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.
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.
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?
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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