Audia: Hepatitis ILA Flashcards
the major problem for viral hepatitis
chronic liver disease and HCC
picornavirus
acute diease
HAV (Hep A virus)
2 enteric acute diseases
HAV and HEV
hepadnavirus
acute
chronic/cancer
HBV (hep B virus)
flavivirus (RNA)
acute, chronic/cancer
HCV
RNA virus
co-infection with HBV
chronic/fulminant
HDV
oral-fecal transmission
infectious hepatitis
NO chronic or carrier state
Hepatitis A
2-4 wk incubation (IgM then IgG)
Hepatitis A
naked capsid
+ssRNA
HAV
replication of HAV:
receptor mediated endocytosis
uncoat and RNA released in cytoplasm
single polyprotein made and chopped up by protease into functional subunits
type of virus that is ready to be translated once it gets into host cell cytoplasm
+ssRNA
extremely stable due to no envelope
Hep A
sx’s of fever, fatigue, nausea, abd pain occur abruptly
Hep A
incubation period is average of 30 days
Hep A
can see jaundice within 2-4 wks as compared to hep B 1-6 months
Hep A
close personal contact
contaminated food/water (shellfish)!
blood exposure (rare)
Hep A
to dx:
time course of sx’s
identify source
serology
Hep A
best way to prevent Hep A
vaccine
hepadnavirus
spreads by blood/bodily fluids
Hep B
can lead to chronic disease and HCC
Hep B
“serum hepatitis”
Hep B
enveloped virus
dsDNA genome
has surface Ag
Hep B
surface antigen for Hep B that actually breaks off as well with the Hep B virus from host cell and acts as decoy to host Ab’s so Hep B can prevail
HBsAg
surface antigen used for HBV vaccine
HBsAg
soluble antigen of HBV and associated with replication
HBeAg
core antigen that will bind with host Ab and indicate carrier/chronic infection
HBcAg
Hep B replication
into host cell (becomes a part of host genome)
uncoat
reverse transcriptase
makes more virus
HBV and HBsAg released
how do people become carriers of Hep B
if exposed and have weak T cell response (mild sx’s but won’t clear virus)
jaundice from liver damage 1-6 months post infection
Hep B
10% of these cases become chronic (cirrhosis)
Hep B
____% of cases of HCC have viral cause
80%
long incubation (3 months ave)
insidious onset
prodromal phase
Hep B acute infection
classic icteric sx’s of liver damage
jaundice, dark urine, pale stool
fulminant disease of HBV when co-infected with what
HDV
what type of hypersensitivity rxns can be associated with Hep B
type III (immune complexes)
detected by liver enzymes
Hep B chronic infection
____% of patients develop cirrhosis or liver failure
10%
80% of all HCC is due to what
HBV
HBV has integration of viral genome into what
host hepatocyte DNA
Hep B transmission
sexual
parenteral
perinatal
Dx w/ clinical sx’s
elevated liver enzymes
serology and virus proteins
Hep B
Rx/prevent Hep B
HBsAg Hep B vaccine
ssRNA
requires co-infection with HBV
HDV (Hep D)
host RNAPII makes RNA copy
replicates genome, makes mRNA
genome is ribozyme
replication for Hep D
blood/bodily fluids transmission
co-infection
Hep D
Dx Hep D
ELISA for delta Ag or Ab
flavivirus
difficult to culture
1-6 month incubation period
can cause chronic disease
Hep C
+RNA genome
enveloped
Hep C
how to make drugs against viruses
selective toxicity
Hep C replication:
Bind to receptor and gets in by endocytosis
Endosome w/ lysosome and pH drops and helps un-coat and release ribonucleic acid into cytoplasm
Replicate and make polyproteins—–then chopped up by protease to make functional pieces
Leave host cell through exocytosis
main mechanism of immune avoidance for Hep C
antigenic drift (error prone replication and causes mutations)
____ are the reservoirs for HCV
humans
Ab to HCV not protective why
antigenic drift
60-85% likelihood of chronic infection
Hep C
no vaccine for this
Hep C
dx by ELISA
hep C
_____ has to have an external coat of Hep B before it can infect hepatocytes and multiply
Hep D
