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MIMM 324 > 20. Orthomyxoviruses 2 > Flashcards

20. Orthomyxoviruses 2 Flashcards

1
Q

how did the 1956 (H2N2), 1967 (H3N2), and 2009 (H1N1) pandemic strains arise?

A

by recombination between human and avian strains, possibly within a pig intermediate host

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2
Q

describe the 1956 (H2N2), 1967 (H3N2), and 2009 (H1N1) pandemic strains

A

all are human strains with NEW avian HA and/or NA genes

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3
Q

why was the 1918 influenza strain unusual?

A

killed young and healthy people

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4
Q

what happened with the 1918 strain infected healthy people?

A
  1. struck suddenly
  2. then too feeble to walk within hours
  3. many die the next day
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5
Q

3 symptoms of 1918 influenza

A
  1. cyanosis (decreased O2 in blood)
  2. hemoptysis (cough up blood)
  3. uncontrolled pulmonary hemorrhage and edema (ARDS)
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6
Q

what caused mortality in fast-progressing 1918 influenza cases?

A

ARDS-like disease

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7
Q

what caused mortality in slow-progressing 1918 influenza cases?

A

secondary bacterial pneumonia and possible neural involvement

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8
Q

how did neural involvement contribute to slower progressing influenza cases?

A
  1. frequency of psychiatric disorders
  2. encephalitis lethargica
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9
Q

what happened when Hultin injected lung tissue from frozen bodies in Alaska into fertilized chicken eggs, mice, rats, and ferrets?

A

nothing! if there was virus it was dead

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10
Q

when was the 1918 virus found?

A

1997

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11
Q

what did the coding sequence of the 1918 influenza virus reveal? (4)

A
  1. 1918 strain was NOT recombinant but a PURE avian strain
  2. 23 aa changes to confer virulent phenotype
  3. sequence did NOT explain virulence
  4. used reverse genetics to generate a live flu virus with the genome
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12
Q

compared to recent strains, how many more 1918 virus particles are released from human lung cells?

A

50x more virus particles

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13
Q

compared to recent strains, describe the body weight, virus particles, and mortality of mice

A
  • 32% more body weight is lost by mice
  • 39,000x more virus particles in mice lung
  • all mice die within 6 days (vs none)
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14
Q

what happens if we express the 1918 virus genes?

A

gives the high-virulence pandemic phenotype

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15
Q

describe the progression of H5N1 outbreaks (3 stages)

A
  1. H5N1 first detected in geese but drew little attention
  2. eradicated by culling all domestic poultry in Hong Kong –> same genotype has not been detected since
  3. emergence of H5N1 with reassortment of genes with same H5 and N1 genes but different internal genes
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16
Q

can H5N1 avian influenza infect humans?

A

yes

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17
Q

describe H5N1 avian influenza in waterfowl

A

causes neurotropic disease and high mortality

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18
Q

describe H5N1 avian influenza in feline species

A

ability to cause death has been transmitted among feline species

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19
Q

describe H5N1 avian influenza in ferrets/mice

A

causes neurotropic disease/death

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20
Q

what type of influenza is H7N9?

A

influenza virus A

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21
Q

What type of people infected with H7N9?

A

ppl working closely with poultry –> no evidence of human-to-human transmission

22
Q

effects of H7N9 in humans

A

severe respiratory illness and mortality rate of 30%

23
Q

9 requirements of new pandemic influenza strain to be as pathogenic as 1918 strain

A
  1. HA with absent human immunity
  2. HA mutation 1 –> allows infection outside lung
  3. HA mutation 2 –> has high affinity to human cells
  4. Polymerase proteins effective in human cells
  5. NS1 increases apoptosis and decreases IGN
  6. Induces cytokine storm
  7. easily infects humans
  8. severe disease in humans
  9. spreads easily from human to human
24
Q

describe the HA mutation 2

A

higher affinity oligosaccharide-binding to the human sialyl-6-lactose receptor than avian sialyl-3-lactose receptor

25
Q

which 4 requirements does H3N2 follow?

A
  1. HA has high affinity to human cells
  2. Polymerase proteins effective in human cells
  3. Easily infects humans
  4. Spreads easily from human to human
26
Q

which 3 requirements does HK H3N2 NOT follow?

A
  1. HA does not allow infection outside lung
  2. NS1 does not increase apoptosis or decrease IFN
  3. No cytokine storm
27
Q

which 1 requirement does avian flu follow?

A

HA has no human immunity

28
Q

which 1 requirement does H7N9 NOT follow?

A

spreads easily from human to human

29
Q

how long does vaccine development typically take?

A

8-9 months to develop

30
Q

what is homeopathy?

A

1 gram of natural substance undergoes dilution of 10^-6 to 10^-9 –> uses placebo effect

31
Q

describe the activity of HA

A

HA binds cell surface receptor of respiratory cell for infection

32
Q

describe the activity of NA

A

NA cleaves the sugars to allow release of viral particles

33
Q

what does a NA inhibitor do?

A

prevents NA activity so no virions can be released

34
Q

what is Oseltamivir?

A

aka Tamiflu

useful for treatment and prophylaxis

but emerging resistance in avian influenza strains

35
Q

how does influenza produce more than 8 proteins if it only has 8 mRNA? 3 examples

A

splicing, bicistronic mRNA, tandem cistrons, etc.

36
Q

describe the 8 steps of viral entry

A
  1. HA binds to sialic acid on host cell receptor
  2. migrates to clathrin-coated pits
  3. enters by endocytosis
  4. endosomal pH decreases
  5. H+ ions enter virions and break charge interactions between nucleocapsids and virion M1 protein
  6. low pH causes conformational change in HA, exposing hydrophobic fusion peptide of HA2 subunit
  7. fusion peptide integrates into vesicle membrane and allows membrane fusion
  8. virus nucleocapsids are released into cytoplasm
37
Q

what allows H+ ions to enter the virions?

A

virus M2 ion channel allows H+ to enter virion from endosome

38
Q

what is unique about transcription and replication of influenza compared to other RNA viruses?

A

occurs in nucleus

39
Q

describe the +RNA used for translation

A

NOT exact copy –> ~20nt shorter than genomic RNA and has cap and poly A tail

40
Q

describe the +RNA used for replication

A

exact copy

41
Q

what is the most abundant viral protein in virus-infected cells?

A

NS1

42
Q

what is the general role of NS1?

A

blocks polyadenylation of cellular mRNAs

43
Q

what 4 things does NS1 bind to?

A
  1. ssRNA
  2. dsRNA
  3. cellular protein: cleavage and polyadenylation specificity factor (CPSF)
  4. polyA binding protein II (PABII)
44
Q

how does NS1 block polyadenylation of cellular mRNAs?

A

binding to RNA and host cell protein

45
Q

why does NS1 block polyadenylation of cellular mRNA but not viral mRNA?

A

different mechanism with different enzymes

46
Q

what do viral proteins PB1 and PB2 do?

A

have cap-binding and endonuclease activities that causes degradation of cellular pre-mRNAs in virus-infected cells

47
Q

overall, what happens to cellular mRNA when cell is infected with influenza?

A

cellular pre-mRNAs are degraded in nucleus and cellular mRNA production/protein synthesis are both suppressed

48
Q

what immune system pathway does NS1 inhibit?

A

PKR antiviral pathway induced by interferon

49
Q

describe the PKR antiviral pathway

A
  1. during virus transcription, dsRNA is formed and interferons are produced
  2. interferons trigger cells to make dsRNA-dependent protein kinase (PKR)
  3. in presence of dsRNA, PKR is activated and blocks ALL protein synthesis
50
Q

how does NS1 block PKR antiviral pathway?

A

binds to dsRNA, reducing its concentration in the cell

51
Q

besides blocking the PKR pathway, what is another way that NS1 interferes with the immune system?

A

prevents maturation of human primary dendritic cells, limiting host T cell activation

52
Q

what is PB1-F?
where is it located?
what is its function?

A

PB1-F is encoded by an alternate reading frame of PB1

localized in mitochondria

causes increased apoptosis in host immune cells responding to influenza virus infection

MIMM 324 (37 decks)

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