Glossary of HBV and HDV
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- What is the structure of the HBV genome? How many ORF's does it have?
- *partially dsDNA
*4 overlapping ORF's
- What constitutes the HBcAg? What do antibodies against this antigen mean?
- *the HBcAg, or core antigen, comes from the capsid of the virus
*anti-HBcAg are not protective and do not confer immunity
- Where does HBeAg come from? What does its presence in the blood signify? How are antibodies against this antigen interpreted?
- *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
- Where does HBsAg come from? What does its presence mean? What do antibodies against this antigen confer?
- *HBsAg comes from the viral envelope and associated proteins
*HBsAg means there is live virus and infection
*anti-HBsAg means resolution and complete immunity
- Decsribe the replication of HBV.
- 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.
- What is the difference between a Dane particle and an Australia antigen?
- The Dane particle is the complete virion whereas the Australia antigen is the empty envelope.
- 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?
- *chronic persistent hepatitis
*chronic active hepatitis
- How are arthritis and glomerulonephritis associated with HBV infection?
- HBV infection can lead to the formation of antigen-antibody complexes whose deposition causes these conditions.
- Why doesn't infection with HBV overstress the host cell?
- The virus regulates its own activity and replication to prevent overstressing the host cell.
- A primary infection of HBV has three outcomes - what are they?
- 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
- Why do immunosupressed individuals often have an asymptomatic presentation of HBV?
- Much of the pathology is associated with CMI and CTL's. These patients have inactive immune system thus little pathology is seen.
- Why might a patient show immunotolerance and fail to have an acute episode during initial infection with HBV?
- Anergic CTL's.
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.
- HBV infection can spread to extrahepatic tissues - what are three such tissues?
*bile duct epithelia
- How is HBV transmitted?
- *in blood and body fluids
- What do the presence of IgM anti-HBcAg and IgG anti-HBcAg signify?
- IgM anti-HBcAg is indicative of a new infection whereas IgG anti-HBcAg is indicative of an old infection.
- What is the "window state" that is sometime seen with the serology of patients with acute/non-chronic HBV infection?
- The point of the infection where HBsAg has disappeared from circulation but anti-HBsAg has not yet appeared, thus serology will be negative.
- When do anti-HBcAg appear in the disease course of HBV?
- The appearance of anti-HBcAg is concurrent with the appearance of symptoms.
- Describe the antigen/antibody profile of a patient with chronic HBV.
- *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
- What is the HBV vaccine? Who should receive it?
- 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.
- Name three compounds used in the treatment of HBV.
- What is the mechanism of action of lamivudine? What problems have been associated with its use?
- 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.
- What is the mechanism of action of Adefovir?
- It is an analog of dAMP which acts as a chain terminator to inhibit DNA synthesis by the viral RT.
- What is an absolute condition of infection with HDV?
- It can only infect host cells concurrently infected by HBV.
- What is the genome structure of HDV? How many ORF's does it encode?
- *a small, circular (-) ssRNA
*it has a single ORF
- What makes HDV unique among (-) RNA viruses?
- 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.
- From where does the HDV get its viral envelope lipoproteins?
- It parasitizes them from HBV.
- How does co-infection with HDV and HBV affect a patient's prognosis?
- This combination is associated with a more aggressive clinical course and higher mortality.
- What are the two types of infection setting seen with HDV?
- *a patient acquires HBV and HDV at the same time
*a HBV patient acquires HDV as a superinfection
- How does a patient's ability to clear HBV affect their ability to deal with HDV?
- Ability to clear HBV is correlated with ability to clear HDV as well.
- How is HDV diagnosed?
- Detection of HDV antigen or antibody against HDV antigen.
- Is there a vaccine for HDV?
- There is not a specific vaccine, but vaccination for HBV confers immunity against HDV.
- Are drugs used to treat HBV effective at treating HDV?
- No - these drugs affect the HBV RT but not the synthesis of HBs antigen. Thus they are ineffective against HDV.
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