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Fungal/Virology > LEC 17 - Orthomyxviruses > Flashcards

LEC 17 - Orthomyxviruses Flashcards

1
Q

Characteristics: Influenza Type A

A

Broad host range

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2
Q

Characteristics - influenza type B

A

Humans

Seals

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3
Q

Characteristics Influenza Type C

A

Minor disease in humans and pigs

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4
Q

What is the structure of the influenza envelope?

A

Contains spikes with hemagglutinin + neuraminidase

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5
Q

What is the genomic structure of influenza?

A

Segmented

ssRNA (-)

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6
Q

What two proteins are contained in the envelope?

A

M1 + M2

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7
Q

Describe M1

A

Envelope matrix protein

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8
Q

Describe M2

A

Ion channels

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9
Q

What is the flu virus sensitive to?

A

Heat

Acid

Solvents + Detergents

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10
Q

What is bound to the RNA of influenza?

A

RNA polymerase complex

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11
Q

What is the components of the influenza nomenclature?

A

Virus type + Host + Geographic origin + Strain # + Year

(H + N subtype)

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12
Q

What are the pandemic vaccines?

A

Avian influenza

H 5 + 7 + 9

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13
Q

What are the regular vaccines?

A

B

H1 (Russian)

H3 (Avian)

H2 (Hong kong)

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14
Q

What is needed to start the replication process with influenza?

A

HA spikes bind to sialic acid receptors on cell = viral host range + tissue trophisms

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15
Q

How does the influenza virus enter the cell?

A

Receptor-mediated endocytosis

Vesicle acidified

M2 allows H+ ions to transverse membrane

Leads to conformation change in HA allowing membrane fusion

Nucleocapsid release from M1 to host

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16
Q

When is the maturation of the influenza virus complete?

A

Virions bud through host membrane lipid rafts w/ inserted viral spike + matrix protein

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17
Q

What is critical for viron release?

A

viral NA

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18
Q

What is the function of viral NA?

A

Cleaves sialic acid receptors that would otherwise bind + trap virus

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19
Q

What must happen to hemagglutinin inorder to allow for infection?

A

Viral protein must undergo postranslational cleavage

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20
Q

Describe HPAI

A

Highly pathogenic avian influenza have HA forms that are cleaved by a wider array of proteases

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21
Q

What are the common symtpoms seen with HPAI influenzas?

A

Produce severe uniformly fatal disease affecting most organs

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22
Q

What two things occurs within a virus that allow it to be so diverse and change so quickly?

A

Antigenic drift + shift

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23
Q

Describe antigenic drift?

A

Point mutation

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24
Q

Describe antigenic shift

A

Resssortment of genome segments

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25
Q

What happens with antigenic shift that allows for influenza virus to be so dangerous?

A

Bird virus + human virus mist in swine cell and by a hybrid virus that is more pathogenic

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26
Q

Where does the low pathogenicitic virus tend to target?

A

Intestinal epithelium

Few disease symtpoms seen

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27
Q

What is the method of transmission of the influenza type A virus?

A

Fecal-oral

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28
Q

What is the common reservior for the influenza type A virus?

A

Water fowl

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29
Q

What does equine influenza cause?

A

Respiratory disease

30
Q

What is the main equine influenza type?

A

H3N8

31
Q

What is the improtance of the flu vaccine with the equine influenza?

A

Counters antigenic drift

32
Q

What symptoms are seen with equine influenza?

A

Fast onset

Reddening nasal mucosa + discharge

Fever

Paroxysmal cough

33
Q

How long does it take a horse to normally recover from equine influenza?

A

2 to 3 weeks

34
Q

What are the signs there is a secondary bacterial infection with EIV?

A

Purulent nasal exudate

Bronchiopneumonia

35
Q

Where does EIV replicated?

A

Respiratory tract epithelium

36
Q

Effects of EIV on upper respiratory tract

A

Destroys ciliated cells

= inflammation + discharge

37
Q

Effects of EIV on lower respiratory tract

A

Traceitis + Bronchitis + Bronchointersitial pneumonia

with congestion alveolar edema

38
Q

How is EIV diagnosed?

A

Clinical symptoms + rtPCR

Nasal or Oropharyngeal areas

Virus culture in eggs or cells lines w/ trypsin

39
Q

How is EIV controlled?

A

Biosecurity

Antibiotics for secondary infections

Watching horses that travel often

40
Q

When is the EIV infections most prevalent?

A

April to October — race season

41
Q

What was the first recognized swine flu?

A

H1N1

42
Q

What is the generic pathogenesis of swine flu?

A

Progressive necrotic, attack on epithleium in respiratory tract

43
Q

Progression rate of swine flu

A

Short incubation period

Abrupt disease onset

44
Q

Symptoms of swine flu

A

Fever

Huddling

Respiratory distress w. paroxysmal cough

Nasal discharge

45
Q

What are the two major variants of H1N1?

A

US strain - similar to original

European strain - avian reservior derived strain

46
Q

Where is it thought that mixing of the flu viruses most likely occurs?

A

Pigs

47
Q

What is the used to diagnose swine flu?

A

rt-PCR

Rapid test kits

Virus isolation

48
Q

What is typed via PCR?

A

Hemagglutinin

Neuramindase

49
Q

When are outbreaks of swine flu most common?

A

Fall and winter

50
Q

What is the general epidemology of swine flu?

A

Explosive spread

No carrier state known

Big economic impact

51
Q

What is the key to controlling the swine flue?

A

Vaccination

52
Q

What is the goal of the swine flu vaccine?

A

To prevent clinical disease

The vaccine does not prevent infection or shedding

53
Q

Why can’t we control all infections with a vaccine that contains H1,2,3 + N1,2?

A

Vaccinate sows - maternal antibodies decline

Vaccines do not stop infection

Constant shift/drift allow flu virus to stay

Virus get to pigs from other sources

54
Q

What is another name for the avian flu?

A

Fowl plague

55
Q

What is the reservoir for the avian flu?

A

Waterfowl

56
Q

What are the symtpoms of a HPAI strain of AVI?

A

Sudden ddeath without any previous signs

57
Q

What are the symptoms of AVI?

A

Respiratory distress

No eggs

Lacrimation

Diarrhea

Edema of head and neck

Cyanosis of comb + wattle

Tremors

Stargazing

58
Q

When does the LPAI strain of AVI cause problems?

A

In Turkeys

59
Q

What symptoms are seen with LPAI strains of AVI?

A

Respiratory distress

Decrease in egg laying

Anorexia

60
Q

Where does AVI replicate?

A

Intestinal + respiratory tracts

61
Q

What does the most virulent forms of HPAI AVI produce in a chicken?

A

Virema

Multifocal lymphoid/visceral organ necrosis

62
Q

What is the two key roles of HA in the infection process of AVI?

A

Attachment

Fusion of host + viral membranes

63
Q

What is HA a large determinant of?

A

Pathogenicity

64
Q

What changes the virulence of AVI?

A

Changes in the AA sequence of the cleavage site

65
Q

What is the change at the AA sequence in AVI that causes it to be a LPAI?

A

one basic AA at the cleavage site

66
Q

Where does HPAI strains of AVI tend to replicate in the body?

A

Liver

Lungs

Kidneys

Brains

67
Q

How is AVI detected?

A

rt-PCR to detect viral M gene

+’s = tested for H5/H7 genes

+’s = Clocal/tracheal swabs cultured

68
Q

What is a notifiable disease when it comes to AVI?

A

HPAI

or LPAI with H5 or H7

69
Q

Where is waterfowl shedding AVI from?

A

Feces

70
Q

How is AVI controlled?

A

HPAI is watched for closing with rapid mass culling when virus is detected

Fungal/Virology (26 decks)

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