Flashcards in Hepatitis Deck (34):
Oral-fecal or parentally spread liver viruses.
6. hepatitis A - E + G
Hepatits A virus (HAV)
Hepatitis B virus (HBV)
Non-A, non-B hepatitis (NANBH)?
Hepatitis C (HCV)
Hepatitis D (HDV) [the delta agent]
Hepatitis E (HEV)
Hepatitis G (HGV)
HAV structure + features
replicates in hepatocytes + Kupffer cells (liver). slowly. non-cytolytic, released by exocytosis.
occur abruptly 15-50 days post-infection.
initial symptoms: fever, fatigue, nausea, loss of appetite, vomiting, abdominal pain.
Liver damage symptoms: Dark urine, Pale stool, Jaundice, Icterus. (rarely jaundice in children)
Complete recovery in 99%. within 2-4 weeks of start of symptoms. up to 2 months. Lifelong immunity.
based on symptoms
anti-HAV IgM ELISA or Radioimmunoassay.
cannot be isolated.
HAV prevention and control
water treatment + avoid uncooked shellfish.
prophylaxis or immune serum globulin treatment (80-90% effective)
Killed HAV vaccines.
all children after 1 year of age. high risk adults + travellers.
(live vaccine in chine, crazy fuckers)
hep E. E = enteric/epidemic.
similar to HAV but later symptoms and more mortality.
serious in preg women.
HBV structure + features
Small enveloped DNA virus, very stable.
small circular, partly (?) dsDNA. encodes RT, replicates thru RNA intermediate. Dane particles, filamentous particle, spherical particle
entry into hepatocyte and uncoating of core. DNA is transcribed in the nucleus into mRNA, RT turns RNA into -DNA, then becomes +DNA. DNA filled core becomes associated with HBsAG, exocytosed.
HBV patho + immune response
tropism for liver.
replicates in liver, symptoms >45 days.
HBsAG presence causes cytopathology (necrosis)
inflammation and CMI: causes symptoms and also resolution.
HBV types of infection. why?
Chronic, acute symptomatic, asymptomatic. Depends on immune response.
weak CMI, echausted CD8 T cells. mild disease, when active liver cirrhosis, failure, major source of spread
HBV acute symptomatic
90% of infections. Strong CMI, after 45 days: nausea, fever, malaise, anorexia. later: jaundice, dark urine, pale stoolsresolution.
1% of acute symptomatic cases, kills you.
initially: jaundice and liver enzymes
HBsAg & HBeAg in serum. anti-HBc&HBe&HBs. quantitative viral load by genomic PCR
HBV control + treatment.
HBV immune globulin: to recently exposed + neonates of + mothers.
Drugs: Iamivudine, entecavir,telbivudine, tenofovir, adefovir dipivoxii, famciclovir.
Vaccination: 1 serotype = yes. yeast recombinant vaccine,: HBsAg Virus like particle. 3 injections.
Hepatitis C virus family
# of genotypes
6 (clades), considerable genetic and antigenic diversity.
HCV structure + features
infects only humans and chimps.
-Acute infection:15-25% clear HCV no treatment
-Chronic HCV: Long term, ~70%
-Hepatic steatosis: fatty liver
-Hepatic Fibrosis: scarring of the liver, still reversible by clearing HCV
-Hepatic Cirrhosis: you
fuked now. severe fibrosis(scarring of living), irreversible
-hepatocellular carcinoma: you have cancer now. (1-5% of cirrhosis people)
HCV pathogenesis features
-down regulates IFN-a response
-down regulate dendritic cell maturation
-major surface proteins E1&E2 drift.
-antibody does nothing, need CMI. but CD8 T cells damage liver and cause cirrhosis.
ELISA: anti-HCV antibody.
denome detection and quantitation by RT-PCR
mostly cannot be grown in culture.
Hepatits G virus
pretty much HCV, almost no symptomatic cases. detectable by RT-PCR
Hepatitis D virus HDV
requires HBV to replicate, often co-infection occurs. causes fulmitant hepatitis (fatal)
anti-HDV antibodies; ELISA and radioummunoassay
RT-PCR for virion genome in blood
ELISA to detect delta antigen.