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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

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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
what spread is it if target organ is same as portal of entry
localised spread
26
what is viral migration from entry portal to target organs aka
dissemination
27
give an example of virus that undergoes dissemination
smallpox | measles
28
what are target organs for smallpoz
respiratory mucosa spleen bone marrow lymph nodes
29
what are the target organs for measles
lymphatic and resp system skin brain
30
how can the nervous system disseminate viruses
rabies and herpes | herpes migrates along a nerve cell
31
how can viruses be disseminated
by blood and nerves
32
how can viruses escape immune system
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
how can a virus be persistant by being episomal
the virus replicates independently of host chromosome
34
how can inhibition of immune and nonspecific defences help viruses evade immune system
downregulate viral gene expression dicrease synthesis of viral and cellular molecules restrict viral gene expression
35
how does Ebola evade immune systemq
produces a decoy antigen to subvert the host immune response
36
how can a virus escape immune system by budding into cytoplasmic vacuoles
HIV does in deep reservoires of WBCs
37
give examples of a virus that is maintained in immune system
Epstein Barr Virus - EBV | Herpes Simplex Virus
38
where is episomal EBV present
in B lymphocyte
39
name some mechanisms EBV uses to avoid immune system
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
what does EBNA protein do
coded by EBV to downregulate epstein barr nuclear antigen to evade immune system
41
which proteins does EBV ecxpress that help it evade immune system
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
what do LM proteins do
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
how does herpes simplex virus evade immune system
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
name a virus that hides in cell to avoid immune sstem
herpes
45
what types of host defences against viral infections exist
generalised - non specific - anatomic barriers, nonspec inhibitors, fever, inflammation,phagocytosis more specific induced defences: NK cells and interferon production
46
name some nonspec defences
``` anatomic barriers nonspec inhibitors phagocytosis fever inflammation general antivirons in eyes ```
47
name some induced defences
NK cells | interferon production
48
what type of defence is fever - how does it work
fever is a nonspec defecnce which reduces mortality/replication for many viral infections small change in T for virus makes replication less efficient
49
is phagocytosis more efficient in bac or virus
bac
50
how have viruses evolved defences for phagocytosis
wait to be engulfed before they start replication
51
what are the outcomes of phagocytosis for the virus
1. virus disruption - influenza, low virulence herpes 2. virus persistance - HIV 3. virus replicaiton - HIV/high virulence herpes
52
give example of virus that persists after phagocytosis
HIV
53
give example of virus thats disrupted after phagocytosis
influenza
54
give example of virus that can multiply after phagocytosis
HIV
55
what do interferons cause
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
what do NK cells - what are they activated by
NK cells activated by interferons and they kill virus infected cells
57
what does interferon do
increase MHC class 1 expression and antigen presentation in all cells
58
what increases MHC Class1 expression and antigen presentation in all cells
interferons
59
what viral strategies exist to avoid immune system
inhibition of humoral immunity inhibition of inflammoatory response blocking of antigen processing and presentation immunosuppression of host
60
how do viruses inhibit humoral immunity
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
how do viruses inhibit inflammatory response
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
how do viruses block antigen processing and presentation
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
how does virus ensure immunosuppression of host
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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