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39 Cards in this Set

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HAV
Hepatitis A Virus
a.k.a. "Infectious Hepatitis"
When studying, think A for Acute, Age-related symptoms and Asymptomatic Infection (children)
And, Antibody-detection (for diagnosis)
HAV
(epidemiology)
World-wide distribution
Predominant in equatorial, developing countries
MOST PREVENTABLE TRAVELER's DISEASE (vaccine)
HAV
(pathogenesis)
Fecal-Oral Transmission (via food/water/contact)
1 month incubation period
Virus shed in feces 2 weeks before symptoms
HAV
(Clinical Manifestations)
VAST MAJORITY RESOLVE COMPLETELY
Children: Asymptomatic
Symptoms of acute-infection increase with age
HAV
(Diagnosis)
IgM Ab to HAV
Hepatitis Viruses
Little PHK-ERs (of Picorniviridae)
Tells you small, (+)ssRNA and naked
Hepeviridae
Family
Non-enveloped, ssRNA
Gensus, Hepevirus
HEV
Hepevirus Genus, Hepeviridae Family (ssRNA, naked)
Major cause of sporadic/water-borne EPIDEMIC hepatitis
Consider HEV w/returning travelers
HEV
(pathogenesis)
Fecal-Oral Route
6 week incubation period
ACUTE Self-Limited Hepatitis
High Mortality during Pregnancy
HEV
(Diagnosis)
IgM to HEV antigen
Rising IgG also diagnostic
HBV
Hepatitis B Virus
Of Hepadnaviridae (enveloped, dsDNA)
HBV
(Replication Anomaly)
Even though dsDNA, first make RNA then reverse transcription to DNA
(weird RNA intermediate!)
Which Hepatitis Virus goes through an RNA intermediate during genome replication?
HBV (of Hepadnaviridae)
Hepadnaviridae
Family
As its name suggests, dsDNA (but with funky RNA intermediate and RT activity)
HBV
(Pathogenesis)
Parenteral Inoculation
(makes sense, the thing is lipid-enveloped so you're not going to go through the GI tract)
Incubation period is 3 months!
Asymptomatic, persistant (children) to symptomatic acute hepatitis (healthy adults)
HBV DNA
Nucleic Acid of HBV
Best marker of active viral replication
Anti-HBs
Indications immunity to HBV acquired by infection or vaccination
Antibody to what HB antigen is suggestive of IMMUNITY?
Anti-HBs
What Antibody is indicative of current/previous infection?
Anti-HBc (the core antigen, of the nucleocapsid)
If IgM, current infection
If IgG, previous infection
Possible outcomes of persistent (chronic) HBV
Chronic HBV (generally asymptomatic infection acquired in childhood)
May lead to chronic hepatits, cirrhosis or hepatocellular carcinoma (HCC)
HBV
(prevention)
Recombinant HBV vaccine using HBV surface antigen
HDV
(pathogenesis)
Coinfection w/HBV
Superinfection in chronic HBV cases (acute/FULMINANT hepatitis, chronic liver disease) <- it's nasty
HDV
(general)
Requires HBV
Delta antigen, encoded on ssRNA (circular)
Enables RNA to get into nucleus & replicate
HDV
(outcome)
If coinfection w/HBV, resolve
If superinfection, majority become chronic
HDV
(Diagnosis)
Serology
Anti-HDV titers (IgM or rising IgG) and HDV antigen
HDV
(Vaccination)
If HBV vaccinated, protected
If HBV (+), vaccine not available for protection against superinfection (they're screwed)
HCV
Of Flaviviridae (falvum = yellow . . . yellow fever, think blood. Also, think IV drug addicts and HepC. Tells you enveloped, (+) ssRNA
HCV
(pathogenesis)
Parenteral transmission (Pam An)
Acute, followed by persistent hepatitis
MOST COMMON CAUSE OF CHRONIC HEPATITIS, possibly resulting in cirrhosis and liver failure
HCV
(Diagnosis)
Antibody to HCV antigen
PCR can be used to monitor viremia and therapy
HCV
(Treatment)
Ribavirin + interferon
Avoid EtOH and get vaccinated for HAV/HBV
HGV
Genus Flavirus
Of Flaviviridae (tells you enveloped, (+) ssRNA)
NOT ASSOCIATED with Hepatitis but role in delaying AIDS!
Torque Tenovirus
Non-enveloped
Long-lasting viremia
Correlation w/Hepatitis but role not proven
Prions
PRoteinaceous INfectious Particles
Abnormal PrP (precursor amyloid protein, of stem/neuronal cells) that catalyzes the conversion of normal protein to aberrant form. Abnl protein forms insoluble fibers and plaques
Prions
(Infection Control)
Prions are resistant to head and most sterilization measures. Therefore, STRICT infection control is ABSOLUTELY NECESSARY
Prions
(Pathogenesis)
Acquired abnormal protein catalyzes the conversion of normal cell protein to aberrant form. Aberrant form accumulates, forms fibers and plaques - resulting in spongiform encephalopathies
Prions
(Transmission?)
May be transmissable (oral route, or transplants), idiopathic or inherited!
Transmissable Spongiform Encephalopathies
Oral/Transplant Transmission
Incubation period can be decades
Absent immune response
Rapidly progressive/fatal
Creutzfeldt-Jakob Disease
Idiopathic Sponogiform Encephalopathy
~60 yeards w/rapid progression toward death (3-4 months)
Variant CJD
Tranmissable Sponogiform Encephalopathy (BSE)
Mean age ~30 w/longer progression period
Link to Mad Cow's Disease