Antivirals Flashcards

1
Q

What surrounds the genetic material in viruses?

A

Capsid (protein shell surrounding the genetic material)

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2
Q

What type of genetic material do the following viruses have: a. Hepatitis B b. Hepatits C c. HIV d. Herpes Simplex Virus e. Influenza

A

a. Hepatitis B It is a DNA virus that also involves reverse transcriptase in its replication b. Hepatitis C RNA virus c. HIV Retrovirus d. Herpes Simplex Virus DNA virus e. Influenza RNA virus

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3
Q

Describe the relative curability of Hep B and Hep C.

A

Hep B – not curable Hep C – CURABLE

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4
Q

At what point do you start treating someone who has recently got infected by Hep B or Hep C?

A

When the infection becomes chronic The immune system, in some people, is able to clear Hep B and Hep C infections by itself

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5
Q

What is the treatment for Hep B? What type of drug is this?

A
  • Tenofovir
  • Nucleotide reverse transcriptase inhibitor
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6
Q

What are the treatment options for Hep C? State the drug types.

A

Ribavirin (+ Peginterferon alfa) Ribavirin is a nucleoside analogue that prevents viral RNA synthesis Boceprivir – protease inhibitor (most effective against Hep C genotype 1)

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7
Q

Describe the receptor interaction involved in HIV attachment and entry.

A

HIV GP120 binds to CD4 GP120 also binds to either CCR5 or CXCR4 Then HIV GP41 penetrates the host cell membrane and the viral capsid enters

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8
Q

State two drugs that interfere with HIV attachment and entry and state their targets.

A
  • Enfuvirtide – GP41 transmembrane glycoprotein
  • Maraviroc –CCR5 chemokine receptor
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9
Q

Name a nucleoside reverse transcriptase inhibitor. How are they activated?

A

Zidovudine Three step phosphorylation

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10
Q

Name a nucleotide reverse transcriptase inhibitor. How are they activated?

A

Tenofovir Fewer than 3 phosphorylation steps

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11
Q

How do non-nucleoside reverse transcriptase inhibitors act? Give an example of an NNRTI.

A

They bind to the reverse transcriptase and cause a change in shape of the enzyme so it blocks HIV replication Example: Efavirenz

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12
Q

Give an example of an integrase inhibitor.

A

Raltegravir

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13
Q

What viral gene encodes all the viral structural proteins?

A

Gag gene

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14
Q

What must happen to the precursor that encodes all viral structural proteins in order to produce fully functioning virus particles?

A

This must be cleaved by a protease into the constituent proteins so that it can make the fully formed virus

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15
Q

Name a drug that acts a protease inhibitor and state one problem with its pharmacokinetics.

A

Saquinavir

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16
Q

What drug can be given to boost the level of the protease inhibitor in the circulation?

A

Ritonavir This decreases the metabolism of saquinavir

17
Q

What is the herpes virus surrounded by?

A

Tegument and a lipid bilayer

18
Q

What do the two different types of herpes cause?

A

HSV1 – cold sores HSV2 – genital herpes usually this way round, not always

19
Q

What is the treatment for HSV?

A

Acyclovir Nucleoside analogue that is specific because its activation requires viral kinases

20
Q

What envelope protein of influenza is important for the release of the virus into the host cell?

A

Neuraminidase

21
Q

Name an inhibitor of this influenza envelope protein

A

Oseltamivir

22
Q

What is the tropism of viral hepititis?

A

Liver hepatocytes

23
Q

What kind of people are immune to HIV?

A

Those with the genetic mutation delta 32 They dont have the CCR5 chemokine receptor so HIV is unable to enter their cells

24
Q

What’s the 1st step of a HIV replication inside a cell?

A

Viral single-stranded RNA -> double stranded DNA by reverse transcriptase

25
Q

What is the difference between the classes of drugs that target HIV replication?

A

Nucleoside RT inhibitors Activated by 3 step phosphorylation process (E.g. Zidovudine) Nucleotide RT inhibitors Fewer phosphorylation steps required (E.g. Tenofovir) Non-nucleoside RT inhibitors No phosphorylation required Not incorporated into viral DNA (E.g. Efavirenz)

26
Q

Why are HIV medications given in combination?

A

If one is jsut given on its own it doesn’t have a large enough effect to destroy the virus to the virus develops resistance to it.

27
Q

What are the targets for hepatitis treatment?

A
  • Hep B: Reverse transcriptase
  • Hep C: RNA synthesis (various mechanisms) Viral protease
28
Q

What are the targets for HIV treatment?

A

Attachment and Entry - HIV GP41 and cellular CCR5 Replication - HIV reverse transcriptase Viral DNA intergration - HIV integrase Assembly and release - HIV protease

29
Q

What is different about Non-nucleoside RT inhibitors compared to other RT inhibitors?

A

No phosphorylation required Not incorporated into viral DNA

30
Q

Why did oseltamivir turn out to be not very useful?

A

You need to take it immediately when you get the virsus (asymptomatic) There is a short incubation period whilst the virus infects its cells After this symptoms appear but by then its too late to take oseltamivir as too many cells are infected

31
Q

What is the tropism of HIV?

A

leukocytes