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Zoonoses > West Nile > Flashcards

West Nile Flashcards

1
Q

Is West nile virus a positive or negative RNA virus?

A

Positive

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2
Q

What genus is west nile?

A

flavivirus

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3
Q

What species is west nile virus?

A

west nile virus

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4
Q

How many lineages does it have?

A

2

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5
Q

How many clades does lineage 1 have?

A

3: 1a, 1b, and 1c

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6
Q

How many proteins does it encode for total? how many are structural and how many are non-structural?

A

10: total
3: structural
7: NS

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7
Q

What is protein E?

A

a glyco protein: structural

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8
Q

what is the function of glycoprotein E?

A

receptor binding, viral attachment, and entry into the cell through membrane fusion

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9
Q

What is protein M

A

membrane protein matrix protein: structural

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10
Q

Where does the virus get the membrane?

A

host

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11
Q

What molecules does the flavivirus mebrane contain?

A

cholesterol and phosphatidylserine,

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12
Q

What are the C proteins, and what do they do?

A

which are 105 amino-acid residues long, to form the nucleocapsid.
The capsid proteins are one of the first proteins created in an infected cell
Structural protein

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13
Q

What are the three structural proteins ?

A

E, M and C

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14
Q

The capsid has been found to prevent apoptosis by affecting what pathway?

A

Akt pathway

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15
Q

What are the non structural protien s and what do they do?

A

NS1 NS1 is a cofactor for viral replication, specifically for regulation of the replication complex.[17]
NS2A NS2A has a variety of functions: it is involved in viral replication, virion assembly, and inducing host cell death.[18]
NS2B A cofactor for NS3 and together forms the NS2B-NS3 protease complex.[14] Contains transmembrane domains which bind the protease to intracellular membranes.
NS3 A serine protease that is responsible for cleaving the polyprotein to produce mature proteins; it also acts as a helicase.[12]
NS4A NS4A is a cofactor for viral replication, specifically regulates the activity of the NS3 helicase.[19]
NS4B Inhibits interferon signaling.[20]
NS5 The largest and most conserved protein of WNV, NS5 acts as a methyltransferase and a RNA polymerase, though it lacks proofreading properties.

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16
Q

How many copies of the E protein are there?

A

180

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17
Q

How many sets does the 180 copies of the E protein form?

A

60

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18
Q

What shape does the 60 copies of 3 E proteins create?

A

icosahedron

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19
Q

How many of the E proteins within a set does a human receptor recognise?

A

2 of the 3

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20
Q

During the budding process the amino particle that is on the end of the ______ protein is released by a proteolytic cleavage process which produces a mature _____ protein, necessary for an infectious West Nile particle. The genomic progeny is assembled into an enveloped, icosahedral nucleocapsid.

A

pre-M

M

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21
Q

What is the secondary bninding factor that the E proteins bind s in the host

A

glycosaminoglycans

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22
Q

What is the primary receptor in the host?

A

DC-SIGN, DC-SIGN-R, and the integrin αvβ3

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23
Q

Where is West Nile found?

A

Middle east
Africa
SW Asia

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24
Q

What are the statistics of the 1999 New york infections?

A 
62 cases and 7 deaths 
lineage 1aNY99
2.6% of the population infected
20% of those mild symptoms
0.7% meningoencephalitis
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25
Q

What animals were infected in the 1999 new york outbreak initially?

A

zoo birds, corvids, and horses

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26
Q

since being introduced to america what percentage has the crown population been decreased by?

A

45%

27
Q

How many cases were reported to the CDC in the USA between 1999-2021?

A

54649

28
Q

How many cases were reported to the CDC in 2009, but how many were there estimated to be?

A

720 cases reported to the CDC, but number of infected estimated at 54,000. Due to under reporting.

29
Q

How many deaths took place between 1999-2021

A

2,376 deaths in the USA

30
Q

As a result of _________ cases dropped until 2003. but there was a peak in _____ because the safety precaustions of people began to fall.

A

herd immunity

2012

31
Q

What time of the year are their peaks in the USA?

A

August and September

32
Q

What countries had an outbreak in 1998?

A
  • Serbia
  • Italy
  • Greece
  • Hungary
  • Romania
33
Q

How many cases were there in Europe in 2020? and how many deaths?

A

66 cases

6 deaths

34
Q

Explain all the steps for the virus entering the cells

A

• Attaching receptor:
o Binding factors:
 Glycosaminoglycans
 Primary receptors:
• DC-SIGN
• DC-SIGN-R
• integrin αvβ3
o antibody recognizes only two of the E proteins in each set of three
o This kind of asymmetry, where you have two proteins binding and one not binding, has not been seen before.”
o The researchers theorize that, although chemically identical, these E proteins exist in different environments relative to each other and might, therefore, have slightly different structures
• Catherin-mediated endocytosis:
o Enters within an endosome: The acidity of the endosome catalyzes the fusion of the endosomal and viral membranes releasing the viral genome into the cytoplasm
• Translation: Translation of the positive-sense single-stranded RNA occurs at the endoplasmic reticulum
o RNA is translated into a polyprotein which is then cleaved by both host and viral proteases NS2B-NS3 to produce mature proteins
• Replication:
o In order to replicate its genome, NS5, a RNA polymerase, forms a replication complex with other nonstructural proteins to produce an intermediary negative-sense single-stranded RNA
o The negative-sense strand serves as a template for synthesis of the final positive-sense RNA
• Virion building:
o Once the positive-sense RNA has been synthesized, the capsid protein, C, encloses the RNA strands into immature virions.
o The rest of the virus is assembled along the endoplasmic reticulum and through the Golgi apparatus, and results in non-infectious immature virions.
o mature viruses are then secreted out of the cell.
• Budding:
o During the budding process the amino particle that is on the end of the pre-M protein is released by a proteolytic cleavage process which produces a mature M protein, necessary for an infectious West Nile particle. The genomic progeny is assembled into an enveloped, icosahedral nucleocapsid.

35
Q

What vectors pass west nile virus?

A

mosquitto

ticks

36
Q

How can west nile be spread? Humans

A

labratory, pregnancy, breast feeding, blood transfussion, organ transplant.

37
Q

How can birds spread west nile? how do they cause outbreaks

A

direct contact, shown to cuase outbreaks along migratory paths

38
Q

How many species of mosquito are there in America that can spread west nile?

A

59 species

39
Q

What is the main genus of mosquitto that spreads west nile?

A

culex genus

40
Q

What is the incubation period of west nile virus?

A

2-14 days

41
Q

what percentage of cases are aymptomatic?

A

80%

42
Q

What are the two forms of the disease?

A
  • West Nile Fever

- West Nile Neuroinvasive Disease

43
Q

Out of the people who get West Nile, how many get West Nile fever? ?/?

A

1/5

44
Q

What are the common symptoms with west nile fever, and what is the one rare symptom?

A
  • Most common form
  • Flu-like symptoms
  • Resolves in 2-6 days
  • Persistent fatigue can occur
    Some patients: Erythematous (red) rash – arms, legs, torso.
45
Q

What percentage of people get the West Nile neuroinvasive disease? ?/?

A

1 in 150

46
Q

What are the symptoms of west nile neuroinvasive disease?

A 
-	Encephalitis
o	Disorientation
o	Ataxia
o	Changes in consciousness
o	Parkinsons-like
	Rigidity in muscles
	Slow movements
-	Meningitis
o	Stiff neck
o	Photophobia
o	fever
-	Acute flaccid paralysis
o	Can affect all muscles
Persistent neurological dysfunction can occur
47
Q

How many species of bird hve been shown to get infected? what are their symptoms?

A

300 species

leg paralysis and tremours

48
Q

What happened to the birds in Utah in 2013?

A

20,000 lake water birds died

29 bald eagles died

49
Q

What symptoms do cats and dogs getr?

A

often asymptomatic: or fever depression, muscle spasms, paralysis and mycarditis

50
Q

What physical symptoms do horses get, what behavioural changes happen in horses?

A

Physical: anorexia, ataxia, weakness, difficulty swollowing, facial oedema, urinary disfuntion

Behavioural: teeth grinding, circling, Tremours and convulsion

51
Q

What ruminants does it affect: what are there symptoms, and how long after infection do they die?

A

Neurological symptoms

Sheep, alpacas, reindeer, and white tailed deer

Death 1-2 days

52
Q

What animals can catch it?

A
  • Bats
  • Horses, Goats, sheep, cattle, Llama, alpaca, deer
  • Rabbit, chipmunk, skunk, squirrels
  • Wolf, black bear
  • Alligator, crocodile
    cat and dogs
53
Q

How can West Nile virus be diagnosed in humans and horses?

A 
Diagnosis – Humans
-	Serology (most common) for IgM
	IgM can persist for a year… so not definitive
o	Serum or Cerebral-spinal fluid
o	IgM capture ELISA
	But Cross reactions with dengue, yellow fever etc. 
o	Plaque neutralisation test 
-	Detection of virus, antigen, or nucleic acids
o	RT-PCR (particularly blood donations)
o	Immunohistochemistry
Horse – Diagnosis
-	Live horses:
o	Serology 
	-4 fold increase in WNV-abs
-	Necropsy 
o	Brain & spinal cord
	RT-PCR
	 Immunohistochemistry
54
Q

What treatment is there for humans?

A 
No specific treatment – just supportive care (fluids etc.)
Clinical trials:
-	Interferon
-	Antisense nucleotides
-	Intravenous immunoglobulin
-	Antiviral drugs
55
Q

What treatment is there for animals?

A

Treatment – animals

  • Several commercial vaccines available for horses
  • Usually 2 doses: 3 - 6 weeks apart
  • Annual revaccination
  • Vaccines sometimes used off-label to protect birds
56
Q

What mosquitto managment is there?

A
  • Surveillance
  • Source reduction
  • Personal protection
  • Biological control
  • Larvicide
  • Adulticide
57
Q

How can surveillence reduce transmission?

A
  • Dead bird testing
  • Sentinel chicken flocks
  • Mosquito collection
    o Test for pathogens
    o Account for species??
  • Larval & adult mosquitoes
    o Map habitats
    o Record keeping
58
Q

What water source reduction can you do?

A 
-	Elimination of larval habitats:
o	Tyres
o	dis-used swimming pools
o	bird baths
o	rain-filled containers
o	guttering
o	water troughs
-	Making habitats unsuitable for larval development
-	Public education
-	Marsh water management
o	Facilitate drainage - allows fish access 
o	Gated – minimally flood during summer
59
Q

What PPE can be used?

A
  • Limit time outdoors at peak biting times
  • Cover limbs - Long trousers & sleeves
  • Use mosquito repellent
    o 50% DEET
    o Do not use DEET on animals
  • Keep window screens intact
  • Replace outdoor light bulbs with yellow bulbs
  • Empty water from all outdoor containers
60
Q

What biological controls are there?

A

Use of natural & introduced predator species to eat larvae and/or pupae
- Mosquito fish
o Gambusia affinis, G. holbrooki
o Fundulus spp., Rivulus spp., killifish
- Other agents used but limited availability
o Fungus, protozoa, nematodes
o Copepods

61
Q

How can larvacides be used?

A
  • Used when source reduction & biological control not feasible
  • More effective & target-specific
  • Less controversial than adulticides
  • Applied to smaller geographic areas
    o Larvae concentrated in specific locations
62
Q

How are adulticides used?

A
  • Used when other control measures are unsuccessful
  • Low efficiency
  • Timing of application & correct type of control increases efficacy
    o Ultra-Low Volume foggers
    o 1 ounce per acre
    o Small droplets contact and kill adults
63
Q

What precautions to take in a lab?

A
  • Mosquito avoidance precautions
    o Insect spray, long sleeves, etc.
  • Wear gloves or double plastic bags to collect dead birds
  • Wash hands after handling specimens in field
  • Manipulate carcasses for necropsy in biosafety cabinet when possible

Zoonoses (23 decks)

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