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HELENP CBG VIROLOGY AND IMMUNITY > CBG Lecture 23: Virus Host (Animal) Interactions > Flashcards

CBG Lecture 23: Virus Host (Animal) Interactions Flashcards

1
Q

what are cells supoprting viral infeciton called

A

permissive

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2
Q

what are permissive cells

A

cells supporting viral infection

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3
Q

what are cytopathic effects

A

structural changes in the host cell

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4
Q

what does infection of permissive cells lead to

A

productive (produce virus) infection which can have cytopathic effects

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5
Q

what does infeciton of non-permissive cells lead to

A

abortive or restrictive infeciton

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6
Q

what are the three forms of persistant infection

A

latent
chronic
acute

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7
Q

what is latent infection

A

produce v little if not any virus, used to avoid immune system - v difficult to get rid of

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8
Q

why might a virus be latent

A

to avoid immune system

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9
Q

what is a chronic infection

A

produce low viral titer over long periods of time

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10
Q

what is an acute infection

A

produce loads of viral particle

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11
Q

what are main viral effects on host cells

A

morphological
biochemical/physiological
genetic

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12
Q

what are main routes of entry

A

respiratory tract
oral cavity
genital tract
skin

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13
Q

give virus that uses respiratory tract to enter

A

influenza

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14
Q

what route does hepA use to enter host

A

oral cavity

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15
Q

give some viruses that use the genital tract to enter

A

herpesvirus

HIV

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16
Q

give some viruses that use the skin to enter

A

rabies

yellow fever

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17
Q

which route does rabies use to enter host

A

skin

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18
Q

which route does yellow fever use to enter host

A

skin

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19
Q

where is the primary viremia

A

sites of entry

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20
Q

where is secondary viremia

A

principle routes of spread through the body and circulatory and nerve systems

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21
Q

what is dissemination

A

spread throughout body as opposed to localised infection

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22
Q

what is pathogenesis/how does it occur

A

occurs by direct cytopathic effects on cells

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23
Q

what is localised spread

A

target organ is same as portal of entry eg. influenza colds+many alimentary tract infections

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24
Q

give examples of viruses that have localised spread

A

influenxa

colds/alimentary tract infections

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25
Q

what spread is it if target organ is same as portal of entry

A

localised spread

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26
Q

what is viral migration from entry portal to target organs aka

A

dissemination

27
Q

give an example of virus that undergoes dissemination

A

smallpox

measles

28
Q

what are target organs for smallpoz

A

respiratory mucosa
spleen
bone marrow
lymph nodes

29
Q

what are the target organs for measles

A

lymphatic and resp system
skin
brain

30
Q

how can the nervous system disseminate viruses

A

rabies and herpes

herpes migrates along a nerve cell

31
Q

how can viruses be disseminated

A

by blood and nerves

32
Q

how can viruses escape immune system

A

1.avoid antibodies neutralising them by spreading directly from cell to cell in syncytia
2. budding into cytoplasmic vacuoles
3. genetic variation -quasispecies
4/inhibition of immune and nonspecific defences - downregulation of viral genes
5. becoming latent
6.protein decoy (ebola)

33
Q

how can a virus be persistant by being episomal

A

the virus replicates independently of host chromosome

34
Q

how can inhibition of immune and nonspecific defences help viruses evade immune system

A

downregulate viral gene expression
dicrease synthesis of viral and cellular molecules
restrict viral gene expression

35
Q

how does Ebola evade immune systemq

A

produces a decoy antigen to subvert the host immune response

36
Q

how can a virus escape immune system by budding into cytoplasmic vacuoles

A

HIV does in deep reservoires of WBCs

37
Q

give examples of a virus that is maintained in immune system

A

Epstein Barr Virus - EBV

Herpes Simplex Virus

38
Q

where is episomal EBV present

A

in B lymphocyte

39
Q

name some mechanisms EBV uses to avoid immune system

A

present in episomal form
uses EBNA protein to downregulate epstein barr nuclear antigen
express LM proteins which interfere with the binding of the cells t T cells so T cells cant recognise this cell as being infected therefore not linked
BUT NK cells might recognise it

40
Q

what does EBNA protein do

A

coded by EBV to downregulate epstein barr nuclear antigen to evade immune system

41
Q

which proteins does EBV ecxpress that help it evade immune system

A

expresses L proteins which interfere with the binding of T cvells to the cell so T cells cant recognise it and kill it - htis doesnt stop NK cells though

42
Q

what do LM proteins do

A

released by EBV and interfere with the binding of T cells to the host cell so that they cant bind and kill host cell

43
Q

how does herpes simplex virus evade immune system

A

dissemination along nerve cell
coldsores are cleared and reappear many time
cell it hides in cant physically be recognised by immune system
latent when in mouth cell

44
Q

name a virus that hides in cell to avoid immune sstem

A

herpes

45
Q

what types of host defences against viral infections exist

A

generalised - non specific - anatomic barriers, nonspec inhibitors, fever, inflammation,phagocytosis
more specific induced defences: NK cells and interferon production

46
Q

name some nonspec defences

A 
anatomic barriers
nonspec inhibitors
phagocytosis
fever
inflammation
general antivirons in eyes
47
Q

name some induced defences

A

NK cells

interferon production

48
Q

what type of defence is fever - how does it work

A

fever is a nonspec defecnce which reduces mortality/replication for many viral infections
small change in T for virus makes replication less efficient

49
Q

is phagocytosis more efficient in bac or virus

A

bac

50
Q

how have viruses evolved defences for phagocytosis

A

wait to be engulfed before they start replication

51
Q

what are the outcomes of phagocytosis for the virus

A
  1. virus disruption - influenza, low virulence herpes
  2. virus persistance - HIV
  3. virus replicaiton - HIV/high virulence herpes
52
Q

give example of virus that persists after phagocytosis

A

HIV

53
Q

give example of virus thats disrupted after phagocytosis

A

influenza

54
Q

give example of virus that can multiply after phagocytosis

A

HIV

55
Q

what do interferons cause

A

antiviral - induce resistance to viral replication in all cells
cause an increase in MHC1 expression (antigen presentation) and activaiton of NK cells to kill virus infected cells

56
Q

what do NK cells - what are they activated by

A

NK cells activated by interferons and they kill virus infected cells

57
Q

what does interferon do

A

increase MHC class 1 expression and antigen presentation in all cells

58
Q

what increases MHC Class1 expression and antigen presentation in all cells

A

interferons

59
Q

what viral strategies exist to avoid immune system

A

inhibition of humoral immunity
inhibition of inflammoatory response
blocking of antigen processing and presentation
immunosuppression of host

60
Q

how do viruses inhibit humoral immunity

A

virally encoded complement control protein to inhibit complement activation of infected cells in vaccinia
virally encoded complement receptor to block complement mediated effector pathways in herpes simplex
virally encoded Fc receptor to block effector functions of antibodies bound to infected cells

61
Q

how do viruses inhibit inflammatory response

A

virally encoded cytokine receptor to block effects of cytokines by inhibiting their interactions with host receptors in rabbit myxoma virus and vaccinia
viral inhibition of adhesion molecule expression to block adhesion of lymphocytes to infected cells -EBV

62
Q

how do viruses block antigen processing and presentation

A

inhibit MHC Class 1 expression to impair recognition of infected cells by cytotoxic T cells -herpes
inhibit preptide transport by TAP - blocks peptide association with MHC Class 1 - herpes simplex

63
Q

how does virus ensure immunosuppression of host

A

virally encoded cytokine homologue of interlekin to inhibit Th1 lymbphocytes and reduce interferon production in EBV

HELENP CBG VIROLOGY AND IMMUNITY (8 decks)

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