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Path: Liver 3 - Acute + Chronic Hepatitis (iii) (HBV (Serological Dx (anti…
Path: Liver 3 - Acute + Chronic Hepatitis (iii)
HBV
leading cause of chronic hep, cirrhosis + liver cancer worldwide
prevalence = 0.1-10% depending on geography + risk factors
high prevalence (>8%) in SE Asia, China, Africa
intermediate prevalence (2-8%) in S Asia, Middle East
low prevalence (<2%) in N Europe, N America
patterns of migration affect prevalence
prevention
avoid/interrupt transmission
vaccination
DNA virus composed of surface + core (contains nuclear material)
only complete virus (surface + core) is infective in blood
HBsAg in surface: anti-HBsAg Ab confers immunity/protection
core contains...
HBcAg (core antigen)
HBeAg (e antigen from viral core - important for viral rep)
HBV DNA (8 different genotypes)
excess surface material can be produced (found as small non-infective particles in blood)
virus not directly cytopathic
immune response to replicating virus triggers necrosis-inflamm activity (damage, control + sometimes clearance)
causes liver damage (acutely, or if rep persists - chronically +/- acute flares)
response can fluctuate, dynamic state, subject to change
response typically absent in infected neonates (immune tolerance persists for decades)
IFN
Serological Dx
establishes dx, disease activity + state
HBsAg +ve: infected
tx can rarely achieve seroconversion to HBsAg -ve + Anti-HBsAg +ve
anti-HB +ve: protective immunity (recovery from infection with loss of HBsAg - i.e. resolved, or vaccine-every other serological marker -ve when vaccinated)
anti-HBc
best marker of exposure to HBV
IgM +ve: recent exposure, acute infection
HBeAg implies whole virus in blood, active rep, infective
anti-HBeAg
appears once HBeAg cleared (seroconversion)
primary aim of tx strategies
low infectivity
low/no viral rep
still HBsAg +ve = inactive carrier
mutant 'escape' strains of HBV exist
lack e antigen
escape Abs
may lead to reinfection
Virology
HBV DNA levels in blood = most reliable marker of active rep + infectivity
HBV Transmission
vertical vs horizontal (parenteral, sexual)
neonates: perinatal vertical transmission in high prevalence areas (if mother HBeAg+ve chronically she has a 90% chance of infecting her neonate
childhood acquisition
intimate non-sexual contact (percut/permucosal)
horizontal transmission in some high prevalence areas (e.g. Africa)
adult acquisition
sexual
blood or blood products
HCWs
IVDUs
horizontal
can occur in low prevalence areas (migration)
HBV infection outcomes
symptomatic in 30% of adults, rarely in neonates
rare cause of ALF
if neonate infected theres a 90% chance this will progress to chronic infection (due to immune tolerance)
if child infected theres a 20-30% chance this will progress to chronic infection
if adult infected theres a <5% chance this will progress to chronic infection (most get acute HBV that resolves)
can recur if immunosuppressed
age @ infection inversely related to risk of progression to chronic infection + also related to likelihood of symptomatic presentation during acute infection
the younger you are the less likely you are to have an immune response - more likely to be an asymptomatic chronic carrier
acute infection with recovery occurs in <10% of neonatal infections but >90% of adult infections
progression to chronic infection occurs in >90% of neonates but <5% of adults
HBV control
vaccination
active immunisation
universal @ birth (ire)
@ risk groups
pooled Anti-HB Ig post-exposure if non immune (passive immunisation)
screen if
signs of acute hep or chronic liver disease
country of origin has > 2% prevalence
pregnant (neonate can get anti-HB Igs)
prior to immunosuppression
high risk
IVDUS
lots of sex partners
MSM
contacts
children of parents from high prevalence areas