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PoM > Immuno - Anti Virals > Flashcards

Immuno - Anti Virals Flashcards

1
Q

How small is the viral genome?

A

1000 nucelotide

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2
Q

How do we observe viruses?

A

Electron microscope

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3
Q

What are Koch’s postulate steps?

A

Isolate virus from diseased individuals and infect healthy individuals with virus to see if it was disease causing or not

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4
Q

What are viruses?

A

Obligate intracellular parasites

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5
Q

What do viruses need to survive and proliferate?

A

Machinery of their host cells

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6
Q

What consists of the viral genome?

A

Either DNA or RNA which can either be single or double stranded

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7
Q

What are the forms of single stranded RNA?

A

Positive or negative. Positive RNA is similar to mRNA therefore can immediately be translated however negative RNA must be transcribed to mRNA and then translated

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8
Q

What happens when a viral genome enters a cell?

A

Genome is replicated partly by viral enzymes but it also relies on host cell machinery. This leads to viral component synthesis and the combination of the new genome with new proteins allows the new virus to be formed and leave the cell.

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9
Q

What are virions?

A

These are complete virus particles

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10
Q

How big are virions?

A

Range from about 10-20 nm

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11
Q

What is a rotavirus?

A

Small spiked virus

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12
Q

What is a rhabdovirus?

A

Bullet shaped/rectangular virus

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13
Q

Describe virus morphology

A

Some are highly symmetrical
Some are non-enveloped
Some are enveloped

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14
Q

How are some viruses enveloped?

A

As they leave their host cell, they derive an envelope from the lipid bilayer, they are then often pleomorphic with an undistinguished shape.

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15
Q

How do we name viruses?

A

Who discovered the virus, the place it was discovered, where it infects the body, its morphology etc..

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16
Q

What is the central dogma surrounding virus replication?

A

DNA —> RNA —> Protein

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17
Q

Why do some viruses not adhere to the central dogma?

A

Some viruses contain RNA as their genome therefore never involve DNA

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18
Q

What do some viruses with RNA genome do?

A

Some viruses convert RNA back to DNA via reverse transcriptase which they integrate into the cell genome and use that for transcription and translation of their proteins.

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19
Q

What do viruses with negative sense RNA do?

A

They carry a complementary strand of their mRNA, so it is copied into a positive copy which is essentially the mRNA (same as the viral genome if it was DNA), which is then translated to the viral proteins

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20
Q

Why are viruses more likely to mutate?

A

RNA and retroviruses use their own polymerases without proof reading mechanisms

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21
Q

Why is the RNA genome typically smaller than a DNA genome?

A

RNA is typically less stable than DNA there is smaller

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22
Q

How do RNA viruses compensate for a small genome?

A

Use various mechanisms to compensate for their small genome. For example they will have overlapping reading frames so that multiple sections of the mRNA are translated to multiple proteins.

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23
Q

What are accessory genes?

A

Non essential genes that can modify the host cell immune response

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24
Q

What are segmented genomes?

A

Physically discrete pieces of nucleic acid encode for distinct proteins

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25
Q

What does segmented genomes allow for?

A

Easy form of evolution - recombination

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26
Q

What is reassortment?

A

Where different genes from different species of virus can co-infect the same cell and mix themselves up e.g. with influenza

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27
Q

How does a virus typically infect a cell?

A

Binds to virus receptors on the host cell and then uses these to inject viral DNA into cell, this then takes advantage of host cell machinery to replicate and to form viral proteins. Replicated DNA/RNA then recombines with the newly formed viral proteins and leave the cell, leaving there out cell to die via apoptosis.

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28
Q

Why do we often have an exponential rate of viral expansion?

A

For every 1 virus that enters the cell we will typically get a lot more viruses e.g. 100 leaving the cell.

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29
Q

What is the cytopathic effect?

A

The result of the virus lysing the cell due to changes of the cell structure after viral infection.

30
Q

What can cause the cytopathic effect?

A

Shut down of host protein synthesis or the accumulation of viral proteins.

31
Q

How can we use a plaque assay to assess viral spread?

A

Viruses can form plaques in monolayers similar to a bacterial colony - therefore we can count the number of plaques from virus to see the spread.

32
Q

What happens in a syncytium assay?

A

Syncytia are when viruses with surface proteins fuse together at a neutral pH, therefore we can count the syncytia.

33
Q

How can we detect a viral genome?

A

PCR

34
Q

How do we detect viral antigen?

A

RFA, ELISA

35
Q

How do we detect viral particles?

A

EM, HA

36
Q

How do we detect antibodies specific to a virus?

A

Serology

37
Q

How can we make viruses de novo?

A

Isolate virus and infect a cell with viral genome, we can then culture the viral expansion to make many more viruses.

38
Q

Why is it hard to achieve a therapeutic index with antiviral drugs?

A

Because viruses are small particles, they are very dependent on their host cell’s machinery.

39
Q

What do most antivirals target?

A

Viral enzymes

40
Q

What are nucleoside analogues?

A

Chemically altered nucleosides which inhibit or interfere with nucleic acid replication but need to achieve some elements of specificity to the viral polymerase

41
Q

What are directly acting antivirals?

A

Drugs that target specific viral factors therefore are very specific to a particular virus.

42
Q

What type of antiviral is acyclovir?

A

Nucleoside analogue

43
Q

How does acyclovir work?

A

Lacks a 3’ OH group so binds to viral DNA and acts as a chain terminator so no more nucleotides can bind to form complete viral DNA. ACV enters infected cells and is phosphorylate to ACVMP via thymidine kinase and then to ACVTP. This then competitively inhibits viral DNA polymerase and terminate the chain of viral DNA.

44
Q

Why is there little resistance to acyclovir?

A

There is a high barrier - when the virus compromises its ability by losing thymidine kinase, it no longer has an advantage over other viruses therefore is less likely rot survive - it is not worth it for the virus to mutate and separate thymidine kinase.

45
Q

How is there high specificity with acyclovir?

A

ACV needs to be phosphorylated to ACVMP to initiate its mechanism process however this occurs via thymidine kinase which is only present n dells infected with the herpes simplex virus

46
Q

What is remdesivir?

A

Nucleoside analogue of adenosine used to treat ebola, COVID and now Hep C

47
Q

What are influenza antivirals?

A

Target unique and essential genes for virus functions

48
Q

What is a requirement for influenza antivirals?

A

They must have an effect abasing all the different types of influenza and should be easy to administer on a yearly basis

49
Q

What is a negative about relenza?

A

The virus readily can acquire relenza resistance

50
Q

Why is oseltamivir more successful than relenza?

A

Oseltamivir is less likely to be a drug that influenza becomes resistant to, and it can be taken orally as Tamiflu therefore is easily administered

51
Q

What is amantadine/ Rimantadine?

A

Cyclic amines with bulky, cage like structures

52
Q

What does amantadine/ Rimantadine function against?

A

Influenza A

53
Q

What is the role of the M2 channel?

A

Allows protons for the acidic endoscope to enter the core of the virus particle and disrupt links between the M1 protein and the nucleus protein, allowing the uncaring of the virus and thus facilitating its effective spread

54
Q

How does amantadine prevent virus spread?

A

Sits in the M2 channel and therefore blocks proton entry and subsequent spread of the virus through uncoating

55
Q

How have viruses mutated to become resistant to amatadine?

A

Single point mutation of M2 channel protein to prevent amantadine from binding.

56
Q

Why is an amantadine resistance mutation favourable for viruses?

A

This mutation leads to very little compromise of virus function as well therefore has little downside for mutation.

57
Q

What is the role of neuraminidase in infleunza?

A

Cleaves the silica acid residues at the end of a virus infection ,and allows the virus to leave the host cell

58
Q

What do NA inhibitors do?

A

Stop NA from cleaving the silica acid residue bond and thus preventing the influenza virus from leaving the host cell

59
Q

What does Baloxavir do?

A

Inhibits the viral polymerase endonuclease for influenza

60
Q

How is Baloxavir ineffective against some mutated viruses?

A

Single point mutation in viral protein confers resistance to Baloxavir

61
Q

What is hepatitis C?

A

Hepatotropic flavivirus

62
Q

What did hepatitis C cause?

A

Hepatocellular carcinoma

63
Q

What can we use to treat HCV?

A

Protease inhibitors
NS5A
NNPI
NS5B polymerase inhibitors

64
Q

What is the disadvantage of HCV antivirals?

A

They are targeted towards the strains of Hep C in the Western World therefore not effective against all strains

65
Q

What can we use for HIV antivirals?

A 
Fusion inhibitors 
Co-receptor antagonists (CCR5 or CXCR4)
Protease inhibitors (CD4)
NRTIs
NNRTIs
InSTIs
ALLINIs
66
Q

What is the life cycle of HIV?

A
  • Env glyocprotein attached to CD4 and co-receptor (CCR5 or CXCR4).
  • Fusion then allows entry of capsid into cell where RNA is reverse transcribed to dsDNA and incorporated into host genome (integrase).
  • Proviral transcription yields viral RNAs which are translated into viral proteins that assemble with unspoiled RNA genome at cell surface.
  • Immature virions bud at cell surface and mature via proteolytic processing.
  • Mature virions then bud and leave the cell
67
Q

What are biologicals?

A

Passive immunotherapy - antibodies taken from recovered individuals or produced from immortalised B cells

68
Q

What is an example of biologicals?

A

Palivizumab used for RSV

69
Q

What is RSV?

A

Respiratory Syncytial Virus

70
Q

How has Palivizumab been developed for treating RSV?

A

Murine derived monoclonal antibodies were specific to the A antigenic site of RSV F protein therefore these sequences were grafted into non-RSV specific human monoclonal antibodies, generating humanised RSV specific antibodies for immunotherapy

PoM (27 decks)

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