Dr. Mubareka's session Flashcards

1
Q

What does IRES stands for?

A

internal ribosomal entry site

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2
Q

function of IRES

A

i) help end-independent ribosomal recruitment
ii) help new interactions with eIFs

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3
Q

where is IRES found?

A

polio
–> picovirus

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4
Q

How is host cell translation shut off with IRES?

A

poliovirus protease 2A cleave eIF4G

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5
Q

Which viruses are enveloped?

A

Flavivirus, Coronavirus, Bunyavirales

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6
Q

Which viruses lack an envelope?

A

piconavirus, orthomyxovirus (influenza), reovirus

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7
Q

What is the source of vaccine derived poliovirus?

A

from oral polio vaccine (when unvaccinated ppl contact with oral vaccinated ones)

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8
Q

What sites are known for evolution of vaccine derived poliovirus?

A

i) revert sites for low neurovirulence
ii) revert site of reduced replicative fitness

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9
Q

How is piconavirus transmitted?

A

fecal-oral, respiratory

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10
Q

Why is cancer cells more susceptible to reovirus infection?

A

Ras expression
–> inhibit dsRNA dependent (PKR)
–> reovirus get endocytosed + replicate inside cells

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11
Q

viruses with non-segmented genome

A

Mononegavirales, Coronavirus, Flavivirus, picovivirus

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12
Q

negative sense viruses

A

Mononegavirales, Orthomyxovirus, Bunyavirales

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13
Q

Function of PKR in viral replication

A

after activated by dsRNA during viral replication
–> stops viral dsRNA synthesis (reovirus)

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14
Q

How does oncolytic virotherapy work for reovirus?

A

i) release of cytokines
ii) activate antigen presenting cells
iii) killing of tumor cells thru NK cells and CD8 T cell

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15
Q

Viruses with segmented genome

A

reovirus, bunyavirales, orthomyxovirus

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16
Q

positive sense viruses

A

piconavirus, flavivirus, coronavirus

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17
Q

viruses belong to neither + and - sense

A

reovirus

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18
Q

Feature special to reovirus

A

RNA always attached to inner capsid

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19
Q

forms of reovirus

A

i) virion
ii) ISVP
iii) core particle

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20
Q

which forms of reovirus is infectious?

A

virion, ISVP

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21
Q

where is N protein found?

A

Bunyavirales

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22
Q

Roles of N protein

A

i) initiates transcription
ii) RNA chaperone
iii) primed mRNA synthesis from genome
iv) form vRNA from cRNA
v) transcription templates as ribonucleoproteins

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23
Q

How does N protein initiates transcription?

A

i) bind to panhandle on vRNA
ii) unwinds panhandle + allow RdRp to interact at 3’ term

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24
Q

what are some injuries linked to hantavirus?

A

acute lung and kidney injury

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25
Q

What contributes to lung and kidney injuries in hantaviral infection?

A

i) increased permeability
ii) thrombocytopenia (less platelets)
ii) complement activation

26
Q

How is permeability increased in hantavirus infection?

A

i) VEGFA upregulated –> downregulates VE cadherin
ii) secretion of bradykinin

27
Q

How does orthomyxovirus initiates transcription?

A

cap snatching

28
Q

Where does cap snatching occur?

A

nucleus for influenza

29
Q

function of PA subunit in transcription initiation of influenza

A

cleave 5’ cap in host transcript

30
Q

describe steps in cap snatching

A

i) viral RNP bind to CTD of Pol II
ii) PB2 capture a capped transcript, then cleaved by PA subunit
iii) PB2 swivels to align 3’ of cleaved gragment to template inPB1 subunit

31
Q

What can enter PB1 in RdRp of influenza?

A

i) NTPs
ii) vRNA

32
Q

Proteins and subunits needed for cap snatching

A

i) RdRp
- PB2 (align the two pieces)
- PA (cleave 5’ cap from trascript)
- PB1

33
Q

What holds vRNA during transcription initiation?

A

binding pocket in PB1 holds 5’ end of vRNA

34
Q

What contributes to the variety in influenza?

A

i) antigenic drift
ii) antigenic shift
iii) recombination

35
Q

How does antigenic shift contirbute to influenza evolution?

A

allow different strains of influenza to mix tgt
–> change surface antigen
–> change genome material

36
Q

How does recombination help with influenza evolution?

A

have segments with genetic material from more than one source
–> increase cleavability of HA

37
Q

How does antigenic drift contribute to influenza evolution?

A

minor changes in virus
–> not recognzied by previous antibodies maybe

38
Q

Thru what process does Ebola get into cells?

A

macropinocytosis

39
Q

What factors on ebola interact with cell surface?

A

glycoprotein 1, 2
(forming trimer)

40
Q

What does Ebola bind on cells for entry?

A

i) attachment factors ( C type lectins)
ii) receptors (TIM-1)

41
Q

what helps with macropinocytosis of ebola?

A

TAM family members (tyrosin kinase receptor)

42
Q

Describe steps in ebola entry

A

i) GP on ebola interact with C type lectin, receptors like TIM-1
ii) virions get in by macropinocytosis
iii) GP cleaved by cathespin B, L –> expose receptor binding site
iv) acidification in endosome
–> GP1 interact with NPC1
–> enter cytosol

43
Q

What happens after ebola genome enters cytosol?

A

i) replicated in cytosol
ii) transcribed into mRNA + translated
–> GP translated in ER
iii) virion assembly

44
Q

Where does ebola infection usuallly occur?

A

dendritic cells, monocytes, macrophages
–> reduced innate immune response
broad cell tropism

45
Q

Why is bat such a great viral reservoir?

A

i) intruded by humans
ii) huge colony + dense
iii) hibernation
iv) flight
v) long life span, synchronized parturition

46
Q

How does flight help bat as a reservoir?

A

allow them to migrate all over and get different viruses
–> their immunity allows them to tolerate virus

47
Q

How ds hibernation help bat as a viral reservoir?

A

lower their body temp
–> allow virus to persist inside them

48
Q

How does human enroachment help bat as a viral reservoir?

A

mix with other viruses present in domestic animals/human
–> acquire receptors within human

49
Q

Strategies used by coronavirus for making subgenomic RNA transcript

A

template switching

50
Q

How does template swithcing works

A

once form TRS-B on 5’ end
–> can skip over some parts of genome
–> TRS-B pair with TRS-L on 3’ end and complete transcription

51
Q

When is S1/S2 junction cleaved in covid?

A

i) trafficking by furin like enzyme
ii) serine protease (TMPRSS2) during attachment
iii) cathepsin in late endosome

52
Q

when is S2’ cleaved by cathepsin

A

enter thru ACE2

53
Q

when is S2’ cleaved by TMPRSS2

A

bind to nearby receptor that has TMPRSS2 close to it

54
Q

What cleaves S protein and when in covid?

A

by furin in golgi apparatus
–> S1 (receptor bind) + S2 (mediate fusion)

55
Q

Common vectors for flavivirus

A

i) A. aegyti
ii) A. albopictus

56
Q

What is the feature of infectious virions in flavivirus?

A

those whose prM is completely cleaved

57
Q

what helps partially mature virions for flavivirus to enter cells?

A

furin protease

58
Q

what happens when more partially mature virions enter cells

A

increase infectivity of immature dengue virus
–> higher conc of antibody

59
Q

In what virus is antibody-dependent enhancement observed?

A

flavivirus

60
Q

What happens in antibody dependent enhancement?

A

i) PRR signalling decrease
–> less interferon production
–> more virions produced

61
Q

Order the geographic distribution of Virus (From most limited to broadest)

A

i) Flavivirus (limited to tropics)
ii) Mononegavirales
iii) Bunyavirales (restriction based on reservoir)
iv) Coronavirus = orthomyxovirus (some geographic restriction)
vi) piconavirus = reovirus
(Global)