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m&i: antimicrobial therapies & challenges + epidemiology of infection > Mechanism of Antivirals > Flashcards

Mechanism of Antivirals Flashcards

1
Q

Explain 3 reasons why even though we have vaccines, we need antivirals

A
  • There are poorly effective or no vaccines for some viruses important to human health
  • Not everyone can be administered a vaccine even if that vaccine is effective
  • Immune response to vaccine administration can take time (and several sequential administrations)
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2
Q

What type of infections might we need to use antivirals for?

A
  • acute infections (aka quick killers) like influenza, ebola, MERS and SARS
  • viruses that we do not have a vaccine for (like HIV - long term) and chronic infections
  • viruses that cause acute inflammatory disease like herpes
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3
Q

What is prophylaxis?

A

Treatment given or action taken to prevent disease

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4
Q

When talking about HIV antivirals what is meant by PEP and PrEP?

A
  • Post-exposure prophylaxis and preventing infection: HIV (PEP)
  • Pre-exposure prophylaxis: HIV (PrEP)
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5
Q

Name some broad different modes of action of antivirals

A
  • Preventing virus absorption into host cell
  • Preventing penetration
  • Preventing viral nucleic acid replication (nucleoside analogues)
  • Preventing maturation of virus
  • Preventing virus release
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6
Q

Explain why developing antiviral drugs that are non-toxic and effective is so hard

A
  • Viruses use cellular proteins which may have other functions
  • Viruses must replicate inside cells - obligate intracellular parasites
  • Viruses take over the host cell replicative machinery
  • Viruses have high mutation rate - quasispecies
  • Anti-virals must be selective in their toxicity
    • i.e. exert their action only on infected cells
  • Some viruses are able to remain in a latent state e.g. herpes, HPV
  • Some viruses are able to integrate their genetic material into host cells
    • e.g. HIV
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7
Q

What viruses does Aciclovir target?

A

Herpes virus family including:

  • Herpes simplex (HSV)
  • Varicella Zoster Virus (VZV)
  • Cytomegalovirus (CMV)
  • Epstein-Barr virus (EBV)
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8
Q

Explain why Aciclovir only works in virus infected cells

A

This is as it starts as an inactive form and is converted to the active form by 2 viral enzymes

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9
Q

The viral enzyme {?} activates Aciclovir

A

The viral enzyme thymidine kinase (TK) activates Aciclovir

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10
Q

Explain what happens to Aciclovir to activate it

A

It is phosphorylated by a viral enzyme thymidine kinase (TK)

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11
Q

Explain how Aciclovir produces its antiviral effect

A

Aciclovir, when phosphorylated (by a viral enzyme?), looks like a DNA base so the viral DNA pol incorporates the active Aciclovir into the DNA

  • Aciclovir is a DNA chain terminator
  • Aciclovir has 30x the affinity for HSV DNA polymerase compared to cellular DNA polymerase
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12
Q

{?} has {?} the affinity for Aciclovir (ACV) compared with cellular phosphokinases

A

HSV thymidine kinase (TK) has 100 x the affinity for Aciclovir (ACV) compared with cellular phosphokinases

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13
Q

What viruses does Ganciclovir treat?

A

CMV (cytomegalovirus)

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14
Q

What type of virus is CMV (cytomegalovirus)?

A

Herpes

  • Herpes virus 4
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15
Q

How does Ganciclovir work?

A

Is basically the same as Aciclovir but just uses a different enzyme that is specific to CMV (so is converted to an active form by a viral enzyme and then will competitively inhibit viral DNA pol?)

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16
Q

Which viral enzyme converts ganciclovir to its active form?

A

CMV phosphotransferase (UL97 kinase)

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17
Q

Name 2 anti-herpes drugs that are not aciclovir or ganciclovir

A
  • Foscarnet
  • Cidofovir
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18
Q

Name the 2 main mechanisms that viruses can become resistant to aciclovir

A

As there are 2 enzymes involved in the pathway, if there are mutations to these 2 specific enzymes then aciclovir can not work

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19
Q

Why is resitance to antivirals in herpes virus very rare?

A

As (in immune competent patients) there is a very low viral load

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20
Q

If a mutation occuurs in {?} in a herpes virus drugs not needing phsophorylation are still effective

A

If a mutation occuurs in Thymidine Kinase in a herpes virus drugs not needing phsophorylation are still effective

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21
Q

If a mutation in a herpes virus occurs in {?} all drugs are rendered less effective

A

If a mutation in a herpes virus occurs in viral DNA polymerase all drugs are rendered less effective

22
Q

What virus does HAART target?

A

HIV

23
Q

What type of genetic material is in HIV?

A

ss + RNA, 2 strands

24
Q

Is HIV enveloped?

A

yes

25
Q

What is gp120 on HIV?

A

The envelope protein, also uses the transmembrane protein gp41
- “ a glycoprotein protruding from the outer surface of the HIV virion that has a molecular weight of 120 and must bind to a CD4 receptor on a T cell bearing such receptors before infection of the cell can occur”

26
Q

Explain what Gag (group specific antigen) is

A

Gag is the major structural protein of HIV and all retroviruses

27
Q

Describe the structure of HIV

A
28
Q

Name 4 types of anti-HIV drugs

A
  1. Anti-reverse transcriptase inhibitors
  2. Protease inhbitors
  3. Integrase inhibitors
  4. Fusion inhibitors
29
Q

Why is it very common for HIV to produce anti-viral resitant HIV mutants?

A

Because it produces a large amount of mutations in its replication (reverse transcriptase lacks proof reading capacity?)

30
Q

What is HAART and why do we do it?

A

Since HIV very often produces antiviral resistant mutants, we use a combination of different types of antiviral HIV drugs (4 types)

  • this therapy is called HAART = highly active anti retroviral therapy
31
Q

What is the most common type (class) of anti-HIV antiviral and name one

A

Nucleoside reverse transcriptase inhibitors (NRTI)

  • AZT
32
Q

Nucleoside reverse transcriptase inhibitors are one type of drug used in the treatment of HIV, explain how these work

A

They are structurally similar to DNA bases so reverse transcriptase incorporates them but they cause chain termination

33
Q

In the treatment of HIV we can use non-nucleoside reverse transcriptase inhibitors, explain how these work

A

These do the same thing as nucleoside RT inhibitors but do not look like nucleotides

  • non competitive inhibition of reverser transcriptase
  • can be used in combination with NRTIs
34
Q

What is meant by a viral swarm in HIV?

A

Due to the high mutation rate and high viral load, HIV can cause a large number of multiple different HIV viruses

  • quasispecies
35
Q

Why does HIV have a high mutation rate?

A

Reverse transcriptase lacks a proof reading capacity

36
Q

What genetic material is in influenza?

A

single stranded (ss) RNA

37
Q

What type of virus do we treat with Amantidine?

A

Influenza

38
Q

How does Amantidine work?

A
  • Inhibit virus uncoating by blocking the influenza encoded M2 protein when inside cells and assembly of haemagglutinin
    • Now rarely used
39
Q

Zanamivir and Oseltamivir (Tamiflu) are used for treatment of flu, how do they work?

A
  • Inhibits virus release from infected cells via inhibition of neuraminidase
    • Oseltamivir-oral
    • Zanamivir- inhaled or IV - less likely for resistance to develop
40
Q

Explain how zanamivir and oseltamivir work

A

Stop the virus (flu) from leaving the cell as an interaction is needed by neuraminidise with the cell surface - they block this interaction

41
Q

How is hepatitis C (HCV) transmitted?

A
  • Unprotected sex
  • Blood and body fluid exposure
  • IV drug use
42
Q

What type of virus (genetic material) is HCV (hepatitis C)?

A

9.6 Kb RNA virus, enveloped, Flavivridae family

43
Q

Since there is no vaccine for HCV, we rely mostly on the broad acting antiviral {?}

A

Since there is no vaccine for HCV, we rely mostly on the broad acting antiviral Ribavirin

44
Q

Explain how Ribavirin works

A
  • Is a nucleoside analogue that is orignially inactive and then is activated by phosphorylation
  • Blocks RNA synthesis (causes chain termination) by inhibiting IMP
45
Q

It is very easy to get mutations that stop the functioning of Ribavirin, and so we now are using {?} to treat {?}

A

It is very easy to get mutations that stop the functioning of Ribavirin, and so we now are using DAAs (direct acting antivirals) to treat HCV (HepC)

46
Q

Describe what DAAs are and their benefits

A
  • Direct acting antivirals
  • Relatively new class of medication
  • Acts to target specitic steps in the HV viral lite cycle
  • shorten the length of therapy, minimize side effects, target the virus itself, improve sustained virologic response (SVR) rate.
  • structural and non-structural proteins - replicate and assemble new virions
  • HCV - first chronic viral infection to be cured without IF or ribavirin.
47
Q

Explain how DAAs work - what 3 things can they inhibit?

A

Inhibit:

  • NS3/4 protease (needed for viral protein formation)
  • NS5A (needed for assembly of virueses)
  • NS5B polymerase (needed for RNA replication)
48
Q

When talking about HCV, describe the genome and how we name the HCV (hep C) proteins

A

HCV is ssRNA
NS = non-structural protein
C = capsid
E = envelope

49
Q

What is the function exactly of the viral protease in HCV

A

I beleive that the whole RNA genome is transcribed into one long protein which is then chopped up by this protease

50
Q

What is post exposure prophylaxis?

A

The emergency management of exposure-prone incidents such as splashes of contaminated fluids, needle injuries etc.

51
Q

Name some viral infections with no effective therapies

A
  • rabies
  • dengue
  • common cold viruses
  • ebola
  • HPV
  • arboviruses
  • ‘Pathogen X’

m&i: antimicrobial therapies & challenges + epidemiology of infection (4 decks)

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