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Phyloepidemiology study of Chronic Hepatitis B
Virus Infection using Next-Generation Sequencing in Saudi Arabia.

 

Understanding the viral diversity of Hepatitis B virus using
Whole genome sequencing and development of antiviral efficacy in vitro model.

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As
stated above, vaccination with HBsAg has been efficacious in the pre-exposure
setting; however, occult infections began to be noted in the late 1980’s55,56 and the first case of a vaccine-induced
escape mutant, in a child in southern Italy, who received passive-active
post-exposure immunization, was described in 1990.57 Mutations within the S gene are known to
be responsible for occult hepatitis B infections, reactivation of hepatitis B,58,59 diagnostic assay failure58,60–63 and reinfection in HBV-infected recipients
of orthotopic liver transplantations.17,64 Occult infections create public health
concerns because asymptomatic carriers can be blood donors.65–67 These mutations are stable and can be
transmitted horizontally and vertically.56,68–71

HBV replicates to high titers in infected
individuals. Because it replicates through an RNA intermediate synthesized by
reverse transcriptase, mutant viral genomes59,72 and quasi-species71–77 are generated. This results in the
production of viral mutants during naturally occurring infections.78,79 Vaccination and the administration of HBIG
and anti-viral drugs like lumavidine exert evolutionary pressures to select
mutants.70,80

The a determinant is
located on the major hydrophilic region (MHR) of the S gene, which is between
amino acids 120 and 160. The MHR forms a two-loop structure. There are two
alternative models for this double loop structure, which involve two pairs of
cysteines forming disulfide bridges at the ends of each loop. The more
generally accepted model envisions disulfide bridging between C124 and C137 and
between C139 and C147.58 The alternative model is built on
disulfide bridging between C107 and C138 and between C139 and C147.63

 

Following infection, the HBV genome is transported to the
nucleus and converted to CCC DNA to yield a double stranded genome which serves
a template for transcription by the host cell RNA polymerase 11. Transcription of the template
gives rise to pre-genomic mRNA and thee sub –genomic mRNAs. The 3.5 kB pre-genomic
mRNA is produced with redundant ends and is used for translation of the core protein
and polymerase enzyme. Following transport of the pre-genomic mRNA and translation
in the cytoplasm, selective encapsidation of the RNA into the nucleocapsid ensues,
along with encapsidation of RNA polymerase. In the immature capsid, he 3.2 kb mRNA
is revers transcribed, to yield the minus strand. The RNA is degraded and the
DNA strand is replicated, producing the second, shorter DNA strand. Early in
the infection cycle, the cellular burden of viral DNA is amplified following
the transportation of mature nucleocapsid to the nucleus in order for
replication to repeat. Viral surface proteins are produced at a later stage of
the infection process, where sub genomic mRNAs are produced and translated. Nucleocapsids
containing DNA genomes then acquire their outer envelope, possibly by budding
into the endoplasmic reticulum (ER) in areas where transmembrane HBsAg are inserted.
The resulting Dane particles are then transported from the cell by normal
pathways of vesicular transport. The particles are assembled and released
without cell lysis, with no evidence of injury to host cells 

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