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Micro Post Midterm > Hepatitis I > Flashcards

Hepatitis I Flashcards

1
Q

types of food associated with Hep A

A

raw undercooked shellfish, oysters, and clams

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2
Q

incubation period of Hep A

A

it is infectious so it has short incubation period

15-40days

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3
Q

is Hep A blood borne

A

it is mainly fecal oral

there is 2 weeks viremia where there is a possibility of blood borne infection

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4
Q

discuss virus shedding of Hep A

A

one starts to shed virus in feces before first symptom but virus shedding stops before the cessation of symptoms

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5
Q

Hep A replicates in what cells

A

kupffer cells and hepatocytes

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6
Q

how do you detect and treat Hep A

A

specific antibodies by ELISA

passive immunoglobulins

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7
Q

type of enzymes does Hep B have

A

it is a partially ds DNA so its viral coded DNA polymerase serves as a reverse transcriptase

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8
Q

incubation period of Hep B

A

50-180 days

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9
Q

what happens during latter half of incubation period of Hep B

A

all secretion from person is infectious – contains HBsAg (includes breast milk, semen, vagina fluid, blood etc)

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10
Q

chronic persistent and chronic active Hep B can both lead to

A

polyartheritis glomerulonephritis

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11
Q

where do all DNA and RNA viruses replicate

A

all DNA viruses replicate in the nucleus with exception of Pox virus

all RNA viruses replicate in the cytoplasm with exception of Influenza

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12
Q

what are step 1-4 of replication of Hep B

A
  • virus core enters the hepatocytes leaving its coat outside the cell
  • viral core is digested by cellular enzymes in order to expose the viral genome - partially dsDNA
  • viral enzymes fill the gap of the partially dsDNA making it into a complete circular dsDNA that moves into the nucleus
  • DNA transcribed into many mRNA and one full length pregenomic RNA
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13
Q

what is difference between the coded mRNAs and the full length pregenomic RNA

A
  • mRNA is going to be translated into structural and non structural proteins
  • pregenomic RNA does not code for anything and is going to become the genomic material for the new replicated virus
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14
Q

what are step 5-8 of replication of Hep B

A
  • mRNA and pregenomic RNA move back into the cytoplasm
  • mRNA gets transcribed into the structural (core, coat) and nonstructural (viral enzymes including RT) proteins
  • viral core assembled by structural proteins and pregenomic RNA and RT enters the core
  • in the core, the RT recognizes the pregenomic RNA and transcribes it into DNA –> RNA-DNA hybrid
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15
Q

what is the RNA-DNA hybrid created by RT in Hep B replication

A

one strand RNA and one incomplete strand DNA (not enough room to transcribe the whole RNA)

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16
Q

what is step 9-12 of Hep B replication

A
  • RNase H activity of RT digests the RNA part of the hybrid leaving a few nucleotides as primer (not enough room to completely digest it)
  • DNA polymerase activity of RT uses the primer to make a second complementary strand of the DNA making it a partially dsDNA
  • this is due to lack of space for RT to complete the two strands of DNA
  • while transcription taking place, core gains its coat and moves towards cell membrane to mature into a complete virus
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17
Q

what is the coat of Hep B made out of

A

glycoprotein

18
Q

what does HBsAg contain

A

dsDNA with RT

19
Q

what is HBeAg and what is it an indicator of

A

soluble antigen that is part of core protein

indicator of serum infectivity

20
Q

where is HBeAg assembled

A

it is not assembled into the virus – it is secreted into the serum

21
Q

function of HBcAg and where is it found

A

protein kinase activity
not found freely in the serum – only in hepatocytes
but you do see the HBcAb antibodies in serum

22
Q

what is the window period in HepB

A

HBsAg = HBsAb hence they are not detectable in the serum so must use HBcAb to detect if person is currently infected with Hep B

23
Q

first antibody to appear in Hep B

A

HBcAb

24
Q

when does viremia of Hep B begin

A

one month before symptoms

25
Q

which antigens of Hep B can be detected in the serum

A

just HBsAg and HBeAg – most definitely not HBcAg you can only detect HBcAb NOT its antigen

26
Q

when do you see the window period in Hep B

A

only in acute infection not in chronic infection

27
Q

does Hep B carry an oncogene

A

no so tumor must arise from the virus involvement in insertional or transactivating mechanism

28
Q

order of functional genes for retrovirus and hepadnavirus

A

retro: gag - pol - env
hepadna: C - P - S

29
Q

first three steps in the pathogenesis of Hep C

A
  • hep C coats itself with LD and VLD lipoproteins and uses hepatocyte cell receptor to enter the cell
  • virus buds into the ER and remains there
  • inhibits apoptosis and INFalpha by binding to TNF receptor and protein kinase R to establish persistence (no cell death)
30
Q

how does Hep C core lead to marked proliferation and what does that pathway do

A
  • HCV core leads to cell proliferation through Wnt/B catenin dependent pathway
  • nuclear accumulation of beta catenin activates c-myc, cyclin D, and WISP-2 genes which dictate proliferation
31
Q

how does Hep C core protein decrease the amount of cyclin dependent inhibitor p21WAF1

A

through inactivation of p53 leading to imbalance in proliferation and apoptosis leaving higher opportunity for malignant transformation which leads to cirrhosis and HCC

32
Q

what is predictor of Hep C disease

A

high ALT (SPGT) value - alanine amino transferase

33
Q

strongest host factor that determines the outcome of Hep C

A

host genetic - polymorphism in IL28B

34
Q

what happens if IL28B has an inactive or altered gene

A

unlike the normal where there will be clearance if there is jaundice or not, this case there will be viral clearance if icteric (jaundice) and then little to no viral clearance if non-icteric

35
Q

what is the importance of Hep C stimulating the production of protein Drp1

A
  • Drp1 induces mitochondria to undergo asymmetric fragmentation
  • you get one healthy mitochondrion and one damaged
  • damaged one is broken down and used as fuel for the virus
  • healthy one keeps the virus infected cell alive
36
Q

what happens if Drp1 protein is silenced in Hep C

A

interferon and apoptotic activity can increase and infected cells will be killed

37
Q

which hepatitis is most likely to cause cirrhosis and HCC

A

Hep C

38
Q

is there a vaccine for Hep B and C

A

yes for Hep B and no for Hep C

39
Q

what is used to treat Hep C then

A

PEGylated interferon alpha and combined oral therapy: daclastavir and sofosbuvir

40
Q

how does daclastavir work

A

it affects viral NS5A –> inhibits viral RNA synthesis and viral assembly/secretion

41
Q

how does sofosbuvir work

A

nucleotide analogue of uridine binding to NS5B—> causes chain termination

Micro Post Midterm (31 decks)

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