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Virology > Coronaviruses > Flashcards

Coronaviruses Flashcards

1
Q

Genome

A

(+)ssRNA

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2
Q

Structure

A

Helical and enveloped

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3
Q

VAP

A

Spike (S)

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4
Q

Host receptor

A

ACE2

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5
Q

Fusion peptide

A

Exposed by cleavage of Spike protein by TMPRSS2

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6
Q

Envelope protein (E)

A

Assembly, membrane channel activity

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7
Q

Membrane glycoprotein (M)

A

Assembly

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8
Q

Nucleocapsid (N)

A

Coats the genome

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9
Q

What is a critical step for entry

A

Processing of Spike by TMPRSS2 to reveal fusion peptide

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10
Q

Life cycle

A
  1. Binding and fusion with Spike-ACE2 and fusion protein
  2. Initial translation of orf1 to make double membrane vesicles
  3. Transcription on virus induced membranes
  4. Transcription of mRNAs
  5. Translation of structural proteins
  6. Genome replication
  7. Budding of RNA/N into an ER vesicle
  8. Furin matures then it’s released
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11
Q

What does the -1 ribosomal Frameshift do?

A

Causes polymerase to fall off

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12
Q

PL2pro

A

Responsible for first few cleavages

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13
Q

3CLpro

A

Responsible for many last cleavages

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14
Q

RNA EXOnuclease

A

Lowers mutation rate by proofreading

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15
Q

Remdesivir

A

Inhibits RNAP by preventing elongation

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16
Q

Problem with Remdesivir

A

Resistance via nsp12 mutations

17
Q

How are the genes arranged and translated?

A

They are nested but each RNA has its own 5’ leader, transcription regulating sequence (TRS), and orf

18
Q

Where did they come from?

A

Zoonotic transmissions mainly via bats

19
Q

SARS1 Pathogenesis

A

Infection of pneumocytes in alveolar epithelium followed by macrophages

Virus mainly in lower respiratory tract

Acute lung damage (partially immune-mediated)

Some virus replication in intestines

Viral load peaks 10 days after infection during symptomatic phase
Virus cleared within 2 weeks but kung damage is so severe many deaths happened after that

20
Q

SARS2 Pathogenesis

A

Much lower fatality rate but much more transmissible = more death

Infection of pneumocytes in alveolar epithelium, macrophages, and nasal cilia

Acute lung damage (partially due to immune-mediated excess cytokines)

Some virus replication outside lungs in intestine and possibly the kidneys

Viral load peaks early in the course of infection and is present before symptoms

21
Q

How is pathogenicity different between SARS1 and SARS2?

A

SARS1 - infectious AFTER symptomatic, virus cleared in about 2 weeks
SARS2 - Lower case fatality but more transmissible so more overall death, also infects nasal cilia, replicates also in kidneys likely, infectious BEFORE being symptomatic

Virology (18 decks)

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