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GI, Liver, GallBladder, Pancreas > M- Hepatitis Viruses > Flashcards

M- Hepatitis Viruses Flashcards

1
Q

What is the mode of transmission of HepA?
Where is infection with this virus most common?
What can stop the spread?

A

Fecal-Oral

  1. food and water
  2. household contacts (most common)
  3. sexual contacts

Common in developing countries- hand washing can stop spread

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2
Q

What is the mode of transmission of HepE?

A

It is transmitted by the fecal-oral route.

  1. Water (most common route)
  2. some food (pork)

Common in developing countries

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3
Q

Describe the genome of Hep A and Hep E.

A

HepA is RNA with 3 domains encoding structural and non-structural proteins
HepE is RNA with 2 domains encoding structural and non-structural proteins

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4
Q

What characteristic of the virion of HepA and HepE allow it to spread by the fecal oral route?

A

They have no lipid coat so detergents are not able to digest and destroy their infectivity.

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5
Q

How does HAV infection present in:

  1. young children
  2. older children and adults
A
  1. asymptomatic

2. jaundice

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6
Q

Who is most likely to present with acute liver failure (fulminant hepatitis) from an HEV infection?

A

Women in the third trimester of pregnancy

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7
Q

What serology markers are measured for HepA?
Which are markers of acute infection?
Which are markers of prior infection?

A

Acute infection:

  1. IgM HAV Ab
  2. Total (IgG+IgM) HAV Ab

Prior infection:
1. Total (IgG+IgM) Ab

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8
Q

What serology markers are measured for HepA?
Which are for acute?
Which are for prior infection?

A

Acute:

  1. IgM HEV Ab
  2. IgG HEV Ab

Prior:
IgG HEV Ab

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9
Q

What is the therapy for HAV and HEV?

A
  1. Supportive- anti-emetics, IV fluid, cholestyramine

If they have fulminant hepatitis they need a transplant

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10
Q

What is prevention AFTER exposure for HAV?

A

within 2 weeks the person can get intramuscular injection of ISG (immune serum globulin) an antibody titer to prevent clinical HepA

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11
Q

What is prevention of HAV before exposure?

A

Active immunoprophylaxis:

a vaccine made of formalin activated HepA antigen

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12
Q

Describe the virion and genome of HBV.

A

Virion: Coat with host lipids

Genome: DNA with overlapping strands

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13
Q

Describe the structural genes and proteins of HBV.
Describe the non-structural genes and proteins of HBV.
Which gene is viral specific and consequently a drug target?

A

Structural:

  1. pre-S1, pre-S2, S (surface antigens)
  2. C gene (core antigen)

Non-structural:

  1. P (polymerase)*** viral specific so drug target
  2. pre-C (e antigen)
  3. X gene
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14
Q

What part of HBV is done by host machinery?

What part of HBV replication is done by viral machinery (polymerase)?

A

Host:
HBV DNA is used to generate RNA transcripts to translate viral proteins (specifically polymerase)

Viral:

  1. polymerase does reverse transcription
  2. RNAse
  3. DNA-dependent DNA synthesis
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15
Q

When can HBc be detected in the blood?

Where does immunohistochemical staining show HBc?

A

It can only be detected in the blood if the surface coat is removed.

Immunohistochemical staining using HBc antibody can demonstrate the presence of HBc in the nucleus of infected cells

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16
Q

What are the 3 ORFs of HBV? Which genes are in each?

A
  1. Polymerase has its own
  2. HBc, HBe and HBs are on one ORF
  3. HBs from a much shorter RNA transcript… This makes surface coat too small to attach to hepatocytes but makes spheres and filaments
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17
Q

What are the three antigen-antibody systems for HBV?

What is each a marker of?

A
  1. HBc Ab- marker of exposure
  2. HBs Ab- marker of vaccination or resolution
  3. HBe Ab- marker of replication
18
Q

What is the first HBV antibody to be detected?

A

HBc IgM - a sign of acute infection

HBc IgG persists later as a marker of exposure

19
Q

Do host or viral factors determine the outcome of a HBV infection?

A

Host.

HBV protein antigens are similar in acute, chronic, fulminant and asymptomatic so it is the HOST cytotoxic T cell immune response that determines how bad the infection is.

20
Q

What is the HBV marker for replication? Why?

A

HBe because it is is translated on the same reading frame as HBc but is upstream.

If HBe Ag is detected, this means that all the machinery necessary for viral replication is available and being used.

High HBe in the blood means it is highly infection due to the replication

21
Q

If HBe is not present in an HBV infection, what does that mean?

A

It means that the virus is not in an infectious state.
HBe is a pre-core sequence that encodes transport to the ER and secretion from the infected hepatocyte.

If HBe is not being translated, the virus remains in the hepatocyte.

22
Q

How is HBV transmitted?

Which way is more associated with an ensuing chronic infection?

A
  1. Percutaneously and through other body secretions

2. Vertical transmission- the baby will develop chronic hepatitis

23
Q

Compare the incubation times for HAV, HEV and HBV.

A

HAV and HEV have a short incubation period (weeks) where HBV has a long incubation period of months

24
Q

What are non-hepatic manifestations of HBV?

A

antigen-antibody complexes form causing:

  1. serum sickness-like syndrome
  2. arthritis
25
Q

What serology test is most informative for HBV if it is negative?

A

HBs Ab because as HBs Ag increases, the HBs Ab will decrease because it forms antigen-antibody complexes.
If HBs Ab is negative, but HBs Ag is positive, it means that the person has a chronic infection.

26
Q

What serological test for HBV is most informative if it is positive?

A

HBe Ab because it is a sign of replication of the virus

27
Q

What are the two groups of people where HBV becomes chronic?

A
  1. Infants that got the virus through vertical transmission

2. Immunocompromised adults

28
Q

Why is chronic hepatitis and cirrhosis rare after an icteric hepatitis in immunocompetent adults?

A

Icteric illness is a sign of immune responsiveness

29
Q

What are the two treatments for chronic HBV?

How does each work?

A

IFN-a:
1. decrease viral replication
2. boost immune response
This converts active (HBe Ag and HBV DNA +)

Anti-retroviral
inhibit reverse transcriptase of HBV

30
Q

How can HBV be prevented after exposure?

A

passive immunoprophylaxis with HBIG (HBs immune globulin)

This is used for sexual contacts and to prevent vertical transmission

31
Q

How is HBV prevented before exposure?

A

recombinant HBs Ag

32
Q

Describe the virion and genome of HDV.

A

It has a HBs coat and has host lipids.
It is made of RNA with a delta antigen.
It resembles a satellite RNA and has self cleavage activity.

33
Q

What are the two ways HDV can infect hosts?

A
  1. Co-infection with HBV
  2. Superinfection in someone with prior HBV

HBV must be present in some capacity because HDV needs HBV machinery to synthesize HBs for the virion

34
Q

In HDV superinfection of an HBV carrier, symptomatic hepatitis follows the appearance of what?

A

delta RNA

35
Q

In superinfectionBof HDV and HBV what serologies would you expect?

A

Acute serologies for HD (IgM HDV Ab)

Chronic HBV

36
Q

Describe the virion and genome of HCV.

A

Virion: lipid coat
Genome: RNA coding structural and non-structural proteins

37
Q

What is the route of acquisition of HCV?

A

Percutaneous

38
Q

What serology is associated with acute HCV?

Chronic?

A

Acute: HCV RNA

Chronic: HCV Ab and HCV RNA

39
Q

What are the non-hepatic manifestations of HCV?

A

circulating Ag-Ab complexes are present that:

  1. cryoprecipitate causing vasculitis
  2. glomerulonephritis
40
Q

What contributes to the chronicity of HCV?

A

mutations in the hypervariable region of the genome to escape immune pressures

41
Q

What is the treatment for HCV?

A

IFNa with ribavirin
IFNa with or w/o a protease inhibitor

The goal is to convert HCV RNA + to - without inflammation

GI, Liver, GallBladder, Pancreas (24 decks)

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