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Flashcards

Coronavirus

Rachael Jones Animal Disease 2 English 5.0Average rating 5.0 out of 5 (1 rating) 44 cards

Cards in this deck (44)

  1. 1From what order is the family Coronaviridae?Nidovirales
  2. 2Give 2 diseases caused by coronavirus.Enteritis/TGE
    Feline peritonitis
  3. 3What are features of Coronavirus?Enveloped virus with characteristic large peplomers (spike-protein) and a core containing +ve RNA helical neuclocapsid
    - Bilipid membrane
    - Can neutralise with anitibodies on the surface
  4. 4What are the stages of replication?Attachment (Aminopeptidase N)
    Endocytosis
    Fusion and nucleocapsid release
    Transcription of polymerase
    Nested RNA transcripts
    Synthesis of nucleoprotein in cytoplasm and spike protein RER/Golgi
    Assembly and budding in Golgi membrane
    Exocytosis of new virus
  5. 5What is the genome of Nidovirals?+ve sense RNA
    5’ cap and leader sequence and a poly A tail
    Translated directly to a protein but uses 3 possible reading frames
  6. 6How many poly-proteins are synthesised?2
  7. 7What do the cleaved polyproteins form?A large RNA polymerase complex
  8. 8What does the polymerase make?-ve sense copy of the genome, plus a set of nested transcripts. Using the same leader sequence then dissociating from the template and re-associating at one of seven downstream complementary sequences only the 5’ end of each mRNA is translated it codes for one protein or in some cases two proteins in different reading frames
  9. 9Why are the nested transcripts made in a gradient?So that it’s efficient and the ones that are needed more and made more
  10. 10What is the issue with all the cutting and pasting?Can lead to problems both for the virus and for treating
  11. 11What is the advantage with the coronavirus budding from E.R and exocytosing?By budding from an intracellular site the virus does not have to kill the cell and can avoid exposing its peplomers on the cell surface were antibodies may bind and mediate complement fixation or ADCC
  12. 12What would happen if the peplomers were exposed?Killed
  13. 13What allows for rapid evolution of new variants?- Lack of proof reading by RNA polymerase enzymes
    - Recombinations between related Coronaviruses or host cell RNA can occur due to repeat sequences used in forming nested transcripts
  14. 14What age of pig are most affected by Porcine Transmissible GastroEnteritis (TGE)?Piglets
  15. 15How does porcine TGE enter the host?Infection occurs by ingestion. The virus is acid labile and protection by milk or food allows passage through stomach.
  16. 16What cells does it target?Entry by attachment to aminopeptidase-N on villous enterocytes. (other cells e.g macrophages)
  17. 17What is the normal function of the enterocytes?Digestion and absorption
  18. 18How does the virus alter/interfere with cell function?- Virus is rapidly cytotoxic to enterocytes
    - Infects the villus enterocytes mainly and therefore destroying those involved in absorption
  19. 19What is the issue with piglets having TGE?The enterocytes are destroyed and they express lactase – without this, lactose is fermented by E.Coli in the small intestines and causing acidification. This makes more of an osmotic effect and causes worse diarrhoea (yellow)
  20. 20What is the main reason that pigs die from having TGE?Diarrhoea which causes dehydration
  21. 21Can pigs recover from TGE?Yes – as long as they receive rehydration therapy due to basal crypts being less affected and recovery can be rapid
  22. 22What would happen if you introduced TGE into a naïve herd?Outbreak of vomiting diarrhoea with fever throughout herd.
    All pigs affected, mortality of piglets near 100%.
    Adult animals recover and may become persistently infected carriers.
    In large production units the disease may become endemic.
    Outbreaks in post weaning piglets that become infected.
    Withdrawal of maternal IgA from milk.
  23. 23What is a disease that is very similar to TGE?Porcine epidemic diarrhoea (PED)
  24. 24What are the effects of having PED?New infection: transient vomiting and diarrhoea in sows and weaners
    - Mortality in younger pigs
    - Epidemics when introduced into new herd
    - Endemic in herds >300 sows
  25. 25How can you differentiate between TGE and PED?Lab testing
    Eg rapid antigen capture ELISA on faeces
  26. 26How can you be protected against coronavirus?- Secretary IgA antibody is protective, systemic IgG is not. Vaccination of sows with live attenuated TGE virus to boost maternal immunity can be used.
    - TGE does not survive long outside of a host.
    - Control of TGE by depopulation and disinfection of affected pens.
    - Removal of Seropositive adults. Virus can be secreted for >100 days in carrier animal
  27. 27What are the clinical signs with respiratory variant of TGE?•Clinical signs : Transient cough 1-2 days
    •Rapid spread between herds by aerosol •Recovered pigs seroconvert to TGE •Recovered pigs are protected from enteric TGE
    •TGE has become rare in UK & mainland Europe (Not Ireland or USA )
  28. 28What is the serological difference between TGE and respiratory TGE?Deletion mutant of TGE
  29. 29What does Bovine Coronavirus cause?Diarrhoea in calves
    Winter dysentery in adult cattle
  30. 30What is the effect of loss of Villi?Giving rise to net fluid secretion diarrhoea malabsorption of sugars and fermentation
  31. 31Where else can Bovine Coronavirus be detected?In respiratory tract and lymph nodes – respiratory symptoms
  32. 32What does Canine Coronavirus cause?Mild enteric disease in puppies
    Can persist in the GIT for months with periodic shedding
  33. 33What is Canine respiratory Coronavirus?Associated with outbreaks of (severe) respiratory disease in kennels. Sequencing shows this virus differs from enteric virus
  34. 34What are the 2 presentations of Feline Enteric Coronavirus?Ubiquitous ‘avirulent’ feline Coronavirus, Chronic infection in some carrier cats
    May cause diarrhoea in kittens.
  35. 35What are the 2 results of having Feline Enteric Coronavirus?1. Resolution of infection and sterile immunity
    2. Sero-conversion Persistent Infection Carrier state (colon)
  36. 36What is Type 1 Feline Enteric Coronavirus?Feline Coronavirus distinct from other Coronaviruses Primary cellular receptor unknown hard to grow most prevalent
  37. 37What is Type 2 Feline Enteric Coronavirus?High degree of similarity with Canine Coronavirus Cellular receptor APN grows well but less common
  38. 38What can persistent infection with either type of Feline Enteric Coronavirus lead to?Feline Infectious Peritonitis (FIP)
  39. 39Why is there evolution of new biotypes?Non proof reading polymerase and cut/paste recombination of coronavirus
  40. 40What are features of FIP?• FIP variants have enhanced replication in macrophages
    •Antibodies to virus enhance macrophage infection by Fc receptor mediated uptake
    •Virus peplomers retained in macrophage golgi therefore are not exposed on the cell surface of infected macrophages.
    •Protection of infected macrophages from ADCC and NK cells
  41. 41What is the cyclical FIP pathology?1. Infection of macrophages,  inflammatory cytokines,  vascular permeability
    2. Immune responses include Helper T-cells antiviral CTL, invasion by neutrophils, perivascular necrosis
    3. Chemotaxis of more monocytes which become virus infected, Antibody enhanced infection via Fc receptors.
    4. Pyro-granulomatous foci containing neutrophils, lymphocytes, macrophages, and deposits of IgG-Virus -C3 complexes
  42. 42What are the clinical signs and gross pathology of FIP?Very variable depending on the organs affected: Malaise sickness due to elevated inflammatory mediators.
    Peritoneum, Liver, kidneys. GI signs may have peritoneal effusion organ enlargement.
    Lungs and pleura: respiratory signs pleural or pericardial effusion.
    CNS skin or ocular lesions also seen
  43. 43What does diagnosis for FIP rely upon?Typical post mortem lesions
  44. 44How can we get immunity to the Coronavirus?1. IgG to S-protein by both active and passive immunisation leads to enhanced monocyte infection and accelerated pathogenesis
    2. T-helper cells may also exacerbate disease by recruiting monocytes to foci of infection.
    3. Cytotoxic T-cells may be important in controlling the initial virus infection removing infected cells.
    4. Temperature attenuated vaccine and nasal inoculation may offer some protection from primary infection.

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Description
Animal Disease 2 (Specific Viruses - DW) Flashcards on Coronavirus, created by Rachael Jones on 04/10/2017.
Created by
Rachael Jones
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