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Figure 66-11. Clinical outcomes of acute hepatitis B infection. (Redrawn from White DO,
Fenner F: Medical virology, ed 3, New York, 1986, Academic Press
From Murray et. al., Medical Microbiology 5th edition, 2005, Chapter 62, published by Mosby Philadelphia,,
Immunological events of acute vs. chronic HBV
infection
A) Acute B) Chronic
From Murray et. al., Medical Microbiology 5th edition, 2005, Chapter 66, published by Mosby Philadelphia,,
Clinical interpretation of the Hepatitis B antigen
panel
Flint, S.J., Enquist, L.W. et. al., “Principles of Virology”ASM Press, 2000, Chapter
7
CDC website: http://www.cdc.gov/ncidod/diseases/hepatitis/slideset/hep_d/slide_1.htm
Notes:
HDV infection can be acquired either as a co-infection with HBV or as a superinfection of persons with chronic HBV
infection. Persons with HBV-HDV co-infection may have more severe acute disease and a higher risk of fulminant
hepatitis (2%-20%) compared with those infected with HBV alone; however, chronic HBV infection appears to occur
less frequently in persons with HBV-HDV co-infection. Chronic HBV carriers who acquire HDV superinfection
usually develop chronic HDV infection. In long-term studies of chronic HBV carriers with HDV superinfection, 70%-
80% have developed evidence of chronic liver diseases with cirrhosis compared with 15%-30% of patients with
chronic HBV infection alone.
Key features of Hepatitis Delta Virus
Figure 66-15. Consequences of deltavirus infection. Deltavirus (d) requires the presence
of hepatitis B virus (HBV) infection. Superinfection of a person already infected with HBV
(carrier) causes more rapid, severe progression than co-infection (shorter arrow).
From Murray et. al., Medical Microbiology 5th edition, 2005, Chapter 66, published by Mosby Philadelphia.
The HDV genome
Figure 88-4 Structure of the HDV RNA Genome. The single-stranded circular RNA genome is indicated by the heavy
black continuous line. The genome has the ability to form an unbranched rod structure, in which approximately 70%
of the bases are engaged in Watson-Crick pairs with counterparts from the opposite side of the circular RNA. In this
unbranched rod structure, the region encoding HDAg (nt 1598-957) is on one side. The RNA editing site is at
position 1012 in the antigenome. The region on the right-hand side contains the autocatalytic cleavage sites
(ribozymes), one in the genome (nt 686) and the other in the antigenome (nt 900). The genome binds HDAg and is
transcribed by a host DNA–dependent RNA polymerase.
Fields Virology 4th edition, 2002, Chapter 88, Lippincott, Williams and Wilkins, 2002 Fig. 88-4
CDC Website: http://www.cdc.gov/ncidod/diseases/hepatitis/slideset/hep_d/slide_6.htm
Diagnosis
A battery of serological tests are used for the diagnosis of acute and
chronic hepatitis B infection.
HBsAg - used as a general marker of infection.
HBsAb - used to document recovery and/or immunity to HBV
infection.
anti-HBc IgM - marker of acute infection.
anti-HBcIgG - past or chronic infection.
HBeAg - indicates active replication of virus and therefore
infectiveness.
Anti-Hbe - virus no longer replicating. However, the patient can still
be positive for HBsAg which is made by integrated HBV.
HBV-DNA - indicates active replication of virus, more accurate than
HBeAg especially in cases of escape mutants. Used mainly for
monitoring response to therapy.
Wong’s virology WEB site: http://virology-
online.com/presentations/hepatitis.htm
Hepatitis B acute infection
Note:
Pattern of
serological
markers
varies
depending
on
whether
the
infection if
acute or
chronic
Notes:
In patients with chronic
HBV infection, both HBsAg
and IgG anti-HBc remain
persistently detectable,
generally for life. HBeAg is
variably present in these
patients. The presence of
HBsAg for 6 months or
more is generally indicative
of chronic infection. In
addition, a negative test for
IgM anti-HBc together with
a positive test for HBsAg in
a single serum specimen
usually indicates that an
individual has chronic HBV
infection.
http://www.cdc.gov/ncidod/diseases/hepatitis/slideset/hep_b/slide_4.htm