Kerriann Parchment GI CBL 2 Part 3 December 2012 Viral
hepatitis serology
Slide 2
Hepatitis A ssRNA virus Transmitted via Fecal-Oral route
Outbreaks are associated with Children in daycare Men who have sex
with men IVDU International travelers Contaminated seafood Usually
causes self-limiting acute illness Does not cause chronic hepatitis
Rarely causes fulminant hepatitis No carrier state
Slide 3
HAV Serology Anti-HAV IgMs are present at the onset of symptoms
and make a reliable marker of acute infection Remains for 4-6
months Anti-HAV IgGs Titers rise when anti-HAV IgMs decline Confer
long-term immunity
Slide 4
Hepatitis B DNA virus Transmitted via parental, sexual fluids,
perinatal Perinatal transmission is the main means of transmission
in high prevalence areas Unprotected sex and IVDU are main means of
transmission in low prevalence areas such as the U.S. Causes: Acute
hepatitis with complete clearance Chronic hepatitis Non-progressive
Progessive resulting in cirrhosis Fulminant hepatitis with massive
necrosis Inactive Carrier state
Slide 5
HBV serology HBV DNA Present when there is active or chronic
disease Inactive carriers or those immunized dont have HBV DNA
Antigens HbsAg- surface antigen that is present during active
disease (acute or chronic) HbcAg- protein present in the core and
is not detectable in serum HbeAg- secretory protein and is marker
of replication Antibodies Anti-Hbs- neutralizes HbsAg and its
presence indicates resolved infection Anti-HbcIgM- marks acute
infection and period during window period (period between
disappearance of HbsAg and anti-Hbs) Anti-Hbc IgG- can appear in
acute resolved infection or chronic HBV Anti-HbeAg- seroconversion
occurs early in acute infections and can occur later in chronic
infections
Slide 6
HBV serology Acute HBV (unresolved) HbsAg Anti-HBc IgM HbeAg
High levels of HBV DNA Acute HBV window period Anti-Hbc IgM Low
levels HBV DNA Resolved HBV infection Anti-Hbc IgG Anti-Hbs Chronic
HBV HbsAg Anti-Hbc IgG Low levels of HBV DNA Inactive chronic
carrier state HbsAg Anti-Hbc IgG Anti-HBe
Slide 7
Hepatitis D Defective RNA virus that co-infects with HBV
Requires HBV to complete virion assembly and secretion HDV can
replicate on its own Acute infections: anti-HDV IgM Chronic
infection: anti-HDV IgG
Slide 8
HCV Compared to HBV, more cases progress to chronic infection
or cirrhosis It is the leading cause of cirrhosis in the U.S.
Transmitted via IVDU Intranasal drug use Blood products
Occupational risks tattoos
Slide 9
HCV serology Acute HCV: HCV RNA can be detected by PCR
Infection will be cleared with development of Anti-HCV antibodies
Spontaneous clearance can occur in 14% of HCV patients
Slide 10
HEV Single stranded RNA virus Fecal oral transmission Disease
is most common in adult between the ages 15-40 Causes self limiting
disease in adults and there is no chronic state However, in
pregnant women, the disease is more severe and can cause fulminant
hepatic failure Anti-HEV Igm- Arise with the onset of symptoms
Anti-HEV IgG- will develop after symptoms resolve (2-4 weeks)
Slide 11
Works Cited Dr. Dubrovskaya. Lecture 14: Viral Hepatitis
Robbins and Cotran Chapter 18: Liver and Biliary Tract