CBG Lecture 23: Virus Host (Animal) Interactions Flashcards
what are cells supoprting viral infeciton called
permissive
what are permissive cells
cells supporting viral infection
what are cytopathic effects
structural changes in the host cell
what does infection of permissive cells lead to
productive (produce virus) infection which can have cytopathic effects
what does infeciton of non-permissive cells lead to
abortive or restrictive infeciton
what are the three forms of persistant infection
latent
chronic
acute
what is latent infection
produce v little if not any virus, used to avoid immune system - v difficult to get rid of
why might a virus be latent
to avoid immune system
what is a chronic infection
produce low viral titer over long periods of time
what is an acute infection
produce loads of viral particle
what are main viral effects on host cells
morphological
biochemical/physiological
genetic
what are main routes of entry
respiratory tract
oral cavity
genital tract
skin
give virus that uses respiratory tract to enter
influenza
what route does hepA use to enter host
oral cavity
give some viruses that use the genital tract to enter
herpesvirus
HIV
give some viruses that use the skin to enter
rabies
yellow fever
which route does rabies use to enter host
skin
which route does yellow fever use to enter host
skin
where is the primary viremia
sites of entry
where is secondary viremia
principle routes of spread through the body and circulatory and nerve systems
what is dissemination
spread throughout body as opposed to localised infection
what is pathogenesis/how does it occur
occurs by direct cytopathic effects on cells
what is localised spread
target organ is same as portal of entry eg. influenza colds+many alimentary tract infections
give examples of viruses that have localised spread
influenxa
colds/alimentary tract infections
what spread is it if target organ is same as portal of entry
localised spread
what is viral migration from entry portal to target organs aka
dissemination
give an example of virus that undergoes dissemination
smallpox
measles
what are target organs for smallpoz
respiratory mucosa
spleen
bone marrow
lymph nodes
what are the target organs for measles
lymphatic and resp system
skin
brain
how can the nervous system disseminate viruses
rabies and herpes
herpes migrates along a nerve cell
how can viruses be disseminated
by blood and nerves
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)
how can a virus be persistant by being episomal
the virus replicates independently of host chromosome
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
how does Ebola evade immune systemq
produces a decoy antigen to subvert the host immune response
how can a virus escape immune system by budding into cytoplasmic vacuoles
HIV does in deep reservoires of WBCs
give examples of a virus that is maintained in immune system
Epstein Barr Virus - EBV
Herpes Simplex Virus
where is episomal EBV present
in B lymphocyte
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
what does EBNA protein do
coded by EBV to downregulate epstein barr nuclear antigen to evade immune system
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
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
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
name a virus that hides in cell to avoid immune sstem
herpes
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
name some nonspec defences
anatomic barriers nonspec inhibitors phagocytosis fever inflammation general antivirons in eyes
name some induced defences
NK cells
interferon production
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
is phagocytosis more efficient in bac or virus
bac
how have viruses evolved defences for phagocytosis
wait to be engulfed before they start replication
what are the outcomes of phagocytosis for the virus
- virus disruption - influenza, low virulence herpes
- virus persistance - HIV
- virus replicaiton - HIV/high virulence herpes
give example of virus that persists after phagocytosis
HIV
give example of virus thats disrupted after phagocytosis
influenza
give example of virus that can multiply after phagocytosis
HIV
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
what do NK cells - what are they activated by
NK cells activated by interferons and they kill virus infected cells
what does interferon do
increase MHC class 1 expression and antigen presentation in all cells
what increases MHC Class1 expression and antigen presentation in all cells
interferons
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
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
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
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
how does virus ensure immunosuppression of host
virally encoded cytokine homologue of interlekin to inhibit Th1 lymbphocytes and reduce interferon production in EBV
