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Gastrointestinal > Hepatitis Viruses > Flashcards

Hepatitis Viruses Flashcards

1
Q

Chronic Hepatitis viruses are those which are

A

Parenterally transmitted

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2
Q

Acute Hepatitis infections are those which are?

A

Enterically transmitted

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3
Q

Hepatitis A general char

A

enterically transmitted (acute)

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4
Q

Hep B general?

A

parenterally transmitted

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5
Q

Hep C general?

A

Parenterally trans

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6
Q

Hep D general?

A

Dependent on co-infection with B

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7
Q

Hep E general?

A

Enterically transmitted

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8
Q

Hep G generall?

A

Parenterally transmitted

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9
Q

Hepatits A morphology

A

ss RNA, positive sense, Icosahedral capsid (no envelope…makes sense because an enveloped virus wouldn’t survive in the GI)

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10
Q

How many serotypes of Hepatits A are there and what implication does this have on the vaccine?

A

One serotype. Means its easy to make a vaccine

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11
Q

Reservoir for Hep A?

A

Humans

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12
Q

HAV spreads via which route?

A

Fecal- oral

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13
Q

Where does HAV replicate?

A

GI tract…incubation period here is about 15-30 days

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14
Q

Where does the virus spread?

A

LIVER (duh), spleen, kidney

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15
Q

Remember, the virus sheds in the GI tract during the asymptomatic incubation period. This is the period of time where it is spread most easily becase the pt doesn;t know they have it.

A

Once virus shedding is over, the pt is not infectious

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16
Q

What symptoms shows up once shedding stops

A

jaundice

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17
Q

Presentation of HAV pt?

A

Jaundice with high liver enzymes

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18
Q

DX of HAV

A

Isolated from the pts feces. Do an ELISA for anti-HAV IgM

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19
Q

At risk populations

A

Day Care Workers
Dudes (gay)
Diners (salad bar eaters especially)
Drug-users

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20
Q

What is a Hepatitis B virion called?

A

Dane Particle

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21
Q

What is the DNA structure of the HBV?

A

Partially dsDNA (one fill length circular DNA strand with another partial strand inside it).

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22
Q

What are the 5 major proteins encoded by the HBV genome?

A
  • DNA polymerase with Reverse Transcriptase capability
  • HBsAG (Hep B surface Antigen) this thing is an attachment protein found mostly in 20nm particles and filaments
  • HBcAG: core antigen, capsid protein
  • HBeAG: Secreted form of HBcAG ( important for diagnosis)
  • x antigen: Influences gene expression
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23
Q

What is the significance of the HBsAG in regards to our immune response?

A

There are trillions of these things (they outnumber the actual virus particles by a long shot) but our immunoglobulins recognize the HBsAG which means that we have a huge immune reaction to the surface antigen fillaments and less of a reaction to the actual virions. They act as a smokescreen of sorts. Allows for infection to become chronic

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24
Q

What is one of teh first thing that happens to the HBV once it enters the cell and uncoats?

A

Completes the synthesis of the second DNA strand to produce a fully double stranded DNA genome

  • Then gets supercoiled—-> enters nucleus
  • Transcribes mRNAs to code for the four proteins
    and one full length copy of the genome in RNA form. Need to get this back to a double stranded DNA structure, this is where the Reverse transcriptase comes in.
  • Once RT converts the RNA to DNA, the viral polymerase begins synthesizing the second DNA strand. Doesn’t finish it though.
  • Gets packaged into a core structure
  • Buds through the ER (picks up an envelope)
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25
Q

HBV is in a sense the exact opposite of HIV

A

ok…HIV is an RNA virus with a double stranded DNA intermediate

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26
Q

HBV endemic where?

A

China and Sub-Saharan Africa where infection occurs earlier, not necessarily more

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27
Q

HBV enters how?

A

Parenterally (not through the mouth) Mostly sexually transmitted

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28
Q

HBV replicates where?

A

Liver

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29
Q

HBV incubation?

A

45-160 days….way longer than HAV

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30
Q

Serological markers of HBV

A

HBsAG surface marker and HBeAG

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31
Q

How do you determine whether a person is chronically infected?

A

If at the 6 mos mark you are still detecting HBeAG and HBsAG instead of antibodies to these things then you can safely assume that the person is chronically infected

32
Q

Screening positive for HBsAG means

A

The person is either recently (acutely) infected or they are chronically infected carrier

33
Q

Screening positive for Anti-HBs

A

Person was infected in the past and it resolved, or the person was vaccinated

34
Q

Screening positive for HBeAG

A

Active infection, high risk of transmission, high Viral levels

35
Q

Screening positive for Anti HBe

A

carrier but low risk of transmission

36
Q

Screening positve for Anti HBc

A

past infection, this will not be positive if they were simply vaccinated

37
Q

IgM Anti-HBc

A

acute infection…IgM is early, IgG is late

38
Q

What markers would you expect to see in a vaccinee?

A

Anti- HBsAG

39
Q

What markers would you see in a high risk carrier?

A

HBeAG, HBV DNA, HBsAG

40
Q

What markers would you see in a resolved acute infection?

A

Anti HBs and Anti HBc (core is not in the vaccine)

41
Q

What markers would you see in a low risk carrier

A

Anti- HBe and HBV DNA and HBsAG

42
Q

HDV morphology>

A

small circular ss RNA, non enveloped but has a capsid

43
Q

Why is HDV defective?

A

It can replicate its genome but it cannot make a receptor therefore it relies on HBV infection to exist

44
Q

What is a HDV co-infection?

A

This occurs when an HDV infection accompanies an acute HBV infection

45
Q

What is a HDV super-infection?

A

Occurs when an HDV infection accompanies a chronic HBV infection

46
Q

What tips you off to a HDV super-infection?

A

A pt with chronic liver disease from HBV suddenly gets worse

47
Q

HCV structure?

A

ss RNA, positive sense, icosahedral capsid, enveloped

48
Q

What is significant about the envelope proteins of HCV?

A

They are combined at first (E1 and E2 combined). They are cleaved by NS3 protease. This NS3 protease is a significant drug target/

49
Q

How many genotypes of HCV are ther

A

6

50
Q

which HCV genotypes are present in the US

A

1,2,3

51
Q

US incidence of HCV?

A

2%

52
Q

Highest incidence of HCV in 45-50 yo men

A

ok

53
Q

The majority of HCV infections come from

A

Drug use

54
Q

Besides drug use, what are some other modes of HCV contraction?

A

Sex, blood transfusions

55
Q

Acute infections of HCV rarely lead to full liver infections

A

truth

56
Q

KNOW

A

HCV pts can have multiple bouts due to reinfection. Antigenic variation accounts for most of the immune escape. This variation is mediated by changes in the hypervariable region (30 AA) of the E2 gene.

57
Q

The cellular damage from HBV and HCV is from our own immune response. These viruses are not cytolytic

A

ok

58
Q

40% of Chronic Hepatitis due to

A

HCV

59
Q

20% of Chronic Hepatitis due to

A

HBV

60
Q

Chronic HBV infection depends most on what?

A

Age of infection

61
Q

Infection with HBV prior to the age of 1 means

A

90% chance you will have chronic HBV
1-5 yo= 30
over 5 yo= 2%

62
Q

90% of hepatitis B infections in adults resolve

A

true

63
Q

85% of infection with HCV

A

chronic

64
Q

Time table for those with HCV left untreated

A

CHronic Hep (10 yrs) Cirrhosis (20) Cancer (30)

65
Q

At risk HCV pts

A

anyone born between 1945- 1965

66
Q

HCV incubation time

A

7-9 weeks

67
Q

DX of HCV

A

Screen pts for HCV core antigen and then test HCV genotype using RT-PCR

68
Q

Least curable form of HCV

A

Genotype 1

69
Q

Most curable form

A

Genotype 2

70
Q

Highest risk for fatality from HEV

A

Pregnant women

71
Q

Reservoir for HEV?

A

Swine

72
Q

Which of the hep viruses causes cirrhosis

A

B,C,D

73
Q

WHich cause acute liver failure

A

A,E

74
Q

Which cannot be cured

A

HCV chronic

75
Q

When should you always be screened for HBV

A

Chemotherapy and HIV treatment

Gastrointestinal (58 decks)

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