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ABBEY MSII U6 > Micro hepatitis viruses > Flashcards

Flashcards in Micro hepatitis viruses Deck (28)
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hepatitis A virology

picornavirus; ssRNA, naked icosahedral capside; environmentally rugged; single serotype (no reinfection and vaccine)


hepatitis A pathogenesis

fecal-oral - infects hepatocytes - often asymptomatic
causes acute hepatitis - NOT hepatotoxic - immunogenic response
1% fulminant hepatitis (quickly lose liver)


hepatitis A on exam

fever, jaundice, gastroenteritis, tenderness around liver, dark urine, pale feces
history: vaccination? foreign travel, daycare, shellfish


hepatitis A labwork

IgM = acute; IgG = resolved or vaccinated; serum ALT = liver damage


hepatitis A treatment

rest, fluids, monitoring; discontinue alcohol and contraindicated meds


hepatitis E virology

small, naked, icosahedral capsid, + ssRNA
one serotype
endemic to asia, africa, mexico


hepatitis E pathogenesis

fecal-oral transmission similar to hep A (acute hepatitis usually resolves) but higher mortality especially in pregnant women!


hepatitis E exam, labwork, treatment

exam: same as hep A (fever, ajundice, gastroenteritis.. travel?..)
labwork: serum ALT
treatment: same as hep A (rest, fluids, monitoring)


hepatitis B virology

hepadnavirus (hepaDNAvirus) - enveloped, DNA genome, partly double-stranded
one serotype, no reinfection , vaccine


how does hepatitis B evade immune system?

-replication produces many INCOMPLETE DECOYS!
-replication in hepatocytes leaves behind integrated viral DNA


hepatitis B pathogenesis

transmitted by blood, sex, birthing
90% have acute hepatitis then clear virus
remaining 10% have fulminant or establish chronic infection


complications of chronic hepatitis B infection

1. cirrhosis (ongoing cytotoxic attempt to clear virus)
2. kidney damage and arthritis (accumulation of antigen-antibody complexes)
3. hepatic cell carcinoma (integrated viral DNA and ongoing hepatocyte replacement in context or virus infection)


hepatitis B labwork

serology for timecourse of infection: surface antigen, surface antibody, core antibody, E antigen


what is anti-HBc indicative of?

no vaccine - prior infection!!


hepatitis B treatment

acute: supportive
DAMAGING chronic: polymerase inhibitors and alpha-interferons


prevention of hepatitis B

vaccination and immune globulin prophylaxis


what is the relationship between hepatitis B and D?

B is a helper virus to D


hepatitis D virology

viriod parasite of hep B
encodes single delta antigen (all other parts obtained from hepB infection same hepatocyte)
NOT capable of solo infection!!


which is worse? co infection or superinfection by hepB+D

superinfection! (pre-existing hep B followed by D) - in co infection, D can't infect all the way because it takes B a while to completely infect - a weak infection by D pretty much


hepatitis D pathogenesis

spread by blood, sex - delta antigen is hepatotoxic - fulminant hepatitis likely


hepatitis D labwork

EIA for delta antigen or antibodies against it


hepatitis D treatment

none effective - liver transplant if meets criteria


hepatitis C virology

favivirus - enveloped, +ssRNA


difference in B and C immune evasion

B makes decoys, C has lots of mutations!


hepatitis C pathogenesis

transmitted by blood, sex, 85% chronic infection with long latency
can proceed to liver failure which is mostly immunogenic


hepatitis C exam

MILD acute hepatitis
diagnose by EIA followed by RIBA and genotyping


hepatitis C treatment (second generation)

acute: pegalyted alpha interferon to reduce risk of chronic infection
chronic: attempt to achieve sustained viral response by combined therapy with:
1. ribavirin (viral chain terminator)
2. pegalyted alpha-interferon
3. HCV protease inhibitors: voceprevir or telaprevir

better for serotypes 2 and 3


hepatitis C treatment (third generatioN)

1. simeprevir serotype 1 with IFN and ribavirin
2. sofosbuvir + ledipasvir
3. sofosbuvir + ribavirin for serotypes 2 and 3