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Medical virology > Coronaviruses > Flashcards

Coronaviruses Flashcards

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USMLE® Step 1 flashcards
1
Q

How many human coronaviruses have been identified?

A
  • 7
  • mostly associated with the common cold
  • not well studied before SAR-CoV-2
  • can be alpha, beta, delta or gamma
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2
Q

What kind of virus is coronavirus?

A
  • ssRNA positive sense
  • nidovirales
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3
Q

What are the 4 main genes in a coronavirus genome?

A
  • structural (S)
  • N protein
  • M protein
  • E protein
  • many accessory proteins
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4
Q

What are some of the roles of the structural protein in the coronavirus genome?

A
  • form large spikes on the virion surface
  • bind specific cellular receptors
  • induces fusion of the viral envelope with the cell membrane
  • induces neutralising Abs and cell mediated immunity
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5
Q

What is the role of the N protein of coronavirus?

A
  • binds viral RNA and aids in its synthesis
  • forms the nucleocapsid
  • also involved in cell-mediated immunity
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6
Q

What is the role of the M protein in the coronavirus genome?

A
  • determines budding site
  • triggers viral assembly
  • forms the shell of the internal viral core
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7
Q

What is the role of the E protein of coronavirus?

A
  • triggers particle assembly
  • associates with the viral envelope to form an ion channel
  • may cause host cell apoptosis
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8
Q

What are the roles of accessory proteins encoded on the coronavirus genome?

A
  • avoiding host immune responses
  • deleting these doesnt affect replication in culture but may in animals
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9
Q

How does coronavirus enter the cell?

A
  • receptor binding and endosome entry
  • or fusion with the cell membrane
  • proteases cleave the spike proteins from the surface as/before the cell enters
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10
Q

How can coronavirus shield itself from the host immune response while building up metabolites/components needed for replication?

A
  • some viral proteins induce double membrane vesicles derived from the ER
  • contain intermediates of RNA replication and have a pore through which the viral genome can interact while staying protected
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11
Q

How does a frameshift came into coronavirus replication?

A
  • not just 1 long ORF like many viruses
  • translation of ORF1 occurs
  • ribosome reaches a complex RNA structure that 5% of the time causes it to slip back 1 nucleotide, miss the stop codon and translate the rest
  • acts as a way to regulate proteins needed in lower quantities such as viral replication proteins
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12
Q

What cleaves the polyproteins produced in coronavirus replication?

A
  • viral encoded proteases
  • NSP5 cleaves ORF1
  • PLpro also involved
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13
Q

What proteins are encoded in the coronavirus genome? nae 6

A
  • RNA dependent polymerase
  • helicase
  • RNA capping enzymes
  • endo+exo nucleases
  • NSP3+4 induce double membrane vesicles
  • NSP1 shuts down host translation
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14
Q

Describe the role of subgenomic RNAs in the coronavirus genome

A
  • produce the accessory proteins
  • made as a result of discontinuous transcription
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15
Q

How does discontinuous transcription lead to the production of subgenomic RNAs?

A
  • replication-translation complex reaches specific TRS elements on the genome
  • RTC jumps to the 5’ end and produces sgRNA -> sgmRNA -> accessory proteins
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16
Q

What is the role of continuous transcription?

A
  • to produce full-length negative sense RNA internediates that act as a template for genome replication
17
Q

What is the genome size of a coronavirus compared to other positive sense RNA viruses?

A
  • much larger
  • has proof-reading enzymes while others dont
  • lower accuracy of others may impose an upper limit on the size of their genomes
18
Q

What are the main ORFs seen in coronaviruses?

A
  • ORF1a = genome expression
  • ORF1b = genome replication
  • 3’ ORFs = virus dissemination
19
Q

How does coronavirus evade the innate immune response? (5)

A
  • encode many proteins to:
  • inhibit interferon signalling or production (NSP1 can stop their translation)
  • inhibiting antiviral proteins like PKR
  • structural proteins like N can interfere with host defense machinery
  • inhibition of inflammasomes
  • inhibition of NK cells
20
Q

What are 3 of the most commonly known and well studied coronaviruses?

A
  • SARS-CoV
  • MERS-CoV
  • SARS-CoV2
21
Q

Describe same clinical difference and similarities between SARS-CoV, MERS-CoV and SARS-CoV2

A
22
Q

How are MERS-CoV and SARS-CoV-2 spread?

A
  • droplets
  • aerosol spread
  • contaminated surfaces
23
Q

Where does SARS-CoV-2 replicate + what is immunity like>

A
  • throughout the respiratory tract
  • unknown duration of immunity
24
Q

Where do SARS-CoV and MERS-CoV replicate + what is immunity like>

A
  • in the lower respiratory tract
  • long-lived memory T cell response proportional to disease
25
Q

What happens once SARS-CoV-2 enters the lungs?

A
  • destruction of cells leads to inflammatory response
  • in some, excessive infiltration of monocytes, macrophages and T cells leads to widespread inflammation, organ damage and cytokine storm
  • in a healthy immune response the virus is cleared here or doesn’t even make it to the lungs
26
Q

Where did human SARS-CoV + MERS-CoV come from?

A
  • camels -> bats
  • bats -> civets and other traded animals
  • civets or camels -> humans
  • mixture of cross-species and zoonotic transmission
27
Q

Where did human SARS-CoV-2 come from?

A
  • bats -> unsure intermediate host (bats?) -> humans
  • mixture of cross-species and zoonotic transmission
28
Q

What is the vaccine situation for coronavirus?

A
  • 12 used worlwide and many in development for SARS-CoV- 2
  • 3 candidates for MERS targeting the S protein
29
Q

How did civet-infecting SARS-CoV move to infect humans?

A
  • spike protein binds ACE-2 with a receptor binding motif
  • civet and humans have similar ACE-2
  • motif only needs a 2 amino acid shift to have high affinity to both ACE-2s
30
Q

What kinds of issues have hampered coronavirus vaccine development in the past?

A
  • some trials enhanced disease
  • used to have a lack of understanding of the immune response to SARS
  • animals cant fully recapitulate human disease
31
Q

How has SARS-CoV-2 adapted to increase infection rate?

A
  • acquired an extra furin cleavage site in the spike protein
  • spike gets cleaved before leaving the host cell priming it for entry to the next one
  • this mutation destabilises the virus but further mutations fixed this
  • also allows binding to a wider variety of respiratory tract cells
32
Q

What do we know about immunity to coronavirus?

A
  • little
  • immunity wanes rapidly
  • poor understanding of how prior infection with other coronaviruses affects later infections
33
Q

What is antigenic cartography>

A
  • mapping relationships between antigenic variants of a virus
  • provides a quantitative + visual summary of antigenic differences
  • can see evolution of the virus and how existing treatments might fare against now/other strains
34
Q

What antivirals are available for coronavirus?

A
  • repurposed drugs
  • mostly inaffective at reducing mortality, need for assisted ventilation or duration of hostpital stays
35
Q
A

Medical virology (15 decks)

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