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has anyone come across this article in uk about hbv phases?

http://www.micropathology.com/images/downloads/Interpretation%20of%20HBV%20diagnostic%20tests%20_4.pdf
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link doesn't work...
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www.micropathology.com/images/downloads/Interpretation%20of%20HBV%20diagnostic%20tests%20_4.pdf
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Copyright Micropathology Ltd Page 1 of 3
www.micropathology.com ***@****
Micropathology Ltd
University ofWarwick Science Park, VentureCentre, SirWilliamLyons Road, Coventry CV4 7EZ
Website: www.micropathology.com E-mail: ***@****
Tel 24hrs: +44 (0) 24 - 76 – 323222
Fax / Ans: +44 (0) 24 - 76 - 323333
The Interpretation of Diagnostic Blood Tests for Hepatitis B Virus (HBV)
HBsAg - Hepatitis B surface antigen
·  Presence indicates infection with HBV
·  Is DETECTED in both acute cases and in HBV carriers
·  Persistence for six months defines carrier status
·  Levels may reflect the amount of virus in the liver and may provide useful information
during treatment monitoring
·  A decline in levels may predict eventual clearance of HBsAg
HBeAg - Hepatitis B e antigen
·  Can be DETECTED in the early phase of HBV infection (usually short lived, 3-6
weeks)
·  Becomes UNDETECTABLE in acute HBV as the virus clears and HBeAb is
DETECTED
·  Can persist in carriers and is usually associated with DETECTABLE HBV DNA
·  During the immune-active phase in HBV carriers a seroconversion occurs when
HBeAg becomes NOT DETECTED as HBeAb becomes DETECTED
·  It is possible for HBeAg and HBeAb to be both DETECTED at the same time or both
NOT DETECTED but this is uncommon
·  NB: Presence of HBeAg is not required for infectivity or replication. It is not part of
the structure of the virus. Some patients with active viral replication do not produce
HBeAg due to the presence of HBV variants
HBeAb - Hepatitis B e antibody - anti-HBe
·  Appearance in acute cases likely to be indicative of spontaneous resolution
·  Carriers who are HBeAg NOT DETECTED, HBeAb DETECTED and HBV DNA NOT
DETECTED are considered to be in the inactive phase. Liver function tests are
usually normal in these cases and they are of low infectivity
·  Carriers who are HBeAg NOT DETECTED, HBeAb DETECTED and HBV DNA
DETECTED usually have abnormal liver function tests and are an infection risk
HBV DNA - Hepatitis B virus DNA
·  Presence indicates infectivity and active viral replication
·  HBV DNA levels in the blood are essential for the diagnosis, decision to treat and
monitoring of patients
·  <103 IU/ml is likely to be associated with disease resolution
·  High levels may be present in carriers with no evidence of liver damage
·  May be NOT DETECTED in blood but DETECTABLE in the liver
Copyright Micropathology Ltd Page 2 of 3
·  Presence in the liver of individuals with UNDETECTABLE HBsAg in blood defines
Occult HBV
HBV genotype and subtypes
·  Eight genotypes defined, designated A,B,C,D,E and F with a number of subtypes
·  Associated with distinct geographical areas
·  Different genotypes may respond differently to anti-viral treatment
·  May influence the severity of liver disease, disease progression and clinical outcome
HBsAb - Hepatitis B surface antibody - anti-HBs
·  Is usually, but not always, DETECTED after the disappearance of HBsAg in acute
infection
·  Is sometimes DETECTED in HBV carriers
·  Is the ONLY antibody produced by successful vaccination
HBcAb - Hepatitis B core antibody - anti-HBc
·  DETECTED in anyone who has been previously exposed or is currently, infected
with HBV
·  In acute infection appears after the appearance of HBsAg and usually before a rise
in liver enzymes
·  Its persistence in all those who have been exposed to HBV makes it a useful
epidemiological marker
·  Is NOT DETECTED in those who have been vaccinated against HBV and have
never been infected with the virus
HBcAb IgM - IgM anti-HBc
·  Routinely used to confirm the diagnosis of acute HBV infection
·  May be the only marker present in cases of acute liver failure where HBsAg has
already become NOT DETECTABLE and anti-HBc is not yet DETECTED but this is
uncommon
·  Levels may be elevated in HBV carriers with an active immune response to the virus
such as those undergoing seroconversion
Note:
·  Transfused blood or transplanted organs of people who are HBsAg NOT
DETECTED, HBcAb DETECTED may transmit HBV to the recipients
·  People who are HBsAg NOT DETECTED, HBcAb DETECTED may reactivate and
become HBsAg DETECTED again if they become immune compromised
·  HBcAg - Hepatitis B core antigen cannot be DETECTED in the blood but can be
DETECTED in the liver
Copyright Micropathology Ltd Page 3 of 3
Phases of HBV infection:
Phase 1: immune-tolerant or replicative phase. In the initial phase of infection there is
little or no immune recognition of HBV. Inflammatory activity is low, liver enzymes are
normal or of low levels, levels of HBV DNA are high, HBeAg is positive and there is no or
minimal pathology on liver biopsy. During this phase the rate of spontaneous HBeAg loss is
very low. This phase is more frequent and more prolonged in those infected perinatally or in
the first years of life. These carriers are highly infectious.
Phase 2: immune-reactive phase. During this phase the immune system recognizes the
virus and tries to eradicate it. There is moderate or severe liver necroinflammation and more
rapid progression to fibrosis compared to the previous phase, liver enzymes are elevated or
fluctuating and HBV DNA and HBeAg levels fall. Seroconversion occurs with loss of HBeAg,
detection of HBeAb and lowering of HBV DNA levels to below 102-103 IU/ml. There is an
increased rate of spontaneous HBeAg loss. This phase may last for several weeks to
several years. Patients in this phase are infectious.
Phase 3: inactive-phase. This may follow seroconversion from HBeAg to HBeAb detection.
HBV DNA levels are very low or undetectable and liver enzymes fall as inflammatory activity
in the liver decreases. This state suggests a favourable long-term outcome with a very low
risk of cirrhosis or HCC in the majority of patients. HBsAg loss and seroconversion to HBsAb
may occur spontaneously in ~1.5% of cases per year, usually following several years of
undetectable HBV DNA. Patients remain infectious but at a lower level.
Phase 4: HBeAg negative chronic HBV may follow seroconversion. This is characterised by
periodic reactivation with fluctuating levels of HBV DNA and aminotransferases and active
hepatitis. These patients harbour HBV variants with nucleotide substitutions in the precore
and/or basal core promoter regions and are either unable to express HBeAg or express low
levels. Patients in this phase are infectious.
Phase 5: HBsAg negative phase. In this phase HBV DNA is generally undetectable in
serum while anti-HBc with or without anti-HBs is detectable. HBsAg loss is associated with a
reduced risk of cirrhosis, decompensation and HCC. The clinical relevance of Occult HBV
where HBV DNA continues to be detectable in the liver in such patients is unclear.
Immunosuppression may lead to reactivation in these patients. Patients are considered noninfectious.
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