Lec 5 - Virus attachment, entry and uncoating Flashcards

1
Q

What 2 types of interactions are involved in binding of the host receptor?

A
  1. Reversible non-covalent binding
  2. Irreversible conformational changes
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2
Q

What is affinity?

A

The strength of binding

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3
Q

What is avidity?

A

The collective strength of all bonds

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4
Q

What is used to measure the strength of interaction and what is the typical value?

A

Dissociation constant K
1x10^-9

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5
Q

What type of cell does influenza A virus bind and how?

A

Epithelial cells of the upper respiratory tract. HA binds sialic acid and NA cleaves this bond for fusion

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6
Q

What is the type of sialic acid bound by human vs avian influenza strains?

A

Human: alpha-2,6-sialic acid
Avian: alpha-2,3-sialic acid

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7
Q

How does virus entry by pore formation work?

A

Virus binds receptors and injects genome through membrane via pore, leaving no spike proteins

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8
Q

How does virus entry by fusion work?

A

Virus binds receptors and fuses with cell membrane by its fusion peptide to release capsid into cell, leaving spike proteins on surface

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9
Q

How does clathrin mediated endocytosis work?

A

Virus enters clathrin coated pit and is endocytosed into vesicle. Acidification by vacuolar ATPase uncoats virus and clathrin is recycled

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10
Q

How does caveolae mediated endocytosis work?

A

Virus enters caveolae coated pit and is endocytosied into vesicle then taken to ER which requires dynamin. ER chaperone proteins uncoat virus

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11
Q

What is a 3rd method of endocytosis of viruses?

A

Phagocytosis by macrophages and neutrophils

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12
Q

How do picornaviruses eg poliovirus replicate in harsh environments eg human gut?

A

Poliovirus has a 4th protein subunit folded beneath the top 3 that’s only revealed after conformational change during binding

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13
Q

Where is the viral fusion peptide found?

A

Viral spike protein after conformational change

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14
Q

How does influenza release its genome?

A
  1. Fusion peptide to penetrate membrane
  2. Scission to split membrane
  3. Apposition to move membrane apart
  4. Hemifusion and pore formation
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15
Q

How does HIV release its genome?

A
  1. SU/gp120 binds CD4
  2. Conformational change so SU/gp120 binds CCR5 or CXCR4
  3. TM/gp41’s fusion pepide allows capsid to enter cell
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16
Q

List influenza’s main proteins

A

HA and NA spike proteins
M2 ion channel
RdRp
Nucleoprotein (NP)
Nuclear export protein (NEP)
M1 matrix protein

17
Q

Describe the polarity of microtubules and the proteins used to transport cargo

A

Positive end at cell periphery and negative end at centrosome/microtubule organising centre (MTOC).
Kineins transport negative to positive
Dyneins transport positive to negative including viral proteins

18
Q

What is the general structure of a nuclear pore complex, and what is required to enter one?

A

Basket structure on nucleus side, filaments on cytoplasm side.
Need nuclear localisation signal

19
Q

How does adenovirus get its genome the nucleus?

A
  1. Clathrin mediated endocytosis
  2. Spike proteins dissociate
  3. Protein VI lyses endosome
  4. Capsid moves to nucleus by cytoskeleton
  5. Conformational changes to capsid and nuclear pore allows entry
20
Q

How does rotavirus evade innate immune receptors inside the cell?

A

Triple capsid dissociates to double layered particle (DLP) where mRNA is made. NSP1 inhibits NF-kb to inhibit IFN stimulated genes