Viral Hepatitis Flashcards
What do all hepatitis viral infections have in common?
ability to cause liver inflammation and disease
Acute only infections
vowels
A, E
Acute/chronic infections
consonants
B, C, D
*need B to have a D infection (needs HBsAg)
Hepatitis G Virus
RNA –> icosahedral –> enveloped –> ss(+) nonsegmented (IV) –> flavivirdae
- same family as HCV and Yellow fever
- contaminated blood products
- current research says not associated with hepatocellular carcinoma or hepatitis
Hepatitis A Virus
RNA –> icosahedral –> nonenveloped –> ss(+) nonsegmented (IV) –> picornaviridae –> enterovirus
- small, naked virus
- capsid structure is EXTREMELY STABLE (can be killed by chlorine water or formalin)
- fecal-oral transmission
- infects cells expressing HAV cell receptor 1 glycoprotein (liver and T cells)
- infection results from immune response to virus –> ONLY ACUTE stage
Clinical Findings of HAV
fever, fatigue, nausea, anorexia, ab pain, dark urine, jaundice
- acute infection detected by anti-HAV IgM
Treatment of HAV
supportive treatment for infected individuals
- IgG for contacted individuals
HAV Vaccine
Hepatitis E Virus
RNA –> icosahedral –> nonenveloped –> ss(+) nonsegmented (IV) –> caliciviridae –> calicivirus
- mimics HAV infection! –> ACUTE infection only
- VERY dangerous in pregnant women
Why HEV bad for pregnancy?
immunological and hormonal factors may be responsible for more severe outcome –> T cells are reduced in pregnancy (HCG)
- damage to sinusoids results from the endotoxin (LPS) from gut flora that is left unchecked by suppressed immune system –> LPS is toxic to hepatocytes –> bad prognosis
Hepatitis B Virus
DNA –> icosahedral –> enveloped –> DS (partial) circular DNA (VII) –> hepadenaviridae –> orthohepadnavirus
- Dane particle infects host cell and a polymerase packaged by virus completes the DS genome –> enters nucleus and completes replication –> exits as Dane particle and HBsAg (decoy)
- blood borne pathogen
Acute or progress to chronic HBV?
immune response will dictate whether patient progresses to chronic infection
- more robust response –> acute only
- less robust response –> chronic infection
Spread of HBV in body
- virus enters blood –> enters liver (if immunized, doesn’t get to liver)
- virus starts to replicate within liver within 3 days of exposure –> symptoms may take up to 45 days
- secondary viremia that can be passed in body fluids (if robust immune response –> no viremia)
- Antibodies to the HBsAg results in Type III hypersensitivity immune complex formation –> itching
Acute serology course
EARLY 1. Spike in liver enzymes 2. HBsAg and HBeAg present 3. Anti-HBc rises WINDOW 1. surface antigen and Anti-HBs not detectable because forming immune complexes together LATE 1. No antigen present 2. Anti-HBs high 3. Anti-HBc and Anti-HBe decrease
Chronic serology course
EARLY 1. Spike in liver enzymes (not like acute phase) 2. HBsAg and HBeAg present 3. Ani-HBc rises LATE 1. HBsAg persistnet 2. HBeAg eventually fades 3. Anti-HBc stays elevated
HBV infection treatment
- prophylaxis with IgG to newborns from HBsAg (+) mom and vaccine
- chronic HBV –> antivirals