Arteriviruses Flashcards

1
Q

What is the order and family of arteriviruses?

A
  • Order- Nidovirales
  • Family-Arteriviridae
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2
Q

What is the genome organisation of arteriviruses?

A
  • Single-Stranded RNA
  • Positive Sense
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3
Q

What is the arterivirus virion structure?

A
  • Singular nucleocapsid protein
  • 6 different enveloped proteins
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4
Q

What are the two cellular receptors of arteriviruses?

A
  • Heparin-like molecules
  • CD163 and sialoadhesins
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5
Q

What are the virus counterparts of arterivirus?

A

Sialic acid in glycan chains of GP5/M and GP2/3/4 trimers

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6
Q

What cell types do arteriviruses target?

A
  • Macrophages, Monocytes, lymphocytes, endothelial cells
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7
Q

What effects do arterivirus have on the infected cells?

A
  • Necrosis or apoptosis directly
  • Supression of type-I interferons
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8
Q

How do arteriviruses replicate?

A
  • Attach to the host receptors
  • Fusion of virus membrane with the host membrane
  • ssRNA genome is released into the cytoplasm
  • Synthesis and proteolysis of replicase polyproteins
  • assembly of new virions via exocytosis
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9
Q

What are the three most important things surrounding arterivirus pathogenesis?

A
  • Dysregulation of cytokine production via macrophages
  • Immuno-supression
  • Persistent Infection
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10
Q

What does equine Arterivirus cause?

A

Equine Viral Arteritis

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11
Q

What are the Clinical Symptoms of Equine Arterivirus?

A
  • Death- in old young or immunocomprimised horses
  • Abortion rate of between 10-60%
  • Influenza-like symptoms in adult horses (lethargy and stiff movement)
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12
Q

How does EAV transmit horizontally?

A

Aerolisation of respiratory tract secretions

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13
Q

How does EAV transmit venereally?

A
  • Acutely infected mares
  • Acutely and chronically infected stallions
  • Natural service and artificial insemination
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14
Q

How does EAV transmit vertically?

A
  • Transplacental transmission, especially when mares get infected late
  • results in abortion, fatal interstitial pneumonia,
  • Fibronecrotic enteritis
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15
Q

When do the viruses become inactivated?

A
  • 20-30 mins at 56-58ºC
  • 2 to 3 days at 37-38ºC
  • Up to 75 days at 4-8ºC
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16
Q

What happens when EAV infects monocytes/ macrophages?

A

release of pro-inflammatory cytokines and TNF-alpha
dysfunction of the vascular endothelium and systemic pathology, pyrexia, cachexia, lipolysis

17
Q

What effects the severity of the EAV virus?

A
  • Virus Strain
  • Horse Breed
  • Donkey species
18
Q

What are the clinical signs of EAV in stallions

A
  • Decreased Fertility
  • Reduced sperm quality
  • Caused by increased scrotal temp and edema
  • Decreased libido
19
Q

What samples may you take for EAV?

A
  • Nasal secretions
  • Blood
  • Semen
20
Q

How would you detect antigens?

A
  • Virus isolation
  • Nucleic acid detection
  • Immunohistochemistry
21
Q

How would you detect antibodies?

A

Serology
Virus neutralisation
ELISA
fluorescent antibody
Fluorescent microsphere immunoassay

22
Q

How would you manage the venereal transmission?

A
  • Separate pregnant mares from other horses
  • Isolate new arrivals
  • Breed carrier stallions only to well vaccinated or seropositive mares
23
Q

How would you prevent/ control transmission in carrier stallions?

A
  • Physically isolate from uninfected horses
  • Clean and disinfect fomites
  • Testing and identification
  • there is no specific treatment other than surgical castration
24
Q

What is the genus of PRRS?

A

Single stranded positive RNA (arterivirus)

25
Q

How many proteins does the PRRS genome encode?

A

7 proteins

26
Q

What are the two distinct PRRS genotypes?

A
  • European
  • American
27
Q

What are the three PRRS subtypes?

A
  • Attenuated strain
  • Immuno-Supressive (type I)
  • Inflammatory (type II)
28
Q

What are the primary target cells for PRRSV tropism?

A
  • Monocyte/ Macrophage lineage
  • infects different subsets of differentiated macrophages in the lungs, lymphoid tissue and placenta
29
Q

How is PRRSV transmitted?

A

* Horizontal transmission
* From contaminated food
* Vertical transmission
* Through transplacental transmission
* Venereal transmission
* During breeding with semen from PI boars
* lateral transmission
* Through fomites or personnel
* Mechanical vectors.
* Flies and mosquitoes might serve as mechanical vectors

30
Q

What is the pathogenesis of PRRS?

A
  • Infection via aerosols/ fomites
  • Mucousal surfaces or lung macrophages
  • Draining regional lymph nodes
  • Target organs are the lung, thymus, uterus, placenta and testis
31
Q

What are the clinical signs of PRRS in young pigs?

A
  • Dyspnoea, nasal exudate
  • Slow growth
  • Reddening of the skin
  • Loss of appetite and lethargy
32
Q

What are the clinical signs of PRRS in pregnant sows?

A
  • Dyspnoea
  • Lethargy
  • Loss of appetite
  • Abortion, stillborn pigs, mummified foetus, weak pigs
33
Q

What are the clinical symptoms of PRRS?

A
  • Fever
  • Mild respiratory distress
34
Q

What samples would you take to determine PRRS?

A
  • Whole blood EDTA
  • Serum
  • Lung/ Respiratory tract
  • Spleen and tonsils
35
Q

What are the three subtypes of PRRS virus?

A
  • Attenuated
  • Immuno-suppressive
  • Inflammatory