A simple brief summary of Hepatitis B virus for medical students. I'll be happy to hear your comments so that we can modify it to gain the max benefit in a simple way. Done by Mays Yousuf

1. Hepatitis B virus facts
HBV is an enveloped DNA virus from hepadnavirus family, with one serotype used in vaccine as HBsAg.
Its natural and only host is the human.
The virus has a partial dsDNA with 4 genes; C,S,X, and P genes that translate 5 protiens.Also, a DNA-
dependent DNA polymerase that can work as a reverse trascriptase.
The envelope has a surface antegin detectable in the acute and chronic phase of infection, and absent
in the window period. The E antegin isn’t always expressed but if, it indicates transmissibility.
Replication cycle: RNA and DNA dependent DNA synthesis
1. HBV enters the cells and is uncoated.
2. In the nucleus, DNA polymerase completes the genome circle so it becomes cdsDNA.
3. mRNA is made by DNA template using cellular RNA polymerase.
4. In the cytosol, a positive mRNA strand is made to be a template fot a minus DNA strand, to positive
DNA progeny strand.
5. Progeny HBV are assembled and released from the cell by budding.
HBV is transmitted by blood transfusion, sexual intercourse, and during delivery.
The virus has an incubation period of 10-12 weeks, follwed by a prodrome, and a convalescence that
ends either with recovery or a chronic carrier state.
The first serologic marker to appear is the HBsAg in the acute phase that becomes undetectable in the
window period, and returns in case of chronic carrier. However, HBsAb is formed later in the course of
disease but still not detectable in states of chronic carrier.
HBcAb appears in the acute phase as IgM for the first 6 months, and in the chronic phase as IgG, and
it’s the most accurate identifier of recent and chronic infections.
Persistence of HBsAg for 6 months after acute infection defines a chronic carrier.
Children born to HBsAg mothers go into a chronic carrier state with no symptoms due to the tolerant
phase of immune system at birth. After a few decades, reactivation with hepatitis occurs, follwed by
seroconversion to HBeAb, and development of either recovery or a chronic carrier state.

2. Risk factors for progression to chronic disease:
An old male with a family history of HCC, and concurrent hepatitis viruses infection who has an
elevated serum HBV DNA, ALT, or AFP levels.
Whom to treat in HBV infection? To those at high risk of progressive liver disease and HCC:
1. HBsAg positive with evidence of chronic infection.
2. Serum HBV DNA > 2000 IU/ml.
3. High ALT serum level.
4. Significant inflammation and necrosis on liver biopsy on follow-up.
Whom to vaccinate with recombinant vaccine? High-risk groups:
1. Active vaccination for health workers, homo- and bisexuals, IV drug abusers, patients on dialysis,
and hemophilia patients. This lasts for 10 years.
2. Combined passive and active vaccination for non-vaccinated health workers, newborn for a HBsAg
mothers, and sexual partners for HBsAg patients.
HBV treatment:
1. Nucleoside analouges: Entecavir (1st
line), Telbivudine, and Tenofovir (1st
line).
2. Nucleotide analouges: Lamivudine, and Adefovir.
3. PegIFN alpha-2b (1st
line).
Interferon causes flu-like illness, myelosuppression, hepatitis, neurologic defects, autoimmune
reactions, and heart failure.
All other drugs reduce DNA levels, and shouldn’t be given in case of renal failure.
Entecavir can be used in Lamivudine resistance.