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GI Micro > Hepatitis Viruses > Flashcards

Hepatitis Viruses Flashcards

1
Q

Enterically Transmitted

A

HAV

HEV

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2
Q

Parenterally Transmitted

A

HBV

HCV

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3
Q

Requires co-infection w/ HBV

A

HDV

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4
Q

Causes acute hepatitis

A

HAV

HEV

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5
Q

Can cause chronic hepatitis and lead to hepatocellular carcinoma

A

HBV (D)

HCV

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6
Q

HAV structure?

A

Non-enveloped icosahedral capsid. ssRNA+ virus. 1 serotype. Human reservoir.

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7
Q

HEV structure?

A

Non-enveloped icosadhedral capsid. ssRNA+ virus. Animal reservoir. Developing countries.

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8
Q

HEV infection is most dangerous to what patient population?

A

Pregnant women. 20% mortality rate.

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9
Q

How is HAV spread?

A

Fecal-oral route

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10
Q

Early childhood dz with HAV presents how?

A

Asymptomatic

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11
Q

What are the patient groups at risk for HAV?

A
  1. Household or sexual contacts
  2. Travelers to endemic areas
  3. Inhabitants of American Indian reservations
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12
Q

What are the patient groups at risk for HAV during an outbreak?

A
  1. Diners
  2. Day care center workers
  3. Gay men
  4. IV drug users
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13
Q

What has decreased the number of HAV outbreaks?

A

Development of vaccine for it.

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14
Q

HBV structure?

A

Enveloped virus termed Dane particle. Partially dsDNA genome 3200 bp. Hepadnavirus family.

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15
Q

What are the 4 major proteins produced by HBV?

A
  1. DNA polymerase (reverse transcriptase)
  2. HSsAg
  3. HBcAg/HBeAg
  4. X Antigen
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16
Q

What does HBsAg do?

A

Serves as attachment protein. Overwhelms cell membrane causing blebs. These rupture and released into blood as 20 nm particles and filaments. Tons of this in the blood hides actual virus from immune system.

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17
Q

What does HBcAg do?

A

Capsid protein. HBeAg is a secreted derivative of HBcAg which serves as an important serologic marker.

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18
Q

What does X antigen do?

A

Influences gene expression and is present in hepatocytes.

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19
Q

Transmission of HBV?

A

Parenteral route.

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20
Q

Where in the human body is HBV present upon infection?

A

Blood, semen, and vaj secretions

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21
Q

Where does transcription for HBV take place?

A

Nucleus. mRNAs are made for the 4 major proteins and a full copy of the genome is also synthesized.

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22
Q

Where is HBV endemic?

A

China and sub-Saharan Africa. Early infection. (Late infection in US and Europe.)

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23
Q

How many weeks after exposure to HBV will ALT spike?

A

16 weeks

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24
Q

Chronic HBV patients clinically appear?

A

Asymptomatic until cirrhosis or HCC appear

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25
Q

ID of carriers or acutely infected person w/ HBV.

A

HBsAg

26
Q

ID of persons who have had HBV infection or received vaccine.

A

Anti-HBs

27
Q

ID of those at increased risk of HBV transmission (active marker).

A

HBeAg

28
Q

ID of HBsAg carriers with low risk of transmission.

A

Anti-HBe

29
Q

ID of persons with past HBV infection.

A

Anti-HBc

30
Q

ID of acute or recent HBV infection.

A

IgM Anti-HBc

31
Q

HDV structure?

A

Circular ssRNA genome. Encodes delta antigen which is its polymerase.

32
Q

Why does HDV require co-infection of HBV?

A

It requires HBsAg bc it doesn’t have its own cell surface receptors.

33
Q

What’s the result of HDV co-infection w/ HBV?

A

Severe acute dz w/ a low risk for chronic HDV infection.

34
Q

When do you get a HDV/HBV superinfection?

A

Occurs when a chronic HBV patient gets infected w/ HDV. There is a high risk for severe chronic liver dz.

35
Q

How do you know a chronic HBV pt has been infected with HDV?

A

The patient’s condition suddenly worsens.

36
Q

HCV structure?

A

Enveloped icosahedral capsid. ssRNA+ genome. Member of Flaviviridae family. Also known as Hepacivirus.

37
Q

What are the major proteins cleaved from HCV’s polyprotein? What do they do?

A
  1. E1 + E2: envelope proteins

2. NS3 Protease: cleaves the polyprotein (important bc it is a target for therapy)

38
Q

What age group is HCV incidence highest in?

A

45-55 year olds (probably more like 50-60 yo now)

39
Q

How long is the incubation period for HCV?

A

7-9 weeks

40
Q

What are the 3 major ways of getting HCV?

A
  1. IV drug use 40%
  2. Sexual contact 15%
  3. Blood transfusion 5%
41
Q

T or F. Acute HCV infections are nearly always fulminant.

A

F: rarely

42
Q

What’s different about a chronic HCV infection?

A

After the initial acute infection, there are minor flare-ups of dz approximately every 2 years.

43
Q

What is responsible for the dz flare-ups with a chronic HCV infection?

A

Production of quasi-species. E2 glycoprotein has a 30 AA sequence that easily mutates which causes a temporary lapse in immunity causing the flare-ups.

44
Q

What causes the liver dz in HBV and HCV infections?

A

Immune destruction of infected hepatocytes. These viruses are not cytolytic themselves.

45
Q

Development of chronic HBV infection depends on what?

A

The age of the patient.

5 yo: 2%

46
Q

What percentage of chronic HBV patients will die of liver dz? When does this occur?

A

25% occurring usually in the 6th decade of life

47
Q

What are the 3 stages of chronic HBV infection?

A
  1. Immune Tolerance: pt usually asymptomatic
  2. Immune Clearance: symptoms appear
  3. Residual Phase
48
Q

T or F. 85% of untreated HCV infections will lead to chronic infection regardless of patient age.

A

T

49
Q

If cirrhosis develops in a chronic HCV pt, how long does it take?

A

10-20 years post-infection

50
Q

If HCC develops in a chronic HCV pt, how long does it take?

A

20-30 years post-infection

51
Q

Chronic HBV and HCV pts must be immunized against what?

A

HAV

52
Q

What is the leading reason for liver transplants?

A

HBV and HCV liver dz

53
Q

Why does it take so long for complications such as cirrhosis or HCC to develop in HBV or HCV patients?

A

The actual viruses are not responsible for cell damage and are not your typical oncogenic viruses. It is the immune destruction that destroys hepatocytes. The more times a cell has to be regenerated, the greater the chance for mutations to occur.

54
Q

Dx of HAV?

A

Detect anti-HAV IgM

55
Q

Dx of HBV?

A

HBsAg, HBeAg, anti-HBe, HBV DNA

56
Q

Dx of HCV?

A

Core (capsid) antigen, HCV RNA

57
Q

Why must you determine the genotype of HCV?

A

Because it determines response to treatment.

58
Q

What are the 5 things used to control HAV infection?

A
  1. Hand washing 10-20 seconds
  2. Passive immunization w/ gamma globulin
  3. Inactivated vaccine (Havrix): ages 12-23 months recommended by CDC
  4. Combination vaccine for HAV + HBV (Twinrix)=Havrix + recombinant HBV vaccine: 18+ years or older
  5. Vaccine or gamma globulin is recommended for travelers to endemic areas
59
Q

What are the 3 things used to control HBV infection?

A
  1. Screen blood supplies for HBsAg, anti-HBc, and HBV DNA
  2. Vaccines
  3. HBIg for exposed individuals: newborns, prophylaxis for travelers
60
Q

What are the 3 HBV vaccines?

A
  1. Plasma-derived HBsAg
  2. Yeast-derived HBsAg
  3. Twinrix
    Childhood immunization recommended.
61
Q

T or F. There is a curative treatment for HCV but not for HBV.

A

T

62
Q

What are the 3 things used to control HCV infections?

A
  1. Screen blood supplies for core antigen and HCV RNA
  2. PEG-IFN + Ribavirin combo therapy
  3. Protease Inhibitors: victrelis, incivek, curative

GI Micro (7 decks)

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