Viruses Flashcards

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1
Q

Influenza Genome

A

ssRNA

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2
Q

Influenza structure (main proteins) (4)

A

HA, NA, M2, M1

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3
Q

Influenza cell entry (5)

A

(1) three spikes of HA bind to sialic acid on HC
(2) receptor mediated endocytosis occurs
(3) low endosomal pH triggers fusion of viral and endosome membrane - low pH induces conformational change in shape of H0 - leads to exposure of HA2 fusion peptide
(4) low pH also opens M2 proton selective channel - acidifies viral core
(5) release of vRNP so free to enter host cell cytoplasm

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4
Q

Influenza transcription and replication (2)

A

(1) converted to positive sense RNA by RNA dependent RNA polymerase (RdRp)
(2) cellular RNA polymerase II binds to DNA and starts transcripiton

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5
Q

Influenza immune responses (3)

A
  1. induces strong IFN production - induces non-permissive state in neighbouring cells
  2. humoral mediated immunity - HA specific antibodies found
  3. RIG-1 is main PRR against influenza virus infections
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6
Q

Influenza M2 ion channel inhibiting drugs

A

Amantadine and Rimantadine

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7
Q

Influenza RNA polymerase inhibitor

A

Favipiravir

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8
Q

Influenza NA inhibitor

A

Zanamivir

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9
Q

Herpes Genome

A

dsDNA

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10
Q

HHV-1

A

Herpes simplex - cold sore - trigeminal ganglion infection (60% US prevalance)

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11
Q

HHV-2

A

Herpes simplex - genital herpes - sacral ganglion (20% US prevalence)

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12
Q

HHV-3

A

Varicella (chicken pox) Zoster (shingles) virus

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13
Q

HHV-4

A

Epstein Virus

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14
Q

Herpes Cell entry (6)

A
  1. gC and gB bind to heparan sulfate
  2. gD binds to HVEM, nectin-q, or 3-0 sulfated heparan sulphate
  3. nectin receptors produce cell-cell adhesion
  4. gD (once bound to HVEM), changes conformation and interacts with gH and gL
  5. interaction results in hemifusion state
  6. gB interaction with gH/gL results in creation of entry pore
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15
Q

Herpes Virus immune evasion (4)

A
  1. Block MHC I expression and promote degradation
  2. inhibit proteosome
  3. block TAP transporter
  4. block expression of activatory NK ligands
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16
Q

Herpes virus treatment (1)

A

acyclovir and glancyclovir - thymidine anlogues

17
Q

HIV genome

A

ssRNA

18
Q

HIV cell entry (4)

A
  1. Gp120 binds to CD4
  2. co-receptor binding (CCR5/CXCR4)
  3. interaction between CD4 and gp120 allows exposure of fusion proteins in the gp41 subunit - inserts into host cell membrane and acts as a tether
  4. mixing of lipids which compose the membranes and entry
19
Q

HIV replication (4)

A

Uses Reverse Transcriptase

  1. polymerase center uses host cell tRNA to use viral RNA as a template - RNA-DNA strand formed
  2. RNaseH center used to degrade RNA component
  3. dsDNA formed
  4. integrase effectively cuts and pastes the viral DNA in to the gebome
20
Q

HIV transcription

A
  1. immediately after replication, only Tat and Rev produced
  2. Tat increases transcription of HIV-1 genes by recruiting cellular transcription factors
  3. primary RNA transcripts undergo extensive splicing - results in over 40 different mRNAs
21
Q

HIV antiviral drugs (3)

A

Tak-220 - prevents binding of CCR5 to gp120
Enfuvirtide - targets membrane fusion
Zidovudine - thymidine analogue which prevents action of RT

22
Q

Hepatitis Genome

A

dsDNA