Hepatitis B pathophysiology: Difference between revisions
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*In the nucleus, second-strand DNA synthesis is completed and the gaps in both strands are repaired to yield a covalently closed circular (ccc) supercoiled DNA molecule that serves as a template for transcription of four viral RNAs that are 3.5, 2.4, 2.1, and 0.7 kb long.<ref>{{cite book | last = Nathanson | first = Neal | title = Viral pathogenesis | publisher = Lippincott-Raven | location = Philadelphia | year = 1997 | isbn = 0781702976 }}</ref><ref>{{cite book | last = Plotkin | first = Stanley | title = Vaccines | publisher = W.B. Saunders Co | location = Philadelphia | year = 1999 | isbn = 0721674437 }}</ref> | *In the nucleus, second-strand DNA synthesis is completed and the gaps in both strands are repaired to yield a covalently closed circular (ccc) supercoiled DNA molecule that serves as a template for transcription of four viral RNAs that are 3.5, 2.4, 2.1, and 0.7 kb long.<ref>{{cite book | last = Nathanson | first = Neal | title = Viral pathogenesis | publisher = Lippincott-Raven | location = Philadelphia | year = 1997 | isbn = 0781702976 }}</ref><ref>{{cite book | last = Plotkin | first = Stanley | title = Vaccines | publisher = W.B. Saunders Co | location = Philadelphia | year = 1999 | isbn = 0721674437 }}</ref> | ||
* These transcripts are polyadenylated and transported to the cytoplasm, where they are translated into the viral nucleocapsid and precore antigen (C, pre-C), polymerase (P), envelope L (large), M (medium), S (small)), and transcriptional transactivating proteins (X).<ref>{{cite book | last = Nathanson | first = Neal | title = Viral pathogenesis | publisher = Lippincott-Raven | location = Philadelphia | year = 1997 | isbn = 0781702976 }}</ref><ref>{{cite book | last = Mandell | first = Gerald | title = Mandell, Douglas, and Bennett's principles and practice of infectious diseases | publisher = Elsevier/Churchill Livingstone | location = New York | year = 2005 | isbn = 0443066434 }}</ref> | |||
===Transmission=== | ===Transmission=== | ||
Revision as of 14:50, 29 July 2014
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Hepatitis B |
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Hepatitis B pathophysiology On the Web |
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American Roentgen Ray Society Images of Hepatitis B pathophysiology |
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Risk calculators and risk factors for Hepatitis B pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Pathogenesis
Intracellular HBV is non-cytopathic and causes little or no damage to the cell.[1]
Life Cycle
- The HBV virion binds to a receptor at the surface of the hepatocyte.[1]
- Severeal cellular receptors have been identified, including the transferrin receptor, the asialoglycoprotien receptor molecule, and human liver endonexin. However, the mechanism of HBsAg binding to a specific receptor to enter cells has not been established yet. Viral nucleocapsids enter the cell and reach the nucleus, where the viral genome is delivered.[1][2][3]
- In the nucleus, second-strand DNA synthesis is completed and the gaps in both strands are repaired to yield a covalently closed circular (ccc) supercoiled DNA molecule that serves as a template for transcription of four viral RNAs that are 3.5, 2.4, 2.1, and 0.7 kb long.[4][5]
- These transcripts are polyadenylated and transported to the cytoplasm, where they are translated into the viral nucleocapsid and precore antigen (C, pre-C), polymerase (P), envelope L (large), M (medium), S (small)), and transcriptional transactivating proteins (X).[6][7]
Transmission
Transmission results from exposure to infectious blood or body fluids containing blood. Possible forms of transmission include (but are not limited to) unprotected sexual contact, blood transfusions, re-use of contaminated needles and syringes, and vertical transmission from mother to child during childbirth. Without intervention, a mother who is positive for the hepatitis B surface antigen confers a 20% risk of passing the infection to her offspring at the time of birth. This risk is as high as 90% if the mother is also positive for the hepatitis B e antigen. HBV can also be transmitted between family members within households, possibly by contact of nonintact skin or mucous membrane with secretions or saliva containing HBV.[8]
Immunopathogenesis
During HBV infection, the host immune response causes both hepatocellular damage and viral clearance. While the innate immune response does not play a significant role in these processes, the adaptive immune response, particularly virus-specific cytotoxic T lymphocytes (CTLs), contributes to nearly all of the liver injury associated with HBV infection. By killing infected cells and by producing antiviral cytokines capable of purging HBV from viable hepatocytes, CTLs also eliminate the virus.[9]
References
- ↑ 1.0 1.1 1.2 "Hepatitis B" (PDF).
- ↑ Nathanson, Neal (1997). Viral pathogenesis. Philadelphia: Lippincott-Raven. ISBN 0781702976.
- ↑ Guidotti LG, Martinez V, Loh YT, Rogler CE, Chisari FV (1994). "Hepatitis B virus nucleocapsid particles do not cross the hepatocyte nuclear membrane in transgenic mice". J Virol. 68 (9): 5469–75. PMC 236947. PMID 8057429.
- ↑ Nathanson, Neal (1997). Viral pathogenesis. Philadelphia: Lippincott-Raven. ISBN 0781702976.
- ↑ Plotkin, Stanley (1999). Vaccines. Philadelphia: W.B. Saunders Co. ISBN 0721674437.
- ↑ Nathanson, Neal (1997). Viral pathogenesis. Philadelphia: Lippincott-Raven. ISBN 0781702976.
- ↑ Mandell, Gerald (2005). Mandell, Douglas, and Bennett's principles and practice of infectious diseases. New York: Elsevier/Churchill Livingstone. ISBN 0443066434.
- ↑ name="pmid791124">Petersen NJ, Barrett DH, Bond WW, Berquist KR, Favero MS, Bender TR, Maynard JE (1976). "Hepatitis B surface antigen in saliva, impetiginous lesions, and the environment in two remote Alaskan villages". Appl. Environ. Microbiol. 32 (4): 572–574. PMID 791124.
- ↑ {{cite journal | author=Iannacone M. et al | title=Pathogenetic and antiviral immune responses against hepatitis B virus | journal=Future Virology | year=2006 | pages=189-196 | volume=1 | issue=2