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POM 4 Immunology > 4.10 Anti-Virals > Flashcards

4.10 Anti-Virals Flashcards

1
Q

What are viruses?

A

Obligate intracellular parasites

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2
Q

Which anti-viral has the highest level of specificity?

A

Acyclovir

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3
Q

What condition is acyclovir used to treat?

A

Herpes

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4
Q

Why is acyclovir so specific?

A

It has to be phosphorylated from ACV to AVCMP by thymidine kinase which is only present in herpes virus infected cells

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5
Q

How does acyclovir work as antiviral?

A

As a nucleoside analogue

It is a chain terminator as it lacks a 3’ OH group, thus phosphodiester bonds cannot form, preventing viral replication

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6
Q

What is a nucleoside inhibitor?

A

Molecule which looks like a nucleoside and is therefore incorporated into the genome, but actually inhibits viral replication

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7
Q

What is RNA in the negative sense?

A

A strand of RNA which is complementary to the mRNA

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8
Q

What sense of genetic material can ribosomes translate?

A

Positive sense

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9
Q

What is a virion?

A

A virus particle outside the cell

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10
Q

Why can ribosomes not be targeted in anti-viral medications?

A

Viruses uses human ribosomes to replicate, meaning they would be attacked

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11
Q

What is the central dogma?

A

DNA is converted by transcriptase into RNA which is translated by ribosomes into proteins

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12
Q

Why do viruses have a high mutation rate?

A

They use their own polymerase to replicate which LACK PROOF READING

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13
Q

RNA is shorter than DNA. How do RNA viruses compensate for this?

A

RNA viruses use complex encoding strategies to make more proteins than expected

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14
Q

Why is it useful for DNA viruses to be large?

A

They have room to acquire accessory genes which could make that virus better at modifying host immune response

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15
Q

What is a segmented genome and how does this impact viruses?

A

Allows easy recombination – reassortment

If different strains of same virus enter cell, the DNA can be mixed to give a mutated virus

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16
Q

What is the size range of viruses?

A

1nm to 1 micrometer

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17
Q

What are two examples of neuramidase inhibitors?

A

Tamiflu and relenza

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18
Q

What is remdisivir a nucleoside inhibitor of?

A

Adenosine

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19
Q

How does remdisivir work as a nucleoside inhibitor?

A

Acts as adenosine and causes chain termination 3 nucleosides later due to the twisting of the molecule

20
Q

What is remdisivir used to treat?

A

Hepatitis C

21
Q

What are 2 examples of adamantanes?

A

Rimantadine, amantadine

22
Q

How does amantadine work as an antiviral?

A

Blocks the M2 ion channel so that H+ cannot enter the endosome

Thus the virus is trapped inside the endosome and cannot replicate

23
Q

Why is the use of amantadine not recommended?

A

Most H3N2 viruses are resistant to it

A single point mutation can mean that amantadine cannot bind M2

24
Q

How do neuraminidase inhibitors (e.g. antiviral tamiflu) work?

A

Inhibits the action of neuraminidase, preventing viral release and infection of more host cells

25
Q

How do neuraminidases (e.g. sialidase) work normally?

A

They cleave bonds between haemagluttinin on influenza and sialic acid on host cell membrane, causing viral release

26
Q

What are tamiflu and relenza used to treat?

A

Influenza

27
Q

What is the lipid envelopes of viruses derived from?

A

The host cell membrane

28
Q

What is the cell membrane of a non-enveloped virus made from?

A

Protein capsid

29
Q

In cultured cells, why are some genes in virus’ genome lost?

A

Some genes limit the host cell immune response to give the virus an advantage

In cultured cells, there is no immune response so these genes are not needed

30
Q

What are the stages of viral replication? AITAE

A

Attachment – of attachment proteins to membrane receptors
Insertion – of nuclear capsid with viral genome
Translation – into viral proteins
Assembly – of proteins into viral material
Exocytosis – of virus from host cell

31
Q

What do direct acting antivirals target?

A

Specific viral factors

32
Q

What are biologicals?

A

Antibodies which are derived from recovered individuals or synthesized in the lab from immobilized B cells

Given directly into the blood

33
Q

What anti-virals are used to treat hepatitis C?

A

Direct Acting Antivirals

34
Q

Between Relenza and Tamiflu, which is more effective and why?

A

Tamiflu – the chemistry of relenza means the virus can more readily acquire resistance so less effective

35
Q

Acyclovir and ribavirin are both antiviral agents that act as nucleoside analogues. Why is acyclovir effective against herpes simplex virus but not influenza?

A

Acyclovir is only converted to its active form inside a cell infected by herpes virus that encodes thymidine kinase, and influenza virus does not encode such an enzyme

36
Q

Tamiflu (oseltamivir) is an antiviral drug that can be used to treat influenza virus infection. The mechanism of action is:

A

To inhibit the neuraminidase enzyme that removes sialic acid from the infected cells surface

This prevents onwards spread of new virus particles

37
Q

Why might a patient with chronic hepatitis C virus treated with an HCV protease inhibitor drug show a loss of a positive viral response over time?

A

The virus has acquired resistance to the drug

The patient has acquired a second infection with a different strain of HCV

The patient has stopped taking the drug

38
Q

Two people in the world are believed to have been ‘cured’ of HIV. How has this been achieved?

A

Bone marrow transplantation from naturally HIV resistant people

Mutation in CCR5 coreceptor gene meant that CCR5 was not expressed and HIV could not enter new cells

39
Q

What is PrEP for HIV?

A

Pre-exposure prophylaxis

Taking HIV antivirals daily to prevent possible HIV infection

40
Q

BHIVA guidelines require that people have an HIV test before going on PrEP. Why is this so important?

A

If the patient is HIV infected, treatment should be given with three drugs at once as two drugs means that resistance is selected more easily

41
Q

Single use of antiviral agents increase the risk of resistance. How is this overcome?

A

Combination therapy

Antiviral resistance becomes less likely as the virus would have to have a mutation against every drug in the combination

42
Q

Describe the HIV replication cycle

A

HIV binds CD4 receptors and fuses with host membrane

Viral RNA is converted to DNA with reverse transcriptase, and viral DNA is incorporated into the host nuclear DNA with integrase

The host cell produces viral RNA and proteins, producing immature HIV

Immature HIV is matured by proteases and cell budding occurs

43
Q

What are four stages of HIV replication which are targeted in combination therapy? VIPR

A
  1. Viral entry inhibition
  2. Integration of viral genome inhibition
  3. Protease inhibition
  4. Reverse transcriptase inhibitors
44
Q

Describe the influenza replication cycle

A

Influenza attaches via glycoproteins, whole virus endocytosed

Virion fuses to endosome lipids, releasing 8 negative sense RNA segments

Segments enter nucleus and RNA-dependent RNA polymerase produces mRNA and replicates it into new genomes

45
Q

What do viruses form in cell monolayers?

A

Plaque – as virus kills cells in the middle layer

46
Q

How can you find out how many virus particles are in a particular preparation of virus?

A

Plaque assay method

Make dilutions and put them into monolayers of cells
After 2/3 days, count the number of plaques formed

47
Q

What is the syncytia assay method?

A

Viruses with surface proteins that fuse at neutral pH also fuse cells together

Thus helps find out how many virus particles are in a sample

POM 4 Immunology (14 decks)

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