Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
31 Cards in this Set
- Front
- Back
How many genera of Reoviridae are there and what form does there nucleic acid take ?
|
9
dsRNA |
|
What genera of Reoviridae is the commonest cause of neonatal diarrhoea ?
|
Rotavirus
|
|
How many capsid layers do rotaviruses have and what properties does this confer on them ?
|
Three
Outer - sticky projections grab host cell Intermediate - (12 copies) RNA polymerase, - internal synth of viral mRNA Inner - capsid has 11 segments of dsRNA lining it |
|
What morphology is typical of rotaviruses?
|
3 layered, non enveloped Icosahedral capsid
Confers good env survival, acid, bile, desiccation & UV resistant survive on pasture from year to year. Quite big |
|
What must happen to rotaviruses before they can infect an enterocyte ?
|
Trypsin / acid degradation of outer capsid
hence restriction of infection site |
|
Post binding to enterocytes rotaviruses enter cells via ---------- and avoid endosome digestion by -------- [Ca]. they also incorporate there ----- capsid in to the endosome ------- disrupting it.
|
endocytosis
decreasing outer membrane |
|
What advantage does internal +sense RNA synthesis confer to rotaviruses ?
|
Prevents cell detecting viruses dsRNA & signalling infection - interferon response.
ssRNA exits via holes in capsid to cytoplasm |
|
Once rotaviruses +sense ssRNA is in the cytoplasm it initiates …….
|
Protein synthesis.
Inner capsid assembly incorporating +sense RNA triggering -ve RNA complementary strand synthesis |
|
What unique final assembly do rotaviruses employ ?
|
outer capsid proteins made in RER, a
ssociate with cell membrane & bud inner capsule through to golgi. End with lipid free outer capsid. Don’t have to kill cell to get out - can escape by lysis or exocytosis. |
|
What unique exit strategy can rotaviruses employ and how does this advantage the virus ?
|
escape by lysis or exocytosis
don't have to kill cell to exit so more particles can be replicated by one host cell |
|
What receptors on host cells can rotaviruses bind to enter cells ?
|
Sialic acid, heparin, intergrins acts as receptors,
but not specific so not spp specific |
|
Why can diarrhoea caused by rotaviruses occur without marked / prior to pathology ?
|
Rotavirus Non Structural Protein 4 effects enterocytes by
- blocks disaccharideases on lumenal membrane - blocks Na Glucose symport - both increase osmotic P - sugar fermented by bacteriain GIT = GAS, & osmotic P - loosens intracellular junctions - cytokine, amine release stimulated |
|
How do rotaviruses cause tight junction loosening ?
|
CA released for ER
- mediates cell cytostuctural relaxation - inhibits SGLT1 |
|
How does rotaviruses mediated cytokine and amine release enhance the diarrhoea?
|
Cytokines
- vasoactive - increase cell permeability - increase fluid & molecule loss to lumen - increase motility of GIT - increase mucous secretion |
|
How should rotavirus infections be treated ?
|
Supportive care
electrolytes & fluids |
|
how does normal cell function enhance diarrhoea in rotavirus infections?
|
Crypt cells function is unaffected so endogenous pumping Cl into lumen ongoing
NSP4 enhances crypt cell Cl secretion. |
|
How can rotavirus infections be diagnosed ?
|
Traditionally - fecal sample under EM
Now strains distinguished by differing RNA segment sizes in agarose gel. Dip stick on farm - 2 lines = +ve. |
|
When can gene reassortment occur in rotaviruses ?
|
2 or more viruses infect same host - swap bits
|
|
How is immunity to rotavirus infections mediated ?
|
Ab to outer capsid VP 7 & 4.
Needs to be lumenal Continuous IgA in milk = protective low damage does not = dz animals may build up immunity by weaning stage. |
|
What strategies can be employed to counter rotavirus infections ?
|
Killed vaccines used to boost maternal antibody levels
Must continue to feed colostrum/milk to dairy calves But many strains - not all included in vaccine Annual booster required |
|
What type of virus is blue tongue, what spp does it affect and what cell type ?
|
Orbivirus
sheeps, cattle, camelids wide variety of cell types |
|
What does this image of midge bites on a sheep show ?
|
Inflammation round bite site -
happy virus infecting lots of cells viraemia spreads to distant sites & other midges |
|
What are the clinical signs of Blue tounge virus ?
|
fever, loss of appetite, conjunctivitis - because BVs inflammed, hyperaemia of mucus membranes, drooling, lameness - hyperaemia of coronary band.
Inflammation in lungs and resp tract - oedema in lung = cyanotic = blue tongue. (often don’t see) symptoms more severe in sheep than cattle. |
|
How does Blue tongue cause death ?
|
Pulmonary oedema
|
|
Blue tongue in insects is not cytopathic but one bite of what mammalian spp host is ---------.
|
sheep
infective |
|
How may blue tongue virus infectivity be increased by midges ?
|
Insect trypsin may cleave virus outer capsid protein and enhance virus infectivity (by sugar digesting enzymes)
|
|
Does insect saliva have an effect on the virus pathogenicity?
|
Yes
- factors in midge saliva affect coagulation pathway, - factor Xa inhibitor, collagenase, - apyrase - prevents ATPO dependent platelet aggregation, - vasodilator proteins = encourage virus to replicate and spread at site of infection. |
|
What factors were thought to affect blue tongue spread to northern climes ?
|
Replication of Blue Tongue virus in culicoides is temperature dependent - 14 days in a row staying above 10C needed for transmission of virus.
Unexpectedly turned up in 2007 ermany / Netherlands wind spread to UK |
|
What made blue tongue potentialy endemic in the UK ?
|
Overwintering: midge adults don’t survive in cold weather. Carrier animals (cattle) must be involved in overwinter survival
Virus overwinters in host T-lymphocytes, T cell activation = virus is reactivated Midge bites causes inflammations - activates T-lymphocytes & therefore virus (Inflamed fibroblasts express WT1 ligand which activates T-cells via WT-1 ligand, which then release virus) |
|
How long does reactivation take in the carrier from activation to transmissibility?
|
4 hours.
|
|
How has BTV8 strain of blue tongue been controlled ?
|
Vaccination in control zone - where no infection occurred
with inactivated BTV8 virus strain specific - variable efficacy - Can have live attenuated virus (but recimbination means can revert to virulent) - Virus like particle - inner and outer capsid proteins made in Bacculovirus spontaneously assemble into capsids with no nucleic acid - Strong neutralising antibody responses - protect from clinical disease but may not prevent infection or carrier status developing |