Viral Description

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    Viral Description & Life Cycle

    Hepatitis B virus (HBV) is a DNA virus of the hepadnaviridae family. The HBV

    virion, also called a Dane particle, is approximately 42 nm in diameter and consists of

    an inner protein core and an outer protein envelope. The outer envelope is composed

    of several proteins, known as hepatitis B surface proteins (HBs), which encase thenucleocapsid, or inner protein shell, made of hepatitis B core proteins (HBc) (Bruss

    and Ganem, 1991). The nucleocapsid is arranged into an icosahedral formation and

    contains the hepatitis B genome and at least one hepatitis B polymerase protein. The

    figure below shows a diagram of the DNA virus.

    Figure 3. Image fromhttp://www.hon.ch/Library/Theme/HepB/hbvirus.GIF

    The viral genome is circular and is characterized by regions that are composed of

    single, double, and triple-stranded DNA. Within the genome are four partially

    overlapping open reading frames (ORFs) that encode seven different HBV genes,

    including but not limited to the hepatitis B surface antigen gene, also called the S

    gene, the hepatitis B core antigen gene, known as the C gene, the X gene, and the

    polymerase (P) gene (Ocama et. al., 2005). The figure below shows an image of the

    viral genome.

    http://www.hon.ch/Library/Theme/HepB/hbvirus.GIFhttp://www.hon.ch/Library/Theme/HepB/hbvirus.GIFhttp://www.hon.ch/Library/Theme/HepB/hbvirus.GIFhttp://www.hon.ch/Library/Theme/HepB/hbvirus.GIF
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    Figure 4. Image fromhttp://www.scielo.br/img/revistas/rhc/v59n4/21391f1.gif

    Unlike other envelope proteins, HBs span the lipid bilayer multiple times. There are

    three different size proteins based on the reading frame, yielding small, medium, and

    large HBs. The large hepatitis B surface antigen is believed to be most responsible for

    conducting viral-host cell attachment. A specific receptor, however, has yet to be

    identified. Another unique feature is that HBs can be secreted as subviral particles,

    lacking all other parts of the virion. Such particles are termed hepatitis B filamentsand hepatitis B spheres, each of which has a diameter of 22nm. Increased levels can

    be found during acute infection. However, because these particles lack core proteins,

    polymerase, and viral DNA, they are non-infectious and do not appear to be

    advantageous to the virus (Bruss and Ganem, 1991).

    Once the virus enters the body of a host, it infects liver cells. In doing so, the viral

    surface proteins fuse with the host cell membrane, allowing the core particle to enter

    the liver cell. Although early steps in viral entry are not clearly defined, the uncoated

    particle (or nucleocapsid) is transported into the nuclear membrane of the host cell.The viral DNA is then brought into the nucleus and is repaired to form a covalently

    closed-circular form, known as cccDNA. Viral DNA is not integrated into the host

    DNA like some viruses. Instead, once the DNA is recircularized, transcription of viral

    DNA and proteins begins and is controlled by four promoter elements and two

    enhancer elements. DNA polymerase then begins copying the DNA. The polymerase

    protein uses its unique shape to initiate reverse transcription and copy the DNA.

    http://www.scielo.br/img/revistas/rhc/v59n4/21391f1.gifhttp://www.scielo.br/img/revistas/rhc/v59n4/21391f1.gifhttp://www.scielo.br/img/revistas/rhc/v59n4/21391f1.gifhttp://www.scielo.br/img/revistas/rhc/v59n4/21391f1.gif
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    Unlike retroviruses, hepadnaviruses bind polymerase proteins into a stem-loop

    formation, which are subsequently packaged by core proteins in the golgi and secreted

    via exocytosis into the blood stream, where it can contact other liver cells and

    continue replication (Rehermann and Michelina, 2005).

    Figure 5. Image fromhttp://mgl.snu.ac.kr/images/HBV%20life%20cycle.jpg

    Bruss, V. & Ganem, D. 1991. The role of envelope proteins in hepatitis B virus

    assembly.Proceedings of the National Academy of Science USA88:1059-1063.

    http://mgl.snu.ac.kr/images/HBV%20life%20cycle.jpghttp://mgl.snu.ac.kr/images/HBV%20life%20cycle.jpghttp://mgl.snu.ac.kr/images/HBV%20life%20cycle.jpghttp://mgl.snu.ac.kr/images/HBV%20life%20cycle.jpg
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    Ocama, P., Opio, C., & Lee, W. 2005. Hepatitis B virus infection: Current status. The

    American Journal of Medicine. 118(12):1413-1420.

    Rehermann, B. and Nascimbeni, M. 2005. Immunology ofhepatitis B virus and

    hepatitis C virus infection.Immunology 5: 215-229.

    Return toChristie's Immunology Home Page

    Christie Brough. Biology 307: Immunology. Dr. S. Sarafova. Davidson College. May

    4, 2007.

    http://www.bio.davidson.edu/people/sosarafova/assets/bio307/chbrough/index.htmlhttp://www.bio.davidson.edu/people/sosarafova/assets/bio307/chbrough/index.htmlhttp://www.bio.davidson.edu/people/sosarafova/assets/bio307/chbrough/index.htmlhttp://www.bio.davidson.edu/people/sosarafova/assets/bio307/chbrough/index.html