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EXAM 5 > Hepatitis > Flashcards

Hepatitis Flashcards

1
Q

HAV basics

A

enteric transmission - fecal-oral

infectious, self-resolving

ssRNA linear, +

no chronic infection

very low mortality

we make neutralizing IgG which KILLS the virus

can have jaundice etc.

picorna - simar to polio

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2
Q

HBV basics

A

parenteral

serum hepatitis

dsDNA circulular, para retrovirus

hepadna

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3
Q

HCV basics

A

parenteral

transfussion

ssRNA linear

chronic in 50% of cases, regardless of age

chronic strongly associated w cirhosis and HCC

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4
Q

HDV

A

parenteral

increased HBV disease if infect after

ssRNA circular

viroid

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5
Q

HEV basics

A

enteric: fecal-loral

community acquired

ssRNA linear, + sense

mortality high in immunocompromised

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6
Q

HBV genome

A

para-retrovirus - does not integrate into chromosomal DNA

replicates by reverse-transcription but packages the DNA intermediate (unlike classic retrovirus)

circular genome - overlapping ORF, barely any room for mutation

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7
Q

acquisition of HBV

A

newborns of long term carriers

IV drug users

transfusion and ransplant

multiple sex partners

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8
Q

Outcomes of HBV

A

asymptomatic, acute, fulminant

acute and asymptomatic can become chronic

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9
Q

fulminant hepatitis

A

viral mutations - replicate so much, directly cytoplastic - 90% mortality

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10
Q

HBV serum particles

A

particles w no DNA

100x

non infectious - decoys

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11
Q

Stages of HBV infection

A
  1. immune tolerance - minimal inflammation and fibrosis (newborns - transplacental tolerance)
  2. immune clearance - loss of immune tolerance and leads to hepatitis, fibrosis, cirhossis, HCC
  3. Inactive carrier state - immune control of infection, little hepatitis
  4. active inflammation - loss of immune control of infection
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12
Q

children primarily have chronic infections from which hepatitis? HBV

A

HBV - tolerance to virus in utero then infected - don’t fight off as well because tolerance + immune response

can’t clear virus - chronic

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13
Q

Marker for active HBV replication

A

HBeAg - marker

early antigen is processed and secreted polypeptide of the core protein

secretion of e angiten correlates with viral DNA replication - used as marker for active infection

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14
Q

HBV polymerase protein

A

RNA and DNA dependent polymerase activity N terminus acts in priming - strand DNA

RNAse H domain - degrade RNA intermediate during replication

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15
Q

HBV life cycle

A

infect cell (LDL?)

core barticle - inserts genomic material into nucleus

covalently closed (partially gapped/duplexed)

plasmid - cccDNA plasmid

transcribed RNA-DNA intermed, into cytoplasm

translated, package ongoing viral RNA

RNA –> cDNA

bud into ER - vesicluar transport to cell membrane - secrete

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16
Q

Early response to HBV

A

innate immunity

HBV infected hepatocytes release Type I IFN

Stim HLA class I on hepatocytes

activate NK, NKT –> make IFN, TNF (dictate chronic infection in newbords)

lead to suppression of HBV replication and liver inflammation

17
Q

Late response to HBV

A

t cell immunity

CTL priming and recruited, destroy infected hepatocytes

18
Q

Factors determining acute v chronic HBV infection

A

age of infected host (newborns more chronic)

strength of cytokine response

immune maturity

19
Q

treatment of HBV

A

entecavir or tenofovir (new nt analogs)

adefovir, telbivudine - older nt analogues (less potent, higher resistance

pegylated IFN alpha - once first line, now bottom

VACCINE!!!

20
Q

HCV transmission

A

injecting illicit drug use

high risk behaviors in the past

sexual activity

21
Q

HCV Outcomes

A

acute infection

subclinical infection (way more common)

chronic liver disease (50%)

22
Q

HCV life cycle

A

receptor binding and endoytosis

fusion and uncoating (+ RNA)

translation and protein processing

RNA replication

package it all in cytoplasm

release

23
Q

NS3

A

HCV

serine protease

cleave polyprotein and release polypeptide

24
Q

phosphoprotein

A

HCV

required for replication

25
Q

immune editing

A

HCV

generates large number of variants over infection to evade immune response

pares ag epitopes and evades immune responnse

no neutralizing ab response

generates many variants

why it is so chronic

26
Q

HCV treatment

A

RNA dep RNA pol inhibitor - Sovaldi

phosphoprotein replication complex inhibor

Harvoni = combo - approaches 100% long term cure

27
Q

HCV antiviral

A

generates many variants

impedes early stages of host response

viral immune editing and glycosylation

disrupts CTLs

serine protease - decreased IFN expression

phosphprotein mutates

28
Q

HCC Mechanism

A

apoptic stimulus (viral proteins, CMI) –> cell death –> genetic lesions (mutations, chromosomal instability, continuous proliferation-regeneration) –> resistance to apoptosis –> neoplasia

EXAM 5 (11 decks)

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