Those who get the HBV at a very tender age have a higher tendency of developing a chronic infection compared to those who contact it later in life. Genotypes of the HBV also have their various mode of higher risk of contraction, some being from an infected mother and others from sexual encounters. Some of the genotypes have a greater tendency of leading to infection than the others but although the nature of the host’s body system and environmental surrounding’s also play a huge role.
Other factors which play a role in infection of the host include a protein known as HBeAg which is derived at the core protein and also the presence of some subviiral particles. Some genotypes have derived ways to increase the size of this protein those increasing their strength of creating an infection. Genotype G is an exception to the expression of this protein and this makes it loose its ability to cause a chronic infection but when it is present with another genotype to provide the HBeAg, chronic infection may occur.
The HBV has mutated in such a way that there is no longer expression of HBeAg but instead there is rapid multiplication so as to make up for those virus that are lost due to the hosts immune system.
Other mutations also occur when the HBV cannot undergo the mutation that changes the form of its stop codon, this new mutation helps these virus particles to suppress HBeAg expression. This type of mutation seems to be genotype specific also and also leads to increased replication of viral particles.
The envelope for HBV is not seen as a necessity i.e. it does not reduce its pathogenicity but in http://cialisfrance24.com the case of a naked viral particle, a protein coat can be made for it from another genome in the same cell. Since protein envelope production is not important, the pathway for its production for it can be shut down in order for the HBV to survive.
In most genome, there has been cases of some missing/deleted genes and are also genotype specific, some of these deletions also prove to cause more chronic infection and some just lead to the lack of non-expression of some other proteins. These deletions has in no way showed any form of it holding back the activities of the HBV.
Splicing or editing of HBV RNA has been shown to create more variation among the different HBV.This splicing has also been proven to increase the strength of infection caused due to it causing over expression of core proteins and also increased DNA replication.
HBV mutants may avoid the immune system and its antibodies by single amino acids substitute but this not mean that they will be able to escape the immune system. They may just be able to hide from it for a little while. The ability for these viruses to mutate to avoid the immune system by various mechanism has made most new vaccines inactive.These vaccines have to be used for a long time and most time these viral particles are able to develop a resistance thee drug.
In conclusion, one of the major reasons why HBV is still very much active in the human population is as a result of direct maternal transmission. The fact that these viruses are able to mutate at such a fast rate in other to avoid the immune system of the host cell and also to shut down certain proteins to increase replication rate just so to maintain their population is also a very big reason they still thrive. These viral particles are also just the starting bodies to many other liver related infections.