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DT4- Exam 3 > Zeng- Hep- Melissa > Flashcards

Zeng- Hep- Melissa Flashcards

1
Q

Where is HAV incidence high?

A
  • Highest in developing Asian and african countries

- Incidence substantially decreased in US with introduction of vaccine

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2
Q

Describe HAV:

Family, genome, structure

A

Picornaviridae
(+) ssRNA
Naked, icosahedral capsid (VP1-3), spherical structure

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3
Q

Describe the neutralizing antigenic epitope for HAV

What does our immune system recognize?

A
  • CONFORMATIONAL EPITOPE vs. typical 3 aa sequence

- VP1 + VP3 form specific structure recognized by human immune system

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4
Q

What is significant about the 5’ noncoding region of HAV genomic RNA?

A
  • IRES (internal ribosomal entry sequence) on 5’ cap

- Forms secondary structure required for cap independent translation (no 5’ cap)

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5
Q

Describe the translational products of HAV mRNA

A
  • RNA has single open reading frame (ORF)
  • Yields single translational (protein) product
  • Product is cleaved into structural and regulatory proteins
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6
Q

What are risk factors for HAV infection? (3)

A
  • poor sanitation/ travel to endemic locations
  • MSM
  • IV drug use
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7
Q

What is the primary route of transmission for HAV in endemic areas? In the US?

A

Endemic areas: fecal-oral

USA: IV drug use/ MSM

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8
Q

Describe two means by which HAV is particularly virulent as an enteric virus

A
  • heat stable (cook to 121F/60C for 30 min)

- acid and detergent stable

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9
Q

How does HAV mediate damage to the liver?

Which immune cells are dominant during acute infection and recovery?

A

Immune mediated damage to hepatocytes

  • CTLs predominate in acute phase of infection
  • NK mediated lysis of HAV infected hepatocytes
  • CD4+ T cells dominate in recovery phase
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10
Q

Do patient develop long lived immunity against HAV after infection? Is vaccination possible?

A
  • Yes, long lived Abs against VP1, VP3 conformational epitope confirm protective immunity
  • Thus, vaccination is very effective
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11
Q

Where geographically is HBV incidence highest?

A

Most common in Asia; 2 billion infections ww/ year

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12
Q

HBV:
Family, genome, structure
What are the important antigens associated with the structure?

A

HepaDNAviridae family

  • Relaxed, partially circular dsDNA
  • Capsid (HBcAg)
  • Enveloped (HBsAg x3, long, medium, short)

**Note: pre-core HBeAg is secreted during replications and indicates INFECTIVITY

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13
Q

Describe the 3 types of HBV viral particles:

A
  1. Dane particle = spherical; complete infectious viron, contains genome
  2. Filamentous subviron= noninfectious, no genome
  3. Spherical subviron= noninfectious, no genome
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14
Q

Describe 4 important characteristics of HBV genome:
What is meant by relaxed circular DNA?
What are two important features of the 5’ end?
What is one feature that facilitates economic usage of the genomic material?

A
  • Relaxed circular (noncovalently closed) partially dsDNA
    (inner (+) strand not full length)
  • Polymerase ATTACHED @ 5’ end
  • RNA primer (PROTEIN) attached at 5’ end
  • Overlapping reading frames (mult. reading frames)
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15
Q

Describe the HBV viral life cycle:

A

Attachment–> nuclear capsid released–>
Nuclear capsid transported to nuclear cell membrane–>
RC DNA released into nucleus–>
Removal of polymerase + RNA from RC DNA–>
DNA synth + ligation ( “repair”) –>
**cccDNA synthesis complete–>
Viral minimicrosome–> Transcription of VIRAL RNA–>
VIRAL RNA exported to cytoplasm –>
Subgeneric + Genomic HBeAg Transcripts–>
Genomic replication–> Assembly of viral particle–> Release

**cccDNA = covalently closed circular DNA

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16
Q

What is HBxAg?

A

Subgeneric transcript formed furring translation of HBV RNA: this confers ability to transform into hepatocellular carcinoma

17
Q

What are the two important genomic length transcripts synthesized turing translation of HBV RNA transcripts?
What are their functional purposes?

A
  1. Precore RNA: codes for HBeAg (secreted, indicates infectivity)
  2. Pregenomic RNA (pgRNA): shorter than precore; no start codon for HBeAg
    - encodes viral polymerase + HBcAg
    - template for genomic DNA synthesis
18
Q

Describe the details of genomic replication:

A 
Epsilon structure on 5' pgRNA binds HBV pol + HBcAg--> 
Immature nucleocapsid--> 
HBV polymerase activity (TP primes, RT reverse transcribes)--> 
Pol-DNA oligo complex forms--> 
Pairs with 3' pgRNA--> 
Reverse transcription of pgRNA--> 
(-) strand DNA synthesized--> 
Serves as template for (+) strand
19
Q

List the 3 specific functions od 5’ Epsilon stem loop structure on pgRNA:

A
  • pol binding site
  • template for DNA oligo synthesis
  • encapsidation signal (associates with HBcAg)
20
Q

What are the three domains of HBV polymerase and what are their functions:

A

TP (Terminal protein) = PROTEIN PRIMER for RT initiation
RT = reverse transcriptase
RH = RNase H

21
Q

Describe the final formation of a complete HBV viral particle:

A

HBsAgs cluster on ER membrane–>
LHBsAg + HBsAg interact–>
Pull nucleocapsid into HBsAg cluster–>
Budding into ER lumen–> secretion

22
Q

What are HBV quasisecies?

A

HBV polymerase lacks proofreading capacity; genome highly prone to mutation

Mixture of genetic variants = quasi species

23
Q

How is HBV transmitted in endemic vs. non endemic areas?

At what age will infection lead to higher rate of chronicity?

A

Endemic:
PERINATAL INFECTION; can be monitored by HBeAg titers; BREASTFEEDING NOT RISK FOR TRANSMISSION
**INFECTION AT YOUNG AGE = ^^ CHRONICITY

Non-endemic:
Sexual + percutaneous spread; low rate of chronicity because patients infected later in life

24
Q

How is hepatic injury mediated in HBV infection?
Describe the humoral response, noncytolytic clearance, and the inlammatory response to infection.
Is there long term immunity after infection subsides?

A

Mediated by IMMUNE RESPONSE
Humoral Anti-HBsAg are protective (long term immunity)

Noncytolytic clearance: CTLs–> IFNY, TNFa, IFNa/b
- Occurs AFTER peak replication, BEFORE hepatitis onset

Inflammatory Response: 
Acute HBV (Specific CD4, CD8)--> Nonspecific T, NK, Neutros
25
Q

HCV

Viral classification, prevalence, mode of transmission?

A

Flavaviridae, (+)ssRNA
2% ww, most common in Egypt
Transmitted via IV drug use

26
Q

HCV: Describe the mechanism of infection

A

HCV E1, E2 heterodimer interacts with cell surface CD81, SR-B1–> weak, delayed cellular and humoral immune response–> mild clinical sx w ^^ chronicity

27
Q

HDV:

Viral classification, prevalence, mode of transmission?

A

Deltaviridae, covalent circular (-) RNA
Up to 30% HBV + patients in cold areas have this
Transmitted parenterally (IV drugs use)

28
Q

HDV: Describe the mechanism of infection

A

Satellite virus (defective) needs HBV coinfection/ superinfection carriers in order to infect

29
Q

HEV:

Viral classification, prevalence, mode of transmission?

A

Calcaviridae, (+) ssRNA
#1 form of hepatitis in endemic regions (70% ppl get it)
Fecal oral transmission especially during WET SEASONS

30
Q

HEV: Describe mechanism of infection

A

Unidentified cell receptor

DT4- Exam 3 (14 decks)

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