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Virology 1 > Hepatitis > Flashcards

Hepatitis Flashcards

1
Q

hepatitis A mode of transmission

A

fecal-oral

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2
Q

hepatitis A virus classification

A

picornavirus - negative sense ssRNA

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3
Q

why is overt disease rare for hep A?

A

it is common where sanitation is poor b/c mothers have immunity to it. this gives their kids passive immunity to it. most kids are exposed early in live, when they have partial immunity that gives rise to active immunity. most people are seroconverted by 5.

in developed countries, the infected individuals are older

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4
Q

how long is the incubation period for hep A

A

30 days

fecal excretion occurs after a few days

viremia takes a week

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5
Q

what cells do hepatitis A viruses infect?

A

liver

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6
Q

what are the symptoms of hep A infection?

A

anorexia, nausea, fever, jaundice, dark urine, and abnormal values from liver function tests

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7
Q

liver function tests

A

used to test for the presence of liver damage.

most common- aspartate amino transferase in the serum. this enzyme is normally in the liver but the virus lysis cells when it replicates to release progeny

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8
Q

describe how heme metabolism is related to hepatitis A

A

normally, heme is converted to bilirubin in the spleen, which is transferred through the blod to the liver, where it is added to the bile and excreted to the GI tract (its why feces are brown)

w/ Hep A, the liver functions poorly, causing an increase in bilirubin systemically. this gets deposited in the skin (causing jaundice), filtered by the kidneys (dark urine), and it doesn’t get to the GI tract (light feces).

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9
Q

compare AST levels in Hep A and Hep B

A

Hep A levels have a sharp peak w/in 2 months of infection, and then drop off sharply

in Heb B, the peak is slower to form and lower. it only becomes evident at 2 months

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10
Q

what are 5 most common ways to produce a Hep A epidemic

A
  1. outdoor summer events w/ inadequate sanitary facilities

2 raw or inadequately cooked shellfish contaminated by sewage

3 w/in one family

4 spread by food handler

5 from fecally contaminated food

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11
Q

T/F- Hep A can be spread via blood transfers

A

T- as long as the virus is viremic

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12
Q

describe the use of passive immunity from IgG in Hep A

A

primarily used after possible exposure, but still useful prophylactically.

it prevents jaundice and malaise, but there is some virus replication and liver damage.

it provides protection for about 4 months

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13
Q

describe Hep A immunization

A

killed virus vaccine. recommended for all children plus travelers, male gay partners, ppl who receive blood products

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14
Q

how do you determine if you are affected w/ hep A

A

serological test for Ab against Hep A

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15
Q

how do you interpret serological data w/ IgM and IgG for Hep A?

A

if both negative- no infection, no vaccine

if IgG pos- previously infected or vaccinated, but not currently

both pos- acute Hep A infection or recent vaccination

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16
Q

what dimensions are important to assess when considering a potential epidemic?

A

1 place- geographical clustering

2 person- do patterns suggest a mode of exposure

3 are new cases around the same time?

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17
Q

Hepatitis E characteristics

A

non-enveloped, + stranded RNA

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18
Q

what is the mode of transmission for Hep E viruses?

A

fecal-oral

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19
Q

what are the symptoms of Hep E?

A

similar to A

fever, nausea, jaundice

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20
Q

what is the Hep E prognosis

A

people generally recover. children often have very mild symptoms.

can become chronic in immunosuppressed pts

bad for pregnant women

21
Q

what kind of virus is Hep B

A

hepadenavirus

enveloped, icosahedral

contains circular DNA mostly double stranded but single stranded some places

it carries a reverse transcriptase

22
Q

what is the incubation period for Hep B

A

70 days

23
Q

how is hep B transmitted?

A

blood transfusions, dirty needles

sexually (especially male to male)

perinatal infections from infected mom to newborn

24
Q

are HB-Ags from the envelope or the capsid?

A

both

25
Q

HBeAg

A

an antigen strongly correlated with infectious Hep B

Abs to HBeAg are not seen in chronically infected pts, but are seen in pts who have successfully cleared the disease

26
Q

what is the mechanism of damage in Hep B?

A

the immune system CTLs see the MHC 1 cells presenting the Hep B and attack, causing damage

27
Q

How many pts move on to chronic Hep B?

A

5%. This is associated with core antigen HBeAg, which predicts chronic hepatitis and liver carcinoma

28
Q

what are outcomes like for perinatally transmitted Hep B?

A

90% of these newborns become chronic carriers, and 25% will die because of hepatitis or cancer

can be helped w/ combo of vaccine and passive IgG

29
Q

describe current vaccines for Hep B

A

subunit vaccines: (inactivated)

purified viral antigens, or viral antigens attached to yeast

30
Q

describe passive immunization for Hep B

A

IgG must be prepared from people w/ high immunity against Hep B. cannot be taken from normal IgG stoes b/c it will not provide protection

31
Q

difference between passive immunity to Hep A and Hep B

A

you can take IgG w/ HA and it is protective. It is not protective against HB, which requires IgG from a pool of highly immune donors

32
Q

chemotherapy for Hep B

A

reverse transcriptase inhibitors, which reduces viral replication to 0, and lowers risk of cancer

33
Q

what precautions are taken to prevent HB infection via blood transfusions

A

no former hepatitis patients

no people who have lied w/ hepatitis pts in 6 months

people who have had a transfusion in 6 months

people w/ HB-Ag in their serum

34
Q

describe the HCV

A

flavivirus

enveloped

plus stranded ssRNA virus

35
Q

what is the most common subtype of HCV?

A

genotype 1 is 70% of cases, genotype 2 is 20%

36
Q

how is Hep C tested for?

A

PCR test

37
Q

what is the transmission method for Hep C?

A

blood/blood contact

STI

perinatally

38
Q

mechanism for Hep C damage?

A

mediated by immune system- CTL/MHC 1

39
Q

describe the timeline of Hep C infection?

A

1-2 weeks- viral RNA detectable

2-6- elevated ALT

4-8 weeks- HCV Ab elevated

after 6 months, 25% clear the virus, 75% develop HCV chronically

40
Q

incubation period for Hep C?

A

60 days

41
Q

prodromal symptoms

A

found in Hep B and C- non specific symptoms that appear before a definitive symptom

in Hep, often arthritis or a rash

42
Q

how do you treat chronic Hep B w/ chemotherapy?

A

alpha interferon w/ polyethylene glycol

drawbacks- expensive, side effects, bad outcomes

Hep B can be treated w/ reverse transcriptase inhibitors

43
Q

hep C chemotherapy

A

pegylated IFN

ribavirin

telaprevir/boceprevir/simeprevir- inhibit essential protease in Hep C

sofosburvir- analog of U, only taken up by viral RNA polymerase and stops replication

Daclatasvir- inhibits a viral protein, and inhibits virion release

usually these drugs are used in combo w/ IFN

44
Q

HBV hepatocellular carcinoma causes

A

rare- only 2% of the 5% that become carriers

HBV DNA integrates near a proto-oncogene and causes in apporpriate expression

excessive damage causes constant regeneration, may predispose to mutations

45
Q

Hep C hepatocellular carcinoma

A

virus does not integrate into the genome

chronic immune response may promote tumor development

46
Q

describe hepatitis D

A

defective RNA virus

circular minus stranded RNA genome

47
Q

describe Hep Ds relationship w/ Hep B

A

only people w/ Hep B can get Hep D b/c Hep D does not produce envelope glycoproteins, but instead must take them from Hep Bs glycoproteins

immunity to Hep B also provides immunity to Hep D

48
Q

how is Hep D detected?

A

Hep D makes on viral protein that is serologically detectable.

PCR analysis is also used

49
Q

Hep D prognosis

A

5% of pts go on to have chronic condition

the infection is worse than singular Hep B infection

mortality rises 10 fold over Hep B infection

Virology 1 (4 decks)

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