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Hepatitis Viruses Flashcards

(75 cards)

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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
HBV is in a sense the exact opposite of HIV
ok...HIV is an RNA virus with a double stranded DNA intermediate
26
HBV endemic where?
China and Sub-Saharan Africa where infection occurs earlier, not necessarily more
27
HBV enters how?
Parenterally (not through the mouth) Mostly sexually transmitted
28
HBV replicates where?
Liver
29
HBV incubation?
45-160 days....way longer than HAV
30
Serological markers of HBV
HBsAG surface marker and HBeAG
31
How do you determine whether a person is chronically infected?
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
Screening positive for HBsAG means
The person is either recently (acutely) infected or they are chronically infected carrier
33
Screening positive for Anti-HBs
Person was infected in the past and it resolved, or the person was vaccinated
34
Screening positive for HBeAG
Active infection, high risk of transmission, high Viral levels
35
Screening positive for Anti HBe
carrier but low risk of transmission
36
Screening positve for Anti HBc
past infection, this will not be positive if they were simply vaccinated
37
IgM Anti-HBc
acute infection...IgM is early, IgG is late
38
What markers would you expect to see in a vaccinee?
Anti- HBsAG
39
What markers would you see in a high risk carrier?
HBeAG, HBV DNA, HBsAG
40
What markers would you see in a resolved acute infection?
Anti HBs and Anti HBc (core is not in the vaccine)
41
What markers would you see in a low risk carrier
Anti- HBe and HBV DNA and HBsAG
42
HDV morphology>
small circular ss RNA, non enveloped but has a capsid
43
Why is HDV defective?
It can replicate its genome but it cannot make a receptor therefore it relies on HBV infection to exist
44
What is a HDV co-infection?
This occurs when an HDV infection accompanies an acute HBV infection
45
What is a HDV super-infection?
Occurs when an HDV infection accompanies a chronic HBV infection
46
What tips you off to a HDV super-infection?
A pt with chronic liver disease from HBV suddenly gets worse
47
HCV structure?
ss RNA, positive sense, icosahedral capsid, enveloped
48
What is significant about the envelope proteins of HCV?
They are combined at first (E1 and E2 combined). They are cleaved by NS3 protease. This NS3 protease is a significant drug target/
49
How many genotypes of HCV are ther
6
50
which HCV genotypes are present in the US
1,2,3
51
US incidence of HCV?
2%
52
Highest incidence of HCV in 45-50 yo men
ok
53
The majority of HCV infections come from
Drug use
54
Besides drug use, what are some other modes of HCV contraction?
Sex, blood transfusions
55
Acute infections of HCV rarely lead to full liver infections
truth
56
KNOW
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
The cellular damage from HBV and HCV is from our own immune response. These viruses are not cytolytic
ok
58
40% of Chronic Hepatitis due to
HCV
59
20% of Chronic Hepatitis due to
HBV
60
Chronic HBV infection depends most on what?
Age of infection
61
Infection with HBV prior to the age of 1 means
90% chance you will have chronic HBV 1-5 yo= 30 over 5 yo= 2%
62
90% of hepatitis B infections in adults resolve
true
63
85% of infection with HCV
chronic
64
Time table for those with HCV left untreated
CHronic Hep (10 yrs) Cirrhosis (20) Cancer (30)
65
At risk HCV pts
anyone born between 1945- 1965
66
HCV incubation time
7-9 weeks
67
DX of HCV
Screen pts for HCV core antigen and then test HCV genotype using RT-PCR
68
Least curable form of HCV
Genotype 1
69
Most curable form
Genotype 2
70
Highest risk for fatality from HEV
Pregnant women
71
Reservoir for HEV?
Swine
72
Which of the hep viruses causes cirrhosis
B,C,D
73
WHich cause acute liver failure
A,E
74
Which cannot be cured
HCV chronic
75
When should you always be screened for HBV
Chemotherapy and HIV treatment

Gastrointestinal (58 decks)

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