MMI 436 > Viral Hepatitis > Flashcards

Viral Hepatitis Flashcards

(34 cards)

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1
Q

Describe the blood supply of the liver

A
  • hepatic artery = normal blood flow
  • hepatic portal vein = collects blood from the stomach, pancrease, gallbladder, small and large intestine, and spleen and deliverys in to the liver
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2
Q

Due to the unique blood supply to the liver, what is the liver constantly exposed to?

A
  • food Ags
  • bacterial products (e.g. LPS)
  • nutrients
  • toxins
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3
Q

What is the function of hepatocytes?

A

generate bile and secrete bile to the gallbladder, sites for viral replicaton

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4
Q

What are the two major functions of bile?

A
  1. digestive - emulsify fats and aid uptake of fat and cholesterol
  2. waste elimination - bilirubin = waste from catabolism of heme from RBCs; liver disease - excess bilirubin –> jaundice
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5
Q

How does blood enter the sinusoids of the liver?

A

via leaky endothelial cells - LSECs

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6
Q

What are the various cell types present in the liver?

A
  • hepatocytes
  • bilirary cells
  • CD4/8 T cells
  • gd T cells
  • NK cells
  • B cells
  • LSECs
  • Kupffer cells - phagocytes
  • stellate cells - healthy liver –> quiscent; liver damge –> secrete collagen –> fibrosis
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7
Q

What is a result of LSECs lacking a basement memb?

A

T cells can get in easily to the sunusoids and see lots of Ags –> bad (can cause uneccessary inflammation) –> solution: the liver is immunoprivileged

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8
Q

Describe the liver under non-inflammatory vs inflammatory conditions

A

non-inflam:

  • Ag presentation by LSECs –> tolerance of T cells
  • CD4 T cells secrete IL-4 and 10 (become Tregs)
  • CD 8 T cells undergo apoptosis

inflam:

  • LSECs down-regulate their MHC expression –> allowing for T cell activation
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9
Q

Describe Kupffer cells (KCs) origin and where they are located

A

origin: derived from YSP
location: exclusively located to the hepatic sinusoids, do not migrate

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10
Q

Describe the activating and inhibiting Rs on NK cells and what their ligans are, what pathway is stronger?

A
  • KIR (inhibting) binds to MHC-I (stronger)
  • KAR (activating )binds to KARL
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11
Q

Describe three different stages of liver injury

A
  1. fibrotic liver: from chronic viral infection, alcohol/drug abuse, high fat diet –> NASH (fatty liver disease)
  2. cirrhotic liver: lots of fibrosis, impaired function
  3. liver cancer: liver failure/death
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12
Q

Describe how we monitor liver injury

A

healthy liver:

  • hepatocyte intracellular proteins are low in blood (e.g. ALT and ALP)
  • hepatocyte secreted proteins are high in blood (e.g. albumin)

fibrotic liver:

  • hepatocyte intracellular proteins are high in blood (e.g. ALT and ALP)
  • hepatocyte secreted proteins are low in blood (e.g. albumin)
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13
Q

HBV - describe the virus mutation rate, and chronic infection frequencies

A

mut rate = low (easier to make vaccine)
chronic infection = 90% (vertical), 10% (horizontal)

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14
Q

Describe modes of horizontal and vertical transmission of HBV, and which transmissions are most common where

A

horizontal:

  • blood and blood products
  • IV drug use
  • sexual tranmission
  • mostly in non-endmeic regions

vertical:

  • mother to infant at the time of birth
  • most common in endemic regions
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15
Q

What HBV Ag does the HBV vaccine target?

A

targets HBsAg

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16
Q

What HBV molecules are used for diagnosis?

Study These Flashcards
A
  • HBV DNA and HBsAg and HBeAg are elevated in blood
  • host Abs against HBcAG, HBeAg, and HBsAg (though not applicable if vaccinated)
17
Q

Describe HBV’s lifecycle

Study These Flashcards
A
  1. entry via NTCP
  2. generation of cccDNA
  3. ts and tl
  4. RT by HBV pol.
  5. assembly
  6. release
18
Q

What HBV viral products are generated during infection?

Study These Flashcards
A
  1. infectious virions
  2. circulating RNAs (present in sub-viral particles)
  3. HBsAg
  4. HBcAg
  5. HBeAg

many different particles –> exasterbate the problem by constantly activating the IS

19
Q

What factors are monitored to determine what stage of chronic HBV infection your in, are these stages sequential?

Study These Flashcards
A

factors = cccDNA, HbeAg, ALT

not sequential - can bounce back and forth between stages

20
Q

Why is it difficult to make a vaccine for HCV?

Study These Flashcards
A

7 major genotypes + high mutation rate –> increase variability between genotypes

21
Q

How is HCV transmitted?

Study These Flashcards
A
  • needle - highly efficient, any contamination of drug paraphernalia
  • sexual transmission - low efficiency, but common route because a) sex is common behaviour and b) large chronic reservoir in population –> increase change of having an infected partner(s)
22
Q

What tests do we use for HCV?

Study These Flashcards
A
  1. NAAT - detects HCV RNA
  2. EIA - detects host Abs to HCV
23
Q

Describe the strucuture of HCV virion

Study These Flashcards
A
  • ss(+)RNA genome
  • VLDL coat –> hides virion
  • capsid
  • env
  • E1 and E2 glycoproteins
24
Q

Describe the HCV life cycle

Study These Flashcards
A
  1. entry via Rs (utilizes recognition by lipoprotein)
  2. uncoating and tl of proteins
  3. assmebly
  4. release
25
What factors do we look at to monitor HCV infection, how do the levels of these factors change over time?
* RNA remains steady * ALT peaks in the acute phase * Anti-HCV abs rise over time (but are most often ineffective)
26
What key thing do we think is necessary to clear an HCV infection?
early induction of HCV nAbs
27
What do PRR signals increase the production of?
IFNa/B
28
What do IFNs stimulate?
ISGs --> dampen ability of virus to spread
29
What signaling pathways do HBV and HCV interfere with?
* infected hepatocyte: RIG-I/TLR3 signaling --> decrease IFNa/B production * IFN stimulated cells: JAK/STAT --> weaked response of ISGs
30
Why is HBV considered a stealth virus?
ISG responses are typically quite weak
31
Describe 6 Bcell/Ab reposnses to HBV
1. Ab sequesteratio by sub viral HBsAg particles 2. virus neutralization (only anti-HBsAg Abs; if lacking --> chronicity) 3. ADCP via KCs 4. ADCC via NK cells 5. Ag uptake and presentation 6. HBV-specific B cells generate antiviral cytokines that: a) supress cccDNA replication, b) downregulated NTCP, c) impair virion assmebly/release
32
Describe HBV-specific CD8 T cell non cytolytic antiviral activities
1. release IFNg and TNFa + express lymphotixin aB on their surface --> mediate antiviral responses in hepatocytes 2. APOBEC3 deaminates cytosine residues in cccDNA --> stop codons --> degradation of cccDNA
33
Describe HBV-specific CD8 T cell cytolytic anti viral activity
release granzyme B and perforin to induce apoptsis of infected hepatocytes
34
What factors cause HCV to progress to chronic infection?
* ISG responses typically greater than HBV, but weaken over time * HCV-specific Abs are typically delayed --> failure to neutralize and clear the virus * chronic type 1 IFN state: induces environent of IL-10 and TGFB = Treg and T cell exhaustion
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