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Chemotherapy intercalation > Lecture 4 Antivirals against influenza virus > Flashcards

Lecture 4 Antivirals against influenza virus Flashcards

1
Q

Name the 3 components that classify the influenza virus

A

RNA
-ve stranded
segmented
Orthomyxoviridae

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2
Q

How many flavours of influenza are there?

A

3 - influenzavirus A-C

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3
Q

Which is the most common influenza in humans?

A

Influenzavirus A

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4
Q

What flavour does the Australian flu come under?

A

Influenzavirus B

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5
Q

What is the lipid bilayer of the virus made from?

A

plasma membrane of the previously infected cell

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6
Q

Which variant M glycoproteins does influenzas A-C encode for?

A

Influenza A = AM2 protein
Influenza B = BM2 protein
Influenza C = CM2 protein

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7
Q

What is the difference between low pathogenicity seasonal flu and high pathogenicity influenza strains?

A

low pathogenicity seasonal flu - mild and common type of flu

high pathogenicity influenza strains - rare and severe, can cause deaths

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8
Q

name 2 examples of high pathogenicity influenza strains

A 
Avian influenza (H5N1)
Spanish influenza (H1N1)
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9
Q

How is influenza virus transmitted?

A

Droplet inhalation - sneeze, cough, breathing = small droplets enter the resp tract
Direct contact - sneezing, coughing and breathing = droplets on surfaces called fomites, contact between surfaces and mucosal cells, mediated by contaminated hands/fingers

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10
Q

What are the symptoms of influenza virus?

A 
Upper resp tract cells affected
Symptoms have rapid onset (24h after contact), peak at day 3, persist for 8/9 days 
Tiredness
Sore throat
Runny nose
Headache
Fever
Cough
Muscle aches
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11
Q

What are the 3 membrane proteins on the influenza virus?

A

M2 protein - specific to flavour of influenza
Neuraminidase (NA)
Haemoglutanin (HA)

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12
Q

What shape is the influenza virus?

A

Rod shaped

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13
Q

What is the the matrix protein?

A

The sheeth beneath the membrane [see slide for image]

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14
Q

Describe the influenza virus life cycle

A

[see slide for image]
Virus binds sialic acid receptor via HA, becomes internalised → Low pH membrane fusion via HA → segments released into cytoplasm → segments imported into nucleus → RNA synthesis → RNA/RNP export → virus assembly at plasma membrane → release of viron

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15
Q

Explain step 1 virus attachment of influenza virus

A

HA recognises sailic acid on the surface of cilliated epithelial cells
HA binds to sialic acid via galactose protein

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16
Q

Explain step 2/3 virus entry of influenza virus

A

Virus is inside the endosome
Escapes when virus envelope (matrix layer) fuses with endosome membrane - mediated by HA protein changing confirmation due to low pH
8 RNA protein segments still cannot get out - release is mediated by M2 protein
M2 (ion channel) forms a pore = influx of H+ ions
Matrix protein layer breaks down and segments are released [see slide for image]

17
Q

Explain step 8 virus release of influenza virus

A

Virus now needs to infect new cells via HA and sialic acid receptor
Need to make sure that HA on released viruses does not bind to receptor on the old cell as this would mean the virus does not spread
Controlled by the NA protein on the virus cell membrane
NA cleaves sialic acid from previously infected cell (essential role)
[see slide for image]

18
Q

Why is a new vaccine needed for influenza every year

A

Influenza virus is rapidly mutating

Every year there is a different strain of the virus

19
Q

Why is a stockpile of antiviral medication for influenza needed despite there being vaccines?

A

Vaccine is slow to make - 9 months
If a pandemic occurred then it would not be quick enough to make a vaccine
Antiviral would work against many strains

20
Q

Name the 2 ways that influenza virus mutation occurs

A

Antigenic drift

Antigenic shift

21
Q

What is antigenic drift?

A

When enzyme genes are copied, mistakes are made
Incorporation of single nucleotide changes into genome
Leads to new virus formation

22
Q

What is antigenic shift?

A

Occurs when 2 different cells infect the same virus

Allows genome segments to mix when virus assembly occurs = different proteins encoded

23
Q

What are the 2 current targets for influenza antivirals?

A

M2 protein

Neuraminidase cleaving protein

24
Q

What are 2 names of drugs in the adamantanes class?

A

Amantadine

Rimantadine

25
Q

Which influenza families does adamantanes target?

A

Low conc = specific for influenza A

High concentration = some general antiviral activity

26
Q

What are the pros of adamantanes?

A

Cheap
Effective
Given as oral or aerosol

27
Q

What are the cons of adamantanes?

A

Must be administered early before the infection e.g. before day 2
Most influenza viruses now resistant due to drift mechanism - mutation in M2 channel
Therefore no longer approved by FDA to treat influenza

28
Q

What is the mechanism of action of adamantanes?

A 
Prevent M2 ion channel activity
Blocks either of the 2 binding sites:
Within the central pore
Within a membrane facing pocket - one of each of the monomers of the tetramere
= prevention of ion channel activity 
Matrix layer remains intact
Virus cannot exit the endosome
29
Q

What is the mechanism of action of Relenza (zanamir) and oseltamivir (tamiflu)?

A

Mimic sialic acid - blocks neurominidase active site so it can no longer bind and digest sialic acid
Produced based on the contact sites between the sailic acid in the neurominidase active state
Produced a molecule that bound with a higher affinity by adding a guanidino group to Glu119 at C4 = now interacts with Glu 225 and Asp 151

30
Q

Do neurominidase inhibitors work?

A

Moderately
Must be given very early on in infection i.e. 48 hours
Symptoms are reduced by 1 day = little impact
Is it worth it? well it may be enough to slow pandemic spread
Stockpiles of Relenza (zanamir) and oseltamivir (tamiflu) exist

31
Q

Are neurominidase inhibitors at risk of resistance?

A

Should not encounter resistance problems as similar structure to sailic acid
However 1% of seasonal strains have shown resistance

Chemotherapy intercalation (14 decks)

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