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hepatitis Flashcards

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1
Q

Hepatitis

A

a clinical syndrome characterized by

inflammation of the liver

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2
Q

why is jaundice associated with hepatitis

A

hepatocyte cell death releases bilirubin, which causes jaundice
bilirubin is a biproduct of heme metabolism in the liver (where heme is detoxified)

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3
Q

hepatitis viruses trophism

A

strong tropism for the liver and preferentially replicate in the hepatocyte
85% of liver cells are hepatocytes
Therefore these viruses primarily cause liverdisease

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4
Q

2 main modes of action for hepatitis viruses
strains?
transmission

A
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5
Q

HepA genome and family

A

linear +ssRNA

picornaviridae

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6
Q

HepA causes what kind of hepatits

A

infectious hepatitis

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7
Q

HepA strucutre

A

icoshedral naked capsid

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8
Q

HepA transmission

A

spread by fecal-oral contamination of food, drink, or shellfish

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9
Q

HAV shedding/ effect on hepatocytes

A

HAV shed into bile ducts and into intestine and passes out of the body in the feces
HAV directly kills hepatocytes

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10
Q

clinical manifestation of HAV infection (HepA)

A

–usually mild intestinal infection

–occasionally viremia occurs, leading to liver infection= jaundice

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11
Q

prevention and treatment HAV

A

killed HAV vaccine (now recommended for all in US, esp. for military, frequent travelers, staff of care facilities)
Post-exposure immune globulin

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12
Q

HAV highly endemic regions: children and adult from non endemic regions

A

In highly endemic regions, almost all children become infected in first few years of life
- most remain asymptomatic
- adults from nonendemic regions who become infected are more likely to display
symptoms

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13
Q

HepB genome and family

A

nicked circular, mostly dsDNA

hepadnaviridae

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14
Q

Hep B envelope

A

enveloped

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15
Q

genome size HepB

A

smallest at 3200 bp

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16
Q

viral particles of hepB

A

–22 nm particle
–Variable tubular/filamentous particle (22 nm diameter)
–42 nm Dane particle (infective form of virus)

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17
Q

surface Ag of HepB

A

L,M, and S, embedded in the lipid bilayer envelope

HBsAg-S is the main component

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18
Q

core Ag of hepB, useful?

A

HBeAg is a processed form of the core, HBcAg.

HBeAg is mostly secreted from infected cells and found in bloodstream. Useful marker for HBV infection.

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19
Q

filament form of hepB enriched for?

A

HBsAg-L

20
Q

HepB replication cycle

A

receptor mediated endo
core particle enters host nuc
undergoes repair to form full dsDNA circle
use of host RNA transcriptase
RNA out of nuc may be translated
RT occurs during viral assembly, unlike retroviruses (DNA made), Reverse transcription is by
viral reverse transcriptase
Budding from ER and vesicular transport to cell mem for release

21
Q

HepB RT priming

A

Priming of reverse transcription by TP (terminal protein domain) of viral polymerase by adding first nucleotide to a tyrosine residue of TP

22
Q

what determine course of HepB infection

A

Cell-mediated immune response- Cytotoxic T lymphocytes kill infected hepatocytes

23
Q

effective CMI with HepB

A
24
Q

non-effective CMI with HepB

A
25
Q

how does HBV kill hepatocytes

A

HBV does not directly kill hepatocytes

Cytotoxic T lymphocytes directed against MHC class I proteins bound to viral antigens on hepatocyte surface

Killing also occurs by cytokine release that promotes inflammation and tissue damage

26
Q

Outcomes of acute HBV infection

A
27
Q

infants and HBv infection outcome

A

90% become chronically infected due to not fully developed Immune response

28
Q

Hepatocellular carcinoma - why?

A

increased cell division due to regeneration - increases chances of mutations
peroxides and free radicals from CTL killing

29
Q 
Serology of HBV infections
HbsAg, ANTI Hb s, ANTI Hb c, ANTI Hb e, HbeAg 
no exposure
prior vax
resolved acute infection
acute/chronic infection 
late stage chronic
A
30
Q

prevention HepB

HBsAg particles produced in?

A

vaccination recommended for all infants in USA

–HBsAg particles produced in yeast

31
Q

treatment HepB

A

–passive immunotherapy within 7 days of exposure

anti RT drugs

32
Q

HepD genome and family

A

circular -ssRNA

deltaviridae

33
Q

HDV depends on what other Hep and why

A

Depends on HBV virus to replicate (provides

envelope protein)

34
Q

chronic HBV and HDV

A

Chronic HBV infection exacerbated by infection with hepatitis delta virus

35
Q

HepC genome and family

A

linear +ssRNA

flaviviridae

36
Q

HepC envelope?

A

enveloped

37
Q

HCV spread routes

A

In addition to HCV transmission through blood and sexual
fluid, HCV also spreads from mother to fetus, by fecal-oral
route, and through organ transplants

38
Q

how does HCV kill hepatocytes

A

HCV also does not directly kill hepatocytes
Cytotoxic T lymphocytes directed against MHC class I proteins bound to viral antigens on
hepatocyte surface
Killing also occurs by cytokine release that promotes inflammation and tissue damage

39
Q

HCV replication cycle

A 
receptor binding and endo
uncoating 
\+RNA translated/ polyprotein made = RNA poly made 
RNA replication (+ to - then to more +) 
virion assembly and release
40
Q

HCV RNA poly error

A 
Viral RNA polymerase
is error-prone, creating
multiple viral variants
(= quasi-species)
(like HIV)
41
Q

HCV infection outcomes

A
42
Q

HepE genome and family

A

linear + ssRNA

caliciviridae

43
Q

HepE replication cycle

A

receptor endo
uncoating and translation of RNA = polypro = viral RNA poly
replication of RNA = full genome and subgenomic for more proteins
assembly and release without budding (naked capsid virus)

44
Q

HepE transmission

A

spread in contaminated food and drink (like HAV)

• human-to human transmission and animal-to-human transmission (common source = pigs) (zoonosis).

45
Q

HEV shedding/ effect on hepatocytes

A

HEV shed into bile ducts and into intestine and passes out of the body in the feces
HEV directly kills hepatocytes

microbiology (42 decks)

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