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viruses Flashcards

1
Q

what makes up a virion

A

genome
capsid
envelope
matrix

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2
Q

what is matrix

A

protein layer connecting capsid and envelope glycoproteins

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3
Q

what capsid symmetry do DNA viruses causing human disease have

A

icosahedral (or complex - pox)

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4
Q

DNA viruses

A

HHAPPP

hepada, herpes, adeno, parvo, pox, papova

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5
Q

what do all helical RNA viruses have

A

an envelope

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6
Q

difference between eclipse and latent period

A

eclipse - no increase in virus

latent - no extracellular virus

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7
Q

stages of replication

A 
attachment 
penetration 
uncoating 
amplification of genome and viral proteins
assembly 
release
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8
Q

where do RNA adn DNA viruses typically replicate

exceptions

A 
DNA - nucleus 
RNA - cytoplasm 
exceptions: 
- HIV RNA but nucleus 
- Pox is DNA but cytoplasm
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9
Q

what does -ve RNA viruses carry

A

RNA dependent RNA polymerase

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10
Q

inclusion bodies

A

accumulated viral proteins at site of viral assembly

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11
Q

3 ways viral genomes continually changing

A

mutation
recombination
reassortment

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12
Q

drug for herpes, why, type of drug

A

acyclovir - herpes virus has herpesvirus thymidine kinase required for activation/adding of P
nucleoside analogue

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13
Q

barriers to viruses in resp tract

A 
mucous 
cilia
alveolar macs
temp gradient (cooler at top)
IgA
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14
Q

what is characteristic of RSV on microscopy

A

multi-nuclear giant cell s

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15
Q

what causes croup

A

parainfluenza

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16
Q

koplick spots

A

diagnostic of measles early on

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17
Q

lifecycle of measles

A

primary viral replication in URT epithelium, infects macs, lymphs, DCs
these drain to lymph nodes and circulation - systemic infection

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18
Q

characteristics of GIT viruses

A

no envelope and bile resistant

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19
Q

reasons for diarrhoea in rotavirus

A

secretion of NSP4 from infected cells

decreased absorption due to enterocyte destruction

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20
Q

major characteristic of EBV

A

polyclonal B cell activation

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21
Q

what produces IFNalpha/beta

A

virally infected mac or DC or normal cell

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22
Q

what activates NK cells

A

IFNalpha/beta

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23
Q

what produces IFNgamma

A

only NK cells and T cells wa

24
Q

what do type 1 vs type 2 interferons do

A

type 1 (IFNalpha/beta) - inhibit viral replication, enhance MHCI expression, activates NK cells

type 2 - gamma - inhibit viral replication, enhances MHCI and II expression

25
Q

ways to evade CD8 T cell recognition

A

antigenic variation
induce apoptosis of MHCI
bind TAP on ER - prevents processing adn presentation on MHCI
bind MHCI and retain in ER
latency - not producing proteins so not susceptible to CD8 attack

26
Q

how do NK cells work

A

have activating R - recognises molecules on cell surface as result of viral infection - KILL
inactivating R - if bind MHCI - OVERIDES KILL
–> so if MHC absent or aberrantly expressed - KILL

27
Q

what activates NK cells a

A

IL12 or IFNalpha/beta

28
Q

what genes does IFN cause upregulation of

A

MHCI and PKR

29
Q

how does PKR work

A

two PKR molecules hook over dsDNA and autophosphorylate

bind to eIF2alpha and phosphorylate - cause inhibition of translation

30
Q

how do viruses evade PKR

A
  • excessive production of small dsDNA
  • proteins that bind to dsDNA to protect
  • virus encoded homologue of eIF2alpha - binds PKR
31
Q

where does influenza virus bind

A

sialic acid R on non-ciliated epithelial cells of RT

32
Q

type of virus influenza

A

enveloped, -ve RNA

33
Q

which flu can infect other species

A

a

34
Q

which flu cause human disease

A

a and b

35
Q

function of haemagglutinin

A

gripper - binds SA containing Rs - initiates entry

36
Q

function of neuraminidase

A

snipper - binds SA and cuts it off

37
Q

difference between different type a flu subtypes

A

different HA and NA

38
Q

current scary forms of flu

A

H1N1 H3N2

39
Q

why is flu virus localised to resp tract

A

needs enzyme tryptase clara to cleave HA to be able to undergo conformational change to escape endosome

40
Q

why do we get reinfected with influenza

A

ab response is lifelong to a particular strain, but flu has antigenic drift

41
Q

flu vaccine conformation

A

trivalent inactivated vaccine

42
Q

antivirals to influenza

A

M2 channel blockers

NA blockers - zanamavir

43
Q

antigenic shift vs drift

A

shift = sudden appearance of new subtype of A (new HA and NA not just mutations in epitope regions (drift))

44
Q

when would you get a flu epidemic

A

when all 5 epitopes of subtype have mutated and vast majority of population has no abs

45
Q

when would you get a flu pandemic

A

when get antigenic shift happens and get sudden appearance of new subtype

46
Q

whats a way to create new influenza subtype

A

reassortment - pig infected with human and avian flu bc has both types of R in RT and get reassortment

47
Q

lifecycle of hep a

A

contaminated water/food - ingestion - replication in intestinal epithelia - blood - rep in liver - bile/faeces

48
Q

hep a vaccine conformation

A

inactivated whole virus

49
Q

hep e lifecycle

A

same as a

50
Q

can you give immunoglobulin to hep a and e

A

no just a - pre and post exposure

51
Q

hep b lifecycle

A
  • partial dsDNA made into cccDNA by viral polymerase
  • host RNA polymerase makes pregenomic RNA (lots of different reading frames)
  • reverse transcription into partial dsDNA
52
Q

what does it mean if HBsAg+

A

chronic carrier

53
Q

strategies of HBV to ensure persistence

A
  1. HBeAg - essential for persistent infection
  2. excess production of HBsAg
  3. HBV cccDNA - can evade a lot of immunity
54
Q

why HCC more common in chronic carriers

A

due to partial integration of HBV genome into hepatocyte genome

55
Q

HBV treatments

A

peg-IFNalpha - for HBeAg+ carriers w chronic active infection
nucleoside analogues - adenfovir

56
Q

can you give hep b vaccines post exposure

A

yes in needle stick injury for e.g.

57
Q

untreated HCV how many become chronic carriers

A

70-90%

exam revision (15 decks)

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