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33 Cards in this Set
- Front
- Back
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What is the structure of the HBV genome? How many ORF's does it have?
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*partially dsDNA
*4 overlapping ORF's |
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What constitutes the HBcAg? What do antibodies against this antigen mean?
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*the HBcAg, or core antigen, comes from the capsid of the virus
*anti-HBcAg are not protective and do not confer immunity |
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Where does HBeAg come from? What does its presence in the blood signify? How are antibodies against this antigen interpreted?
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*HBeAg is a soluble component of the viral core
*presence of HBeAg means active disease and high infectivity *presence of anti-HBeAg is a good clinical sign |
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Where does HBsAg come from? What does its presence mean? What do antibodies against this antigen confer?
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*HBsAg comes from the viral envelope and associated proteins
*HBsAg means there is live virus and infection *anti-HBsAg means resolution and complete immunity |
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Decsribe the replication of HBV.
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The viral DNA is filled in to yield a cccDNA which exists in the host nucleus. cccDNA is transcribed by host RNA pol. The RNA transcript leaves the nucleus and is packaged in a capsid. The viral RT converts the RNA transcript into a pdsDNA genome inside of the capsid.
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What is the difference between a Dane particle and an Australia antigen?
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The Dane particle is the complete virion whereas the Australia antigen is the empty envelope.
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Chronic HBV can pass through several stages, culminating in PHC...what are these stages? How long can the transition from acute infection to PHC take?
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*chronic persistent hepatitis
*chronic active hepatitis *cirrhosis *PHC *30 years |
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How are arthritis and glomerulonephritis associated with HBV infection?
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HBV infection can lead to the formation of antigen-antibody complexes whose deposition causes these conditions.
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Why doesn't infection with HBV overstress the host cell?
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The virus regulates its own activity and replication to prevent overstressing the host cell.
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A primary infection of HBV has three outcomes - what are they?
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1.Acute episode induces a strong immune response which clears the infection and bestows immunity.
2.Acute episode induces an intermediate immune response that fails to clear the infection; persistent infection and chronic state 3.No acute episode and immunotolerance; persistent infection and chronic state |
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Why do immunosupressed individuals often have an asymptomatic presentation of HBV?
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Much of the pathology is associated with CMI and CTL's. These patients have inactive immune system thus little pathology is seen.
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Why might a patient show immunotolerance and fail to have an acute episode during initial infection with HBV?
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Anergic CTL's.
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T/F:
Integration of viral and tumor DNA is required for the conversion of chronic HBV to PHC. |
False: though HBV DNA is often found integrated into tumor DNA this is not required for development of PHC.
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HBV infection can spread to extrahepatic tissues - what are three such tissues?
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*spleen
*bile duct epithelia *kidney *pancreas *lymphocytes |
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How is HBV transmitted?
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*in blood and body fluids
*needles *sex *vertical/perinatal |
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What do the presence of IgM anti-HBcAg and IgG anti-HBcAg signify?
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IgM anti-HBcAg is indicative of a new infection whereas IgG anti-HBcAg is indicative of an old infection.
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What is the "window state" that is sometime seen with the serology of patients with acute/non-chronic HBV infection?
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The point of the infection where HBsAg has disappeared from circulation but anti-HBsAg has not yet appeared, thus serology will be negative.
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When do anti-HBcAg appear in the disease course of HBV?
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The appearance of anti-HBcAg is concurrent with the appearance of symptoms.
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Describe the antigen/antibody profile of a patient with chronic HBV.
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*an initial sharp rise then plateau in HBsAg and HBeAg
*there is a sharp rise then decline of IgM anti-HBcAg with an associated rise in IgG anti-HBcAg *there is a rise in anti-HBeAg several years after the initial infection |
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What is the HBV vaccine? Who should receive it?
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The vaccine is a recombinant HBsAg. It should be given to all newborns and workers with occupational risk. Also it is effective in the post-exposure setting if given within one week.
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Name three compounds used in the treatment of HBV.
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1.Lamivudine
2.Interferon alpha 3.Adefovir |
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What is the mechanism of action of lamivudine? What problems have been associated with its use?
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Lamuvidine (3TC) is an analog of cytosine that when tri-phosphorylated will act as a chain terminator and inhibit DNA synthesis by the viral RT. Many patients experience post-treatment rebound of viremia; also there is emergining resistance to the drug.
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What is the mechanism of action of Adefovir?
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It is an analog of dAMP which acts as a chain terminator to inhibit DNA synthesis by the viral RT.
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What is an absolute condition of infection with HDV?
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It can only infect host cells concurrently infected by HBV.
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What is the genome structure of HDV? How many ORF's does it encode?
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*a small, circular (-) ssRNA
*it has a single ORF |
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What makes HDV unique among (-) RNA viruses?
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It does not code for its own RNA-dependent RNA pol, and seems instead to be transcribed by the host DNA-dependent RNA pol II.
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From where does the HDV get its viral envelope lipoproteins?
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It parasitizes them from HBV.
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How does co-infection with HDV and HBV affect a patient's prognosis?
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This combination is associated with a more aggressive clinical course and higher mortality.
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What are the two types of infection setting seen with HDV?
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*a patient acquires HBV and HDV at the same time
*a HBV patient acquires HDV as a superinfection |
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How does a patient's ability to clear HBV affect their ability to deal with HDV?
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Ability to clear HBV is correlated with ability to clear HDV as well.
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How is HDV diagnosed?
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Detection of HDV antigen or antibody against HDV antigen.
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Is there a vaccine for HDV?
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There is not a specific vaccine, but vaccination for HBV confers immunity against HDV.
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Are drugs used to treat HBV effective at treating HDV?
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No - these drugs affect the HBV RT but not the synthesis of HBs antigen. Thus they are ineffective against HDV.
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