a low resistance propensity have been developed and approved.
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Avatar_m_tn
What about HBV? Any prediction of a cure?
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Avatar_m_tn
Unfortunately, no. It is very frustrating to see no major breakthroughs, except for REP9AC, in the last 10 years.Either HBV is not a serious disease or it is not taken seriously. Sigh.
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Avatar_m_tn
GI 13020
Myrcludex B
Rep9AC'
ARC520
GS9620

all potential cures developed in the last few years, now we just have to wait
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Avatar_m_tn
Thank you studyforhope...

We are very fortunate to have you on this forum. All of the information and support you provide is greatly appreciated it.

Thanks again for your insight on my questions.
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Avatar_m_tn
What will happen if you being chronic with one hbv genotype get infected by another? You will beome chronic with two genotypes or the last you got is acute and therefore resolved after  6 months?
Or maybe immune response for the fresh virus would clear the both?
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Avatar_m_tn
A superinfection with another genotype or just another strain can have many outcomes.
Depending on fitness and new reactable Tcell epitopes there could be balanced coexistence or a flare which could lead to the elimination of the vast majority of cells infected with the epitope recognizable strain. A collateral clearance of the immunoadapted primary HBV strain is also possible, but rarely to completion. The cccDNA of the primary strain could be removed from an infected cell by very high localized IFNgamma secretion of activated CTLs from the engagement with the epitopes presented on the neighboring cell infected with the new, epitope equipped strain.
But this outcome will be rare. Most likely , after the flare, a slow rebound of the unaffected HBV strain will occur.
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Avatar_m_tn
The flip side is: superinfection can change from a disease inactive state to one that is active?
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Avatar_m_tn
Yes, this is one of the possible outcomes, activation of disease, when semiefficient immune activity is induced by the newcomer strain.
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Avatar_m_tn
Can you please explain in simple terms 'How does hepb vaccine works'? Thank you very much.
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Avatar_m_tn
This off topic. But this is the simple answer:

The outer coat of the HBV  virion is build of surface antigen proteins.

The vaccine also  contains tiny spheres of surface antigen proteins on their surface that have a precisely defined shape, just like on the virion surface.

The vaccine induces the production of antibodies that can bind strongly to these shapes.

Once those antibodies are present and virions are entering the body, far away from the liver, these antibodies will bind all around to the surface of the intruding virions.

These coated virions are unable to hook up to the receptors waiting for them on the liver cell surface.

Thus no entry and no infection is possible.
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