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Virology > Hepatitis Viruses > Flashcards

Hepatitis Viruses Flashcards

1
Q

What causes the most chronic viral hepatitis in the US?

A

hepatitis C

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2
Q

Which hepatitis viruses cause acute infection?

A

A, E

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3
Q

what kind of virus family is hepatitis A of

A

picornavirus

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4
Q

Unlike many RNA viruses, what is notable about the serotypes of hepatitis A?

A

has only a single serotype

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5
Q

how is hep a transmitted

A

fecal oral

contaminated food, water, shellfish, poor hygiene

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6
Q

symptoms of hep a virus

A

asymptomatic

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7
Q

can someone who has gotten hep A be infected again?

A

no, its protective antibodies provide lifelong immunity

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8
Q

what is notable about the capsid of picornaviruses

A

stable to acid, drying, detergents

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9
Q

how does hepatitis A enter its site?

A

enters cells through receptor enriched in liver

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10
Q

what is different about hep A from the other picornaviruses

A

it’s not cytolytic– just shed from cells

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11
Q

tissue culture system for hepatitis viruses

A

no good one for A, B

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12
Q

pathology in the liver from hep A is due to

A

most likely immunopathology

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13
Q

incubation time of hep A

A

30 days

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14
Q

symptoms of hep A

A

jaundice in some pts

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15
Q

What comes first, IgM or IgG

A

IgM

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16
Q

prevention for hep A

A

inactivated hep A vaccine used for high risk people: infants, travel, chronic liver disease, ppl working w HAV

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17
Q

frequency of hep A infection in the US in recent years

A

has decreased since 90s, after vaccine licensed

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18
Q

family of Hep E virus

A

calicivirus

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19
Q

genome of HEV

A

+ sense ss RNA

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20
Q

shape of HEV

A

icosahedral

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21
Q

what is HEV known as

A

enteric virus

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22
Q

transmission of HEV

A

fecally contaminated water
minimal person to person

US cases usually from travel

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23
Q

incidence of HEV in the US

A

sporadic, not endemic

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24
Q

prevalance of HBV in US

A

low

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25
Q

what is notable about the outcomes of Hep B virus infections?

A

they are different depending on age

young-chronic infection chance higher, but symptomatic infec lower

older children, adults–chronic infec chance lower, symptomatic infec chance higher

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26
Q

family of HBV

A

hepadnavirus, genotypes A-H

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27
Q

envelope or not for HBV

A

enveloped

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28
Q

what is the receptor for HBV

A

sodium bild acid cotransporter

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29
Q

genome of HBV

A

circular DNA that is partly double stranded

30
Q

life cycle of HBV

A 
genome enters
DNA synthesis to make complete dsDNA
then goes to nucleus
trnascribed to mRNA
mRNA translated in cytoplasm

mRNA reverse transcribed to ssDNA, DNA is made partially DS!!!!

viral particles are released, as well as sub-viral particles of sAg

31
Q

what is notable about the DNA of HBV?

A

it can integrate into the chromosome and stay in the cell

32
Q

what do HBV infected cells release?

A

infectious viruses as well as non infectious HbsAg particles

33
Q

HbsAg

A

antigen without DNA–not infectious

34
Q

what was the foundation for the HBV vaccine

A

HbsAg

35
Q

risk factors for acute hep B in US

A

sex

intravenous drug users

36
Q

transmission of HBV from what?

A 
nursing
vaginal secretions
blood
semen
saliva
37
Q

how can one get a HBV infec

A

neonates nursing
sex
IV drug use
blood

38
Q

how does HBV spread in the body in infection?

A

goes to blood
Ab develops
goes to liver, where it replicates–with cell mediated immunity, you have symptoms and resolution, or it can go back to blood, infect, etc

39
Q

symptoms of HBV

A 
RUQ pain
nausea
anorexia
malaise
jaundice
dark urine
40
Q

when do you start shedding HBV after infec?

A

2 months later

41
Q

timeline of antibody development against HBV

A

anti HBc first
then Anti HBe
AntiHBs

42
Q

outcomes of HBV infec in ADULTS

A

90% have resolution

9% have HbsAg for more than 6 months–which can go on to be resolution, or asymptomatic carrier state, or chronic persistent hepatitis, or chronic active hepatitis (can lead to hepatic cell carcinoma)

43
Q

what influences the outcome of HBV infec?

A

immune control
presence of HDV (delta agent)

immune control–if limited cell med response, get chronic disease and mild symptoms, can lead to cirrhosis or primary hepatocellular carcinoma or fulminant hepatitis

Delta agent can cause a chronically infected HBV individual to get fulminant hepatitis

44
Q

hep D virus

A

viroid–can only grow in HBV infected cells

45
Q

genome of Hep D virus

A

small RNA that is a riboyzme that processes itself

46
Q

What does the genome of hep D encode

A

1 antigen that is packaged in Hep B sAg

47
Q

what type of infection is hep D?

A

coinfection that is acute

superinfection (after the HBV infec)

48
Q

implications of Hep D for disease

A

higher risk of severe chronic liver disease

49
Q

why chronic HBV infec leads to high incidenc of hepatocllular carcinoma

A

injury to liver->proliferation of cells that are usually quiescent–genetic errors can accumulate

integration of viral DNA into host chromosome causes genomic instability–can cause changes in host gene expr

virally encoded X protein–associated w/ signal transduc cascades that can be oncogenic–X lowers p53 activity

HCC in mice is associated w/ surface antigen expr ession and X expression

50
Q

incidence of acute Hep B in the US in recent years

A

has decreased since 80s and 90s when HBsAg screening of pregnant was recommended, immunization was recommended for infants,

51
Q

prevention of HBV

A

screen blood
vaccination
blood/body fluid precautions

52
Q

treatment of HBV

A

polymerase inhibitors
nucleoside analogs
IFN alpha

53
Q

family of hep C

A

flavivirus

54
Q

genome of hep C

A

+ strand RNA

55
Q

enveloped or not for hep C

A

enveloped, associated with VLDL

56
Q

what is notable about transcription for Hep C

A

error prone RNA polymerase leads to many quasi-species, so no vaccine

57
Q

what does genome of hep C encode

A

multiple immunomodulators enabling its persistance

58
Q

what is liver damage in Hep C a result of

A

mostly immunopathology

59
Q

what does hep C increase the risk of

A

hepatocellular carcinoma

60
Q

hep C causes highc incidence of chronic and ___ infections

A

asymptomatic

61
Q

what mediates translation for hep C

A

IRES

62
Q

what happens w the protein translated by hep C

A

protelytic processing

63
Q

which virus has a close relationship w intracellular lipids and membranes

A

Hep C

64
Q

sources of infection for Hep C

A

intrav drug use
sex
transfusion

65
Q

incidence of hep C of late

A

has gone down since the 90s because of screening of blood

66
Q

outcomes of HCV infec in ADULTS

A

15% -recovery and clearance
85% - persistent infection

applies for immunocompetent

67
Q

what can persistent HCV infec cause

A

chronic hepatitis–leading possibly to liver failure, or cirrhosis, or hepatocllular carcinoma

68
Q

why does HCV chronic infec lead to high incidence of hepatocellular carcinoma

A

HCV core protein regulates many cell tumor suppressors (p53, Rb), pathways in proliferation

HCV core protein induces steatosis, leading to oxidative stress, increased cell prolif

inhibit NK cells

enhance cell growth

69
Q

role of miRNA 122

A

enhances translation and/or replication for HCV by binding and regulating its mRNA

70
Q

most prevalant genotype of HCV

A

1

71
Q

HCV therapy

A

direct acting against viral components

host targeting

72
Q

when is hep A virus shed?

A

in feces before symptoms appear

Virology (15 decks)

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