Orthomyxoviruses Flashcards

1
Q

true or false: influenza viruses have almost an unlimited amount of serotypes

A

true

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2
Q

true or false: influenza is an endemic disease

A

false it is an epidemic disease
worst months: February

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3
Q

True or false: influenza is a pandemic disease

A

true

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4
Q

when did asian flu was a thing

A

in 1957 in usa, rhode island
girl scouts fucked up

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5
Q

What does Flu do

A

-it affects and kills cells of our respiratory tract
-wipes out mucocilary defenses

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6
Q

What is a part of the structure of influenza?

A

-HA: hemagglutinin 16 completely distinct gene types A
-NA: neuraminidase 9 completely distinct gene types A
-NS1: major non structural protein
-Helical nucleocapsid
-lipid bi layer membrane
-polymerase: 3 peoteins
-M1 protein: matrix protein

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7
Q

true or false: NS1 is expressed in influenza infected cells

A

true

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8
Q

What are the three groups of influenza

A

A, B and C which is based on the nucleoprotein type

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9
Q

True or false: influenza viruses from different groups can recombine

A

false: they can’t

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10
Q

which type of influenza viruse4s can infect only humans

A

B and C

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11
Q

Which type of influenza virus can infect all mammalian and avian species

A

A

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12
Q

True or false: only C influenza viruses can cause pandemics

A

false it is A

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13
Q

True or false: there is no antigenic cross-reactivity between different hemagglutinin and neuraminidase types

A

true

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14
Q

first influenza pandemic

A

h3n2

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15
Q

spanish flu name of strain and when did it started

A

1918 H1N1

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16
Q

First isolation of influenza

A

in 1933 H1N1

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17
Q

Asian flu 2

A

H2N2 1957

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18
Q

Hong kong flu

A

h3n2 1967 and in 1976 there was h1n1 too

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19
Q

MEXICAN FLU

A

h1n1 2009

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20
Q

how do they make influenza vaccines

A

you take the attenuated donor virus with the new antigenic variant and then you get the attenuated vaccine virus

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21
Q

What is the reservoir for Influenza A viruses

A

waterfowl basically they have a cloaca where the bladder, the vagina and the colon kinda all merge together

22
Q

Avian influenza true or false: multiplies in cloacae without causing disease

A

trie

23
Q

True or false: in avian influenza only one strain can exist in individual bird

A

false, multiple can coexist

24
Q

true or false: there is high level of genetic reassortment in avian influenza

A

true

25
Q

True or false: there is little to no selective pressure and little;e genetic change in avian flu

A

true

26
Q

the 2009 h1n1 was a mix of what?

A

eurasian flu, h1n1, human h3n2 and avian

27
Q

how did the 1956, 1967 and 2009 pandemic strains arose

A

-by recombination between human and avian strains possibly within a pig intermediate host
- these 3 pandemic strains: human strains with new avian HA+/- NA genes

28
Q

true or false: the 1956 flu pandemic caused the most deaths

A

false
*The 1918 pandemic strain caused far
and away the worst human mortality
of a known flu pandemic
- 10-20 times that of 1956 or 1967

29
Q

why was the 1918 strain unusual

A
  • It commonly killed young and healthy
    victims
  • Healthy asymptomatic persons:
  • Could be struck suddenly
  • Rendered too feeble to walk within hours
  • Many would die the next day
  • Symptoms included:
  • Cyanosis
  • Hemoptysis
  • Later uncontrolled pulmonary
    hemorrhage and edema - ARDS
30
Q

mortality 1918 flu

A

Mortality in fast-progressing cases
-Primarily from ARDS-like disease
-Mortality in slower-progressing cases
-Primarily from 2o bacterial pneumonia
-Possible neural involvement:
- Frequency of psychiatric disorders
- Encephalitis lethargica

31
Q

how many people dies from the 1918 flu

A

100 million worldwide
approx 60% of peeps got it and the mortality rate was 2.5-6%

32
Q

WHAT DID THE COMPLETE 1918 INFLUENZA VIRUS CODING SEQUENCE REVEALED?

A

1) 1918 strain NOT a human/avian recombinant
but a PURE avian strain
(2) 23 a.a. changes out of 5,672
(3) Sequence did not explain virulence
(4) Decision to use reverse genetics to generate a live
flu virus with the genome of the 1918 pandemic virus

33
Q

TRUE OR FALSE: THE 1918 strain would not fuck us up rn

A

FALSE IT WOULD

34
Q

h5n1 1996

A

in china in chickens a lot of people got sick
they killed all them chickens

35
Q

true or false: no evidence of sustained human to human transmission in h7n9

A

true

36
Q

What would be required to
produce a new pandemic
strain of influenza that would
be as pathogenic as the 1918
strain?

A

1) HA protein to which humans have little or no immunity
(2) HA mutation 1  facile infection of non-respiratory tissues
(including macrophages) allowing spread outside lung
(3) HA mutation 2  higher affinity oligosaccharide-binding
to the human sialyl-6-lactose receptor than
to the avian sialyl-3-lactose receptor
(4) Polymerase proteins direct facile RNA synthesis in human cells
(5) Viral NS1 protein has mutations directing
- high level induction of apoptosis
- high level inhibition of IFN induction
(6) Induction of severe pro-inflammatory effects (cytokine storm)
(7) Ability to easily infect humans
(8) Ability to cause significant disease in humans
(9) Ability to spread easily from humans to humans

37
Q

Difference between h1n1 1918 and current h7N9

A

does not spread easily human to human

38
Q

what are the drugs attck against flu

A

neuranimidase inhibitor
blocks the cleavage of the receptor aka hemagglutinin and the cell receptor so that no new virion can be released
-tamiflu

39
Q

what are the 2 surface proteins of the flu

A

Na and HA

40
Q

how many mechanisms are there to make express proteins

A

6

41
Q

true or false: influenza replicates in the nucleus

A

true
Unlike almost all other RNA viruses, influenza virus
nucleocapsids are transported to and are transcribed and
replicated in the host cell nucleus

42
Q

how does influenza gets in cell

A

sialic acid receptor and clathrin coated pir

43
Q

which proteins binds to the cell receptor

A

HA

44
Q

is influenza an rna virus or DNA

A
  • ssRNA
45
Q

true or false: there is a pH conformation change in influenza

A

true in endosomal membrane

46
Q

Influenza virus RNA transcription:

A
  • PB2 recognizes and binds 5’ cap structures found on all
    eukaryotic mRNAs
  • PB2 binds to caps of newly-synthesized pre-mRNAs in the cell
    nucleus
  • PB1 then acts as a nuclease, cleaving the bound pre-mRNA at
    an A or G residue 10–13 nt from its 5’ cap
  • This capped RNA fragment, still bound to PB2, is used as
    primer to copy genome RNA
    -
47
Q

role of PB1

A

-PB1 acts as an RNA polymerase

48
Q

Role of PA

A
  • Role of PA is not well understood
  • Resulting viral mRNAs have heterogeneous sequences for the
    first 10–13 nt
  • Flu can thus make capped messenger RNAs even though they
    do not code for a capping enzyme
49
Q

What does NS1 do

A

The NS1 protein interferes with polyadenylation of cellular
mRNAs
NS1 protein is the most abundant viral protein in virus-infected
cells
NS1 binds to both single- and double-stranded RNA and to two
host cell proteins:
(1) cleavage and polyadenylation specificity factor (CPSF)
(2) poly(A)-binding protein II (PABII)
Binding of NS1 to these proteins inhibits normal 3’ end cleavage
and polyadenylation of cellular mRNAs
Polyadenylation of viral mRNAs occurs by a distinct mechanism
and does not depend on these cellular enzymes

50
Q

Cap-binding and endonuclease activities of the influenza PB2 and PB1 proteins leads to

A

Cap-binding and endonuclease activities of the influenza PB2 and PB1 proteins leads to degradation of cellular pre-mRNAs in virus-
infected cells
As a combined result of interference with 3’ end processing and 5’ end cleavage
- most cellular pre-mRNAs are degraded in the nucleus
- cellular mRNA production and protein synthesis are suppressed

51
Q

Influenza virus and the immune system:

A

NS1 inhibits activation of the interferon-induced PKR antiviral pathway
During influenza virus transcription, some ds-RNAs are inevitably formed
Virus infection → interferon production
→ cells produce double-stranded RNA-dependent protein kinase (PKR)
In the presence of ds-RNA, PKR is activated and blocks both cellular and viral protein synthesis