Hepatitis A virus Flashcards
Hepatitis A virus
Picornaviridare “ Infection hepatitis”
Hepatitis B virus
Hepadnaviridae “Serum Hepatitis”
Hepatitis C Virus
Flaviridae “Serum Heptatitis”
Hepatitis D virus
Satellite, co-infect with HBV
Hepatitis E virus
no family established, “infections hepatitis”
Hepatitis F and G
no family established; Flaviviridae
Primary causes of Chronic liver disease
Hepatitis C; Alcohol; Hepatitis C + Alcohol; Unknown;
Hepatitis A, acute or chronic
- acute infection, not chronic
- most common vaccine preventable diseases in the world
Genome of Hepatitis A
- Single stranded
- Positive
- RNA
- viral protein on the 5’ end
Capsid structure of Hepatitis A
- icosahedral
- 4 viral polypeptides(VP1-VP4)
Envelope of Hepatitis A
-does not contain one
Family of Hepatitis A
Picornavirus
Hepatitis A is stable in what kind of conditions?
- acid at pH 1
- solvents
- detergents
- salt water, groundwater(months)
- drying
- cold(3C) and high(61C) temperature
Inactivation of Hepatitis A by?
- chlorine treatment
- Formalin
- Peracetic acid
- Beta propiolactone
- UV
Replication process of Hepatitis A
- Receptor binding
- RNA uncoating
- Translation and proteolytic processing
- RNA processing
- Virion assembly
- Maturation and release
Incubation of Acute Hepatitis
-period is 2 to 6 weeks, mean of 4 wks
Prodrome phase of Acute hepatitis
- mild flu like
- anorexia, nausea, vomiting
- fatigue, malaise, myalgia, headache
- low grade fever
Icteric phase of Acute hepatitis
- dark urine; pale stool
- jaundice
- abdominal pain
- itch(pruritus)
Recovery of acute hepatitis
- symptoms generally wane during jaundice period
- complete recovery 99% of the time
Physical appearance of jaundice
- aka Icterus
- yellowing of skin, conjunctiva, mucous membrane
Cause of jaundice
-increased levels of bilirubin(unconjugated)
Normal process of death of RBCs
- heme converted to bilirubin in spleen and hepatocytes
- bilirubin processed by liver, becomes conjugated
- enters bile and excreted via feces
Conjugated bilirubin excretion method
-water soluble and excreted via kidneys
Pathogenesis of Hepatitis A
- ingestion
- replication in oropharynx/GI
- transported to liver
- shed in bile, transported to intestines
- shed in feces
- brief viremia
- cellular immune response
Hepatitis Virus course
- ALT(alanine transaminase) highest 1 month after exposure
- IgM antiHAV increases then decreases 1-5months
- Total antiHAV log growth increase after 1month
Epidemiology of Hepatitis A
- close personal contact
- contaminated food, water
- blood exposure
Prevalence of antibodies for hepatitis A
- highest in N.A., Australia, Western Europe
- lowest everywhere else
Diagnosis of hepatitis A
-detection of HAV-IgM in serum
Diagnosis of past infection of hepatitis A
-detection of HAV-IgG in serum
HAV IgG/ HAV IgM interpretations
(+/+) - acute HAV infection
(-/+) - acute HAV infection, but early phase
(+/-) - no acute HAV infection, immunity
(-/-) - no acute HAV infection, no immunity
Control of Hepatitis A
- infected people immune for life *
- good hygiene, block transmission
- passive or active immunization
Hepatitis A vaccinations
-present and 3 types
