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 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.
Hepatitis B virus is a precursor to several other illness such as liver cirrhosis and hepatocellular carcinoma and from their names you notice that they all have to do with the liver.
The virus which is one of the smallest DNA virus has a protein coat which encloses a double stranded deoxyribose nucleic acid. When the virus infects the hepatocytes which are the main cells of the parenchymal tissue of the liver, its DNA particle changes to a form which enables transcription of the viruses mRNAs with the aid of the hosts RNA polymerase. This eventually leads to Virus replication and the production of its protein coat.
The transformed form of the nucleic acid which is the covalently closed circular DNA form has several characteristics such as its ability to have every of its nucleotide code for something and this makes its structure both compact and efficient. The protein coat of the new viral particles are produced during translation of AUG codons which are the start codons. The virus possess 7 viral proteins which needs several transcripts to enable their expression.
As mentioned earlier the HBV is compact and its compactness can lead to it having multiple effects on naturally occurring mutation from a single gene and this leads to difficulty in our efforts to figure out its pathogenic pathway.
The HBV genome is able to generate 4 polyadenylated RNAs through the aid of 4 promoters found on different position on the genome These 4 RNAs are transcribed by 2 enhancer elements and also by a transactivator known as HBx which is capable of causing multiple effects from a single gene. This transactivator is needed for HBV infection to occur and can also result in cancer of the liver.
The previous RNAs are transported to the cytoplasm of the host cell so that it can lead to protein translation and also replication of DNA.During this process, hepatitis B antigen is secreted and this protein is required for infection to be established. The pregenomic RNA which is the shorter version of the 3.5kb polyadenylated RNA produced and responsible for expression of core proteins is the only HBV transcript that is needed for genome replication.
Infection of a HBV does not directly lead to liver cirrhosis and HCC but however repeated actions of destruction and regeneration of the liver cells as a result of trying to flush out HBV may result to these diseases.
There are 8 genotypes of the HBV which are further dived into several subgenotypes with the exception of 3 genotypes, with each having little variation from the next. These genotypes of HBV are also restricted to certain regions of the world. Some genotypes such as genotype g which is popular among homosexual men are known to interact with several other diseases which can also result in more diseases originating. Although most of the genotypes of HBV are geographically specific, 1 host may possess more than 1 type of genotype of HBV (although 1 dominates over the other) as a result of increased migration. In cases of more than 1 HBV genotype infecting the same host, there may be formation of recombinant virus as a result of interaction between both viral genome.
In recent times, an additional 2 genotypes were discovered, although they had similarities with other genotypes, they possessed variations that could not be left unnoticed. The new genotype I is geographically specific to Southern China and also has a relationship with the development of HCC. Genotype J was isolated from an 88 year old man believed to have been infected during his stay at a south eastern Asian island. Genotype J is believed to be a recombinant of two HBV from different species.
To be continue…
Welcome to Skool 2. This is my first post. I finally managed to push myself to get things rolling.
Get those thoughts out and start acting on them. Time wait for no one.