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MMI 436 > Viral Hepatitis > Flashcards

Viral Hepatitis Flashcards

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?

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

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?

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?

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?

A

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

21
Q

How is HCV transmitted?

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?

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

Describe the strucuture of HCV virion

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

Describe the HCV life cycle

A
  1. entry via Rs (utilizes recognition by lipoprotein)
  2. uncoating and tl of proteins
  3. assmebly
  4. release
25
Q

What factors do we look at to monitor HCV infection, how do the levels of these factors change over time?

A
  • RNA remains steady
  • ALT peaks in the acute phase
  • Anti-HCV abs rise over time (but are most often ineffective)
26
Q

What key thing do we think is necessary to clear an HCV infection?

A

early induction of HCV nAbs

27
Q

What do PRR signals increase the production of?

A

IFNa/B

28
Q

What do IFNs stimulate?

A

ISGs –> dampen ability of virus to spread

29
Q

What signaling pathways do HBV and HCV interfere with?

A
  • infected hepatocyte: RIG-I/TLR3 signaling –> decrease IFNa/B production
  • IFN stimulated cells: JAK/STAT –> weaked response of ISGs
30
Q

Why is HBV considered a stealth virus?

A

ISG responses are typically quite weak

31
Q

Describe 6 Bcell/Ab reposnses to HBV

A
  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
Q

Describe HBV-specific CD8 T cell non cytolytic antiviral activities

A
  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
Q

Describe HBV-specific CD8 T cell cytolytic anti viral activity

A

release granzyme B and perforin to induce apoptsis of infected hepatocytes

34
Q

What factors cause HCV to progress to chronic infection?

A
  • 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

MMI 436 (14 decks)

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