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Flaviviridae

Rachael Jones Animal Disease 2 Englisch 55 Karten

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  1. 1Give to genus is the Flaviviridae family.1. Flavivirus
    2. Pestivirus
  2. 2Give diseases in Flavivirus.Worldwide diseases of humans and animals
    Wesselbronvirus, Yellow fever, Dengue,
    Many types of tick borne encephalitis
  3. 3What are key structural points about the virus structure?+ve sense RNA genome; spherical nucleocapsid with icosahedral symmetry; enveloped by tight lipid with indistinct peplomers
  4. 4What are features of the Flavivirus in sheep and the effects that it has?Louping ill virus of sheep – good example of arbovirus; tick-borne (Ixodes ricinus); also of economic importance in grouse; trans-stadial transmission; peaks in spring/autumn. Causes CNS signs. Controlled by vaccination.
  5. 5Give 3 pestiviruses.- Bovine Virus Diarrhoea
    - Classical swine fever
    - border disease
  6. 6What are features of Bovine virus Diarrhoea?At a herd level causes lower fertility (embryonic death, abortions), with sporadic cases of mucosal disease (which has 100% mortality). Immunosuppression causes exacerbation of other infections. Infection of pregnant cows from day 90-120 of pregnancy can lead to persistent infection in calf, which can mutate to a cytopathic strain which causes mucosal disease
  7. 7What are features of Border disease in sheep?Mid-gestation infection leads to persistently infected lambs and “hairy shakers”
  8. 8What pestivirus is notifiable in the UK?Classical swine fever
  9. 9What is the replication of the Flavivirus?- Infection is by endocytosis following attachment of the peplomers to cell
    surface ligands.
    - There is a single (polycistronic) open reading frame; this is translated
    into a large polyprotein which is then cleaved to form the different virus proteins.
    - The virus assembles and buds from the endoplasmic reticulum, from where it is exocytosed without the need for cell lysis.
    - Also these viruses do not cause rapid shutdown of host cell protein synthesis and are often not cytopathic in cell culture
  10. 10What are the receptors of the Louping III virus?Sialic acid on glycolipids /gangliosides, found on a wide variety of cells including nerves. - non species specific
  11. 11What is the pathogenesis for Flavivirus?- Infection from bite of carrier tick.
    •Replication at site of entry in leucocytes/macrophages DCs.
    •Spread to local lymph node where more cells are infected.
    •1oFeverassociated with interferon response and vireamiaspread to other lymphoid organs.
    •Further replication and continuing prolonged viraemia(not a true persistent infection).
    •Opportunity for infection of ticks (extededduration of feeding)
  12. 12What occurs in some animals if they don't deal with the virus infection?Animals prolonged vireamia allows spread to CNS and onset of neurological signs.
    2o fever(ataxia, tremors, louping, paralysis, death)
  13. 13How does prolonged vireamia occur?1. Blood: viraemia and infected lymphoid cells
    2. Infection of endothelium
    3. Infection of neurones, microglia astrocytes: Death of nerve cells
  14. 14What is perivascular suffing?Infiltration of lmphocytes, monocytes
    and dendriticcells across inflamed endothelium.
  15. 15What tick carries Louping ill?Ixodes ricinus
  16. 16Where is there a reservoir of Louping ill?Host: may birds and small mammals, Red grouse, Voles, Hares etc
    with sporadic epidemics in livestock and humans
    Can infect sheep, goats, cattle, deer, horses
  17. 17How does the host acquire the Louping ill virus?Has to feed on an infected host
    - no transovarial transmission
    - Once the tick is infected it will be infected through all the stages of life
  18. 18What do different stages of ticks life prefer to feed on?Larval = small mammals and birds
    Adults = larger mammals, sheep, cattle, horses, humans and deer
  19. 19When will the disease in sheep occur most commonly?Spring or autumn associated with the peak levels of tick activity
  20. 20What happens when a sheep has been infected by a tick with louping ill?- Virus replicates in leucocytes and monocytes at the bite site and within the draining lymph node.
    - Followed by a viraemia and infection of other lymphoid organs.
    - Prolonged viraemia
    - Also replicate in endothelial cells - cross the blood brain barrier and infects cells in the CNS.
  21. 21What are the clinical signs of Louping ill?- Following CNS invasion
    - Non-suppurative encephalomyelitis.
    - ever, tremors, hyper-excitability, altered gait (louping), progressing to coma and death.
    - Not all develop neurological problems
  22. 22What can lead to increased mortality rate with Louping ill?Immunosuppression caused by co-infection with Ehrlichia phagocytophila will lead to increased mortality rates
  23. 23How can you become immune to Louping ill?- Neutralising antibodies are protective for CNS infection
    - Vaccine of inactivated cell culture given to breeding ewes
    - Lambs protected by maternal antibodies - most disease seen in sheep from 6 months-2 years
  24. 24How can you diagnose Louping ill?Confirmed by virus isolation, the presence of IgM antibodies indicating recent infection, or immunohistology of brain tissue.
  25. 25What is the most common Pestivirus for infecting cattle worldwide?Bovine Viral Diarrhoea/ mucosal disease
  26. 26Does BVD actually cause diarrhoea as one of the main signs?No - may occur but not main clinical presentation
  27. 27What are the main signs of BVD and the economic problems faced?Herd are lowered fertility due to abortions, embryonic death etc. with sporadic cases of mucosal disease once the virus is established
  28. 28What are the 2 types of the BVD virus?Biotype 1
    Biotype 2
  29. 29What are the differences between the 2 types of BVD virus?Produce similar diseases but the type 2 virus is also associated with a thrombocytopaenic, haemorrhagic syndrome
  30. 30How does BVD cause disease?Starts with non-cytopathic strain; the non-cytopathic strains can then mutate into cytopathic strains, during the course of persistent infection
  31. 31How does the BVD replicate?1)Adhesion
    2)Endocytosis(clathrin)
    3)Low pH/ fusionnucleocapsidrelease
    4)Synthesis of polyprotein
    5)Protein cleavage (host and virus proteases)
    6)Genome replication via RNAintermediate
    7)Virus assembly
    8)Budding from ER
    9)Maturation and exocytosis
  32. 32What are the key features of the replication of BVD?- Receptor CD46 (complement control protein).
    - Virus Polyproteincleaved by Host protease and virus NSP2/3 protease.
    - Does not shut down host protein synthesis.
    - Blocks Type 1 interferon production.
    - Non lyticinfection with exocytosis.
    - Most strains non cytopathic.
    - Persistent infection of cell lines in vitro, cattle in vivo.
    - Disease associated with conversion to cytopathicstrain with NSP3 mutations.
  33. 33How do the non-cytopathetic strains cause immunosuppression in BVD?- Npro (N-terminal protease) acts to inhibit transcription of interferon within the cell.
    - A capsid glycoprotein (Erns) has an intrinsic RNase activity and is secreted from infected cells, enabling it to degrade both ss- and dsRNA and preventing RNA (released from infected cells by this or any other virus!) from activating the innate immune response.
    - Infection induces a lymphopenia
  34. 34What do the cytopathic strains of BVD cause?Mucosal disease
  35. 35How do the cytopathic strains arise?Due to genetic recombination and may contain incorporated host cell RNA or duplicated virus sequences
  36. 36What do the cytopathic strains do?Induce pro-inflammatory host interferon responses and frequently have mutations in the non-structural protease NSP3.
  37. 37How is the BVD disease spread?- Oro-nasal route with a non-cytopathic strain
    - Replicates within the nasal epithelium (probably in mucosal lymphoid cells).
    -Followed by a viraemia, with virus found in both T and B lymphocytes the numbers of which decrease (lymphopaenia).
    - Despite the immunosuppression caused by infection, most animals will mount an effective (although often delayed) immune response and recover from infection uneventfully
  38. 38Give reasons why the disease will vary even with the same strain?The age of the animals at infection and the immune status of the herd
  39. 39When can outbreaks of BVDV occur?Following mixing of calves that have been bought at markets and transported to fattening unit or by introduction of carriers into uninfected herds as well as by aerosol transmission form neighbouring premises
  40. 40What occurs if the disease is milk due to non-cytopathic virus?- High morbidity, few clinical signs, transient fever and recover, antibody response to virus
  41. 41What occurs in moderate/severe outbreaks of BVD?- fever depression, diarrhoea, erosions in mouth some deaths.
    - + immuno-suppression may exacerbate respiratory disease.
    Recovered animals seroconvert to BPV
  42. 42What occurs in infecting of pregnant cow by the non cytopathic strain in the 1st 30 days?- Trans-placental infection of foetus
    - Early embryonic death
    - Cow mounts immune response and clears the virus
  43. 43What occurs in infecting of pregnant cow by the non cytopathic strain in days 30-90?- Trans-placental infection of foetus
    - Embryonic/ foetal death
    - Cow mounts immune response and clears the virus
  44. 44What occurs in infecting of pregnant cow by the non cytopathic strain in days >125?- Cow and calf mounts immune response and clears the virus
    : Some Foetal defects may occur, retinal dysplasia , cerebellar hypoplasia, cerebral cavitation low birth weight, neonatal death.
  45. 45What occurs in infecting of pregnant cow by the non cytopathic strain in days 90-120?Infection during a critical period of calves immune system development
    - Cow mounts immune response and clears the virus
    - Calf survives, but is immuno-tolerant to virus
    - Lifelong persistent infection with no antibodies or immune response
  46. 46What occurs in endemic herds?- High levels of immunity (80% seropositive) virus infection of susceptible adults is rare
    - Newborn calves are protected by maternal antibody
    - Heifers are most likely to become infected when they join the main herd
    (i.e. during second pregnancy)
    - Persistent infection of cows at around 1% of animals
  47. 47When might mucosal disease develop?Persistently infected (tolerant) with non cytopathic strain
  48. 48What is present in samples taken from persistently infected animals?Virus isolated from these cases contain both the non-cytopathic virus of the original infection and new cytopathic variants which have arisen by recombination or mutation that occur during the continuous replication cycles of the virus in persistent infection.
  49. 49Why might persistently infected animals get mucosal disease?- Associated with the appearance of cytopathic variants of the virus in the blood of infected animals
    - These arise from virus mutants of the original strain. (deletions, duplications rearrangements re-combinations
    or insertion of cellular sequences)
    - All lead to production of an 80kd. NS3 that mediates the cytopathic effect.
    - Virus acquires a tropism for the mucosal immune system e.g. peyers patch, lamina propria and MLN
  50. 50Give features of the onset and clinical signs seen.Onset may be acute or gradual, pyrexia, anorexia, profuse watery diarrhoea, nasal discharge erosive stomatitis, dehydration emaciation and death
  51. 51What is seen on pathology?- Erosions in mouth, oesophagus, forestomachs
    - Inflammation, hyperemia, intestines
    - Necrosis of peyer's patches and lymphoid tissues
  52. 52How can you diagnose BVD?- Tissue culture (plus Immunofluoresence, non cytopathic).
    - Detection of viral RNA by RTPCR. (ear punch test)
    - Serology by ELISA
    (remember no antibody in tolerant carriers)
    - milk antibody for herd test.
    - Antigen capture ELISA for persistent infection.
  53. 53What is the control programme for BVD?1.Testing and removal of persistently infected animalsVirus capture assay +ve/antibody –ve
    2. Vaccination of remaining animals 1st dose inactivated vaccine (no response to NSP3) 2nd booster dose (live attenuated vaccine)
    3.Continue to monitor and remove of virus +veanimals
    4.Vaccination of replacements @ 6 months
    5.Maintain bio-security
  54. 54What are the control drawbacks?- Testing and removal to generate BVD free herd
    - Risk of heard breakdown
    - Vaccine not all totally effective,
    may not protect from all strains of virus
    and are not certain to prevent foetal infection.
    - Some evidence that attenuated vaccines may contribute to disease onset in tolerant animals (BVDV can be spread by dirty needles)
  55. 55—

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Animal Disease 2 (Specific Viruses - DW) Karteikarten am Flaviviridae, erstellt von Rachael Jones am 03/11/2017.
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