Hep Flashcards

1
Q

Hepatitis G classification

A
RNA virus
Icosahedral Nucleocapsid
Enveloped
SS (+) Nonsegmented
Flavivirdae
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2
Q

Hepatitis G is in the same family as these two virusus

A

HCV

YFV

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3
Q

How does one usually acquire Hep G?

A

Exposure to contaminated blood products (multiple blood transfusions, IV drug users)

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4
Q

If one has Hep G they may be coinfected with one of these viruses (2)

A

HBV
HCV
(or both)

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5
Q

How is Hepatitis G diagnosed

A

detection of the genome by RNA via RT PCR

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6
Q

Which two Hep viruses are Fecal to Oral transmitted?

A

A and E

Think acute infections

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7
Q

Which three Hep viruses are through blood/sexual contact

A

HBV, HCV, HDV

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8
Q

Short incubating viruses (2-8 weeks)

A

HAV and HEV

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9
Q

Long incubating viruses (2-24 weeks)

A

HBV, HCV and HDV

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10
Q

Can all Hep viruses cause an acute infection?

A

Yes

Only HBV, HCV and HDV will progress to chronic

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11
Q

Hepatitis A classification

A
RNA virus
Icosahedral nucleocapsid
SS (+) non segmented
Picoraviridae
Enterovirus
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12
Q

Describe the structural features of Hepatitis A

A

Small, naked virus

VPg protein is attacked at the genome containing polyA tail

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13
Q

What happens after the RNA for Hep A is translated?

A

RNA is translated all at once then cleaved down to subsequent products that have specific functions (example : structural vs non structural)

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14
Q

How can Hep A virus be inactivated?

A

Chlorine treatment in drinking water
Formalin
UV radiation

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15
Q

Mechanism of Hep A infection

A

Fecal to oral
Infects cells expressing HAV cell receptor 1 (HAVCR1)
Virus replicates in large quantities in liver and shed in stool 10 days before onset of jaundice

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16
Q

What actually causes the pathogenic effects of hepA?

A

Hep A isn’t cytotoxic

It’s the immune response to the viral infected liver cells (by cytotoxic T cells)

17
Q

Most common cause of liver failure in the US (and subsequent transplant)

A

Chronic HCV

18
Q

How do viral hepatitis infections often present?

A
febrile illness of prolonged duration
jaundice
fatigue
abdominal pain
loss of appetite
nausea
vomiting
19
Q

Hepatitis infection labs

A

High AST, ALT, BIL and total protein

20
Q

Why can arthritis and rash occur with hepatitis

A

immune complex associated vascultis

21
Q

Risk factors for HAV

A

contaminated seafood or imported berries

22
Q

Risk factors for HBV

A

Multiple sexual partners and unprotected intercourse

23
Q

Risk factors for HCV

A

intravenous drug use and blood transfusion (prior to 1990)

24
Q

Entecavir

A

HBV

Guanosine nucleoside analog that inhibits HBV polymerase

25
Q

Pegylated interferon alpha 2A

A

HCV + AIDS/KS
HBV

Cytokine with immunomodulating, antineoplastic and antiviral properties

26
Q

Tenofovir disoproxril fumerate (TDF)

A

HBV

Inhibits activity of HBV polymerase by competing with dATP causing DNA chain termination

27
Q

Brief review of ELISA

A

HAV IgM serum of individual
HAV antigen on plate.
Add serum
If ab against the HAV virus, will bind and stick
Then use second ab that changes color
anywhere with color has the IgM antibody from the individual

28
Q

Where does peak liver damage occur in HAV

A

When the CTL and IgM response occurs

29
Q

Exposure prophylaxis for HAV?

A
If healthy (1-40 yo) - HepA vaccine
Others get pooled human immunoglobin
30
Q

When is hep E especially dangerous

A

3rd Trimester of tregnancy

31
Q

Hep E classification

A

RNA
Icosahedral Nucleocapsid
SS (+) Nonseg. Genome
Caliciviridae

32
Q

Why is Hep E dangerous in pregnant women

A

Immunological and hormonal factors - T cell imbalance

33
Q

HBV classification

A
DNA virus
Icosahedral
Enveloped
DS circular DNA (VII)
Hepadnaviridae
Orthohepadnavirdae
34
Q

What is the ‘infectious’ virion in HBV

A

Dane particle