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Hepatitis atu2 > Hepatitis Viruses > Flashcards

Hepatitis Viruses Flashcards

1
Q

What is the relationship between different hepatitis viruses ?

A

Just that they cause hepatitis and are split on acute and chronic

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2
Q

What are the acute Hepatitis viruses ?

What are the chronic hepatitis viruses?

A

A/E are acute

B/C/D are chronic

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3
Q

The liver facts

A

Weighs up to 2kg
Key function in metabolism/homeostasis

Blood supply from small intestine via portal vein. And from aorta via hepatic artery

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4
Q

How often does blood in the body go through liver

A

Every 8 mins where it is constantly sampled and altered

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5
Q

Ultrastructure of Liver?

A

Blood from hepatic artery and portal vein mix in the sinusoid which is loomed with endothelial cells called fenestrations
- fenestrations enable blood to diffuse through the endothelial later to hepatocytes

Space between hepatocytes and endothelium is know as Space of Disse and contains macrophages etc

Other side of hepatocytes is bile canaliculus, which enables hepatocytes to release bile into bile duct

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6
Q

How much of the liver is hepatocytes?

A

Number 2x10^11
60% of liver
80% of mass

Metabolically active but not replicating

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7
Q

What do hepatocytes do?

A

Metabolise carbohydrates,fats and proteins into glucose

Glucose->glycogen ->glucose

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8
Q

What are the functions of hepatocytes

A

Fat metabolism

Protein metabolism

Detoxification

Bile production

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9
Q

How are hepatocytes involved in fat metabolism?

A

Oxidation of triglycerides (lipids) produces energy

Synthesise lipoproteins

Conversion of excess carb+protein-> lipid, which is exported to adipose tissue for storage

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10
Q

How are hepatocytes involved in protein metabolism?

A

Aminotransferases perform Deamination + trans animation of amino acids –> glucose/lipid

Remove ammonia via urea synthesis

Synthesise non-essential amino acids and serum proteins, e.g. Albumins and clotting factors

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11
Q

How are hepatocytes involved in detoxification?

A

Metabolic waste ammonia, insecticide residues, drugs and alcohol

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12
Q

How are hepatocytes involved in bile production?

A

Bile acids derived from cholesterol and crucial for digestion of fat and fat soluble vitamins in small intestine

Key route for excretion of waste products

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13
Q

Percentage excreted in bile recirculating and what is cycle

A

Liver -> gall bladder-> small intestine

Then 5% excreted or recirculated back to liver

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14
Q

How does normal Uninfectwd liver function

A
  1. Phagocyte uptakes senescent RBC
  2. Phagocyte breaks this down into components, including gene –>bilirubin(green,yellow)
  3. Released and conjugated to albumin, to keep it soluble
  4. Bilirubin is taken up by hepatocytes, conjugate to glucuronic acid
  5. This is released into bile and into small intestine
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15
Q

Pathology of acute hepatitis?

A

Jaundice is due to hepatocytes dysfunction due to inability to break down bilirubin

Accumulation of toxins also causes 
Abdominal swelling and pain
Prolonged itchy skin
Dark urine
Pale stools
Bloody/tat like stool
Chronic fatigue and loss of appetite
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16
Q

How to diagnose acute hepatitis?

A

Look at serum levels of liver enzyme/metabolic products as hepatocytes damage results in
Increased alanine aminotransferase as released from damaged hepatocytes

Decreased albumin

Increased bilirubin

17
Q

Chronic hepatitis shows?

A

Results in induction of liver Fibrosis/scarring, involves deposition of ECM macromolecules(collagen etc), induced by hepatic stellate cells - is reversible however

Fibrosis can develop into liver cirrhosis
- more widespread damage, leading to liver failure, resulting in restricted blood flow due to EVM buildup- portal hypertension

Can develop into hepatocellular carcinoma - a very aggressive and difficult to treat cancer

Can only be diagnosed by liver biopsy

18
Q

Features of acute hepatitis viruses?

A

Non-enveloped and enteric transmission can’t survive in bile due to high acidity and high concentration of detergents

19
Q

Features of chronic hepatitis viruses?

A

Enveloped viruses and parenteral blood transmission

20
Q

What is Hepatits A virus?

A

HAV
A PICORNAVIRUS
7.5kb linear +ve ssRNA genome
30nm in diameter

Has 5’IRES + VPg, polyA tail, producing single poly protein, cleaved into p1,p2, p3 which are then cleaved into all the proteins

Patients produce huge amounts of HAV which can be viewed via EM of faeces

21
Q

Epidemiology of HAV?

A

Prevalent in Southern Hemisphere e.g. South Africa/Asia/America

Low in Northern Europe

Spread via close personal contact
Household/sexual/child day care centres
Contaminated food/water (infected handlers/shellfish)- most common

Blood exposure (IV drugs/transfusions) -rare
Endemic countries have exposure of less than 100% aged 10
22
Q

How has HAV evolved?

A

Thought to only be present in primates with 3 closet related simian genotyoes and 3 closely related human genotypes

Felix see Lee studies show more distributed
-13 novel species found in bats, hedgehogs, rodents and shrews.
Showed no evidence of disease but high amounts of virus in liver

23
Q

HAV clinical features ?

A

Usually mild disease
Fatality rate 0.4%
1.75% in >49year olds

Average incubation 30 days with sudden onset symptoms fever, malaise , abdominal discomfort and jaundice

Can be followed by monitoring blood born markers ALT/Ab be HAV

24
Q

HAV therapy options?

A

Vaccines
E.g. One based on virus grown in MRC-5 cells, formaldehyde inactivated and aluminium adjuvant

Epaxal(crucell) - virosome based (no AI), artificial liposomes containing lecithin/cephalin studded with influenza NA/HA and intact HAV particles - well tolerated and highly immunogenic. One dose ensures 97% seroprotection at 2 weeks

25
Q

What is Hepatitis E virus

A

Linear, 7.5kn +ve sense ssRNA genome with 3 overlapping ORFs, with a genome structure relating to Caliciviruses and Togaviruses (rubella)

HEV is sole member of Hepeviridae

26
Q

Contents of HEV ORFs

A

ORF1 encodes all proteins for replication. methyl-transferase(MT), which cleaves +transfers m7g cap, Protease(Pro), Helicase(Hel) and RNA pol (Pol)

ORF2 produces the capsid protein

ORF3 overlaps with ORF2 but not fully characterised

27
Q

Epidemiology of HEV

A

Prevalent in equatorial regions, e.g. Mexico ? Northeast Africa , south/Southeast Asia

4 different genotyoes
Large outbreaks occur due to faecally contaminated drinking water
Accounts for 50% of sporadic hepatitis viruses in endemic areas

Considered zoonosis
Pigs, deer, rodents birds

Evidence for animal human transmission via infected pig products

28
Q

Look at the infection time progression graph in notes

A

Do it and make sure you know

29
Q

HEV infection

A

Similar symptoms to HAV
Higher fatality rate 1%-3%
High fatality in pregnant woman 25%

30
Q

HEV vaccination?

A

GSK+US army developed one 201-2004 with high 95% efficacy but wasn’t pursued

One with 99% efficacy licensed 2012 in China

31
Q

HAV,HEV and multi-vesicular bodies

A

HAV and HEV interact with ESCRT to bud into MVBs, within exosomes Tom mimic enveloped viruses

Interaction mediated via specific domains

  • Late domain PSAP within ORF3 which interacts with TSG101
  • YPXXXL domain of VP2 which interacts with ALIX(2 YPXXXLs thus 2 ALIX)

End result HAV/HEV are released into blood with an effective envelope

Viruses exploit phagocytes for direct internalisation
Have PS on exosome external surface which interacts with specific Receptors on phagocytes

Hepatitis atu2 (5 decks)

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