Antiviral II Flashcards

1
Q

T or F: Viruses are intra cellular parasites..

A

True

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2
Q

Do viruses possess both DNA AND RNA ?

A

No, they have either or.

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3
Q

What are the steps for DNA virus replication?

A

Attachment, entry and uncoating, DNA synthesis via replication, expression of genes(capsid protein), maturation, release.

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4
Q

What primary difference is found in retrovirus replication vs dna replication?

A

RNA VIRUS enters and undergoes dsDNA synthesis with reverse transcriptase sand integrates itself, becomes a provirus.

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5
Q

Most of the clinical pharmacological inhibitors are involved in what process of the host cell?

A

Genome replication and gene expression.

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6
Q

What is the main target for inhibition of viral genome replication ?

A

Viral DNA-dependent DNA polymerase

Viral RNA-dependent RNA polymerase

Viral RNA-dependent DNA polymerase (Reverse Transcriptase)

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7
Q

Nucleoside analogs are used to target thymindine kinase and DNA Pol but must be converted from prodrug to its active form . What is the active form ? What converts it ?

A

Acyclo-guanosine triphosphate.

Thymindine Kinase

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8
Q

A poor substrate for human cellular TK and DNA Pol is ?

A

Acyclovir

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9
Q

Thymindine kinase phosphorylates acyclovir because ?

A

Tk is promiscuous and will phosphorylate anything that is looks like a nucleoside.

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10
Q

Review : Slide 11 describes the key features of acyclovir triphosphate which is the effector of inhibition of DNA pol. When incorporated, what occurs to the phosphate and the enzyme

A

Acyclovir triphosphate becomes monophosphate and changes the conformation of the enzyme , DNA pol.

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11
Q

Acyclovir serves as a chain inhibitor because it lacks a 3’ hydroxyl group. What does it also alter ?

A

It alters the catalytic site of the enzyme, DNA Pol.

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12
Q
Resistance is mostly due to mutation in either .
A. TK
B. DNA POL
C.  Both
D. Neither
A

C. Both

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13
Q
Which mechanism is most common?
A. TK deficient mutant
B. TK low producer mutant 
C. Mutant that produces an altered TK. 
D. NEITHER
A

A. Selection of TK-deficient mutant

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14
Q

DNA poly. Resistance is mediated by mutation enhancing the excision of the analog after? (The most common feature)

A

It has been incorporated into DNA chain

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15
Q

Valacyclovir a valine ester has a good oral bioavailability what other two prodrugs have a good oral bioavailability?

A

Famciclover and Valganciclovir

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16
Q

Which acyclovir derivative is most toxic due to its addition of the 3’ CHOH group?

A

Valganciclovir

17
Q

T or F. Cidofovir is approved for HIV PATIENTS.

A

True

18
Q

HIV Genome organization includes all the following, which one of them is derived from polyproteins A and B?

LTRs
Phi sequence - packaging of RNA into mature viral particles.
gag- the interior core of the viral particle
Pol- protease
Env

A

Gag and pol

19
Q

Similar to herpesviruses, What infections does HIV form ?

A

Latent

20
Q

There are no drugs for latent infections caused by HIV but which target is not actively used by anti-HIV drugs?

A. Viral fusion
B. Reverse transcription
C. Maturation
D. Integration

A

D. Integration

21
Q

Lamivudine is less toxic than AZT. What does it inhibit!?

A

HIV and Hepatitis B reverse transcriptase.

22
Q

Emtricitabine inhibits HV RT, WHAT GROUP DISTINGUISHES IT FROM LAMIVUDINE ?

A

Contains that 5-fluoro-group

23
Q

Reasons why we need to make a cocktail of different drugs? Which is missing?

  1. Low efficacy of each drug alone
  2. -
  3. Multiple resistance mutations decrease the fitness of the virus
A
  1. Mutations conferring resistance to one drug do not confer resistance to others
  2. Mutations at the different sites can adversely affect one another
24
Q

Anti-SARS nucleoside analogs cause delay of chain termination, what drugs do so?

A

Remdesivir and Molnupiravir

25
Q

To inhibit both viral DNA and RNA polymerase this drug does not require the activation of viral or cellular TK What drug is this?

A

Foscarnet

26
Q

Efavirenz, nevirapine and delavirdine all inhibit

A

HIV RT.

27
Q

T or F: Nevirapine binds on the backside of RT and changes the shape of the active site, blocking its action and works well with AZT

A

Yes, it works great with Azidothymidine.

28
Q

The main target of viral maturation is essential in all of these except?
A. Essential for HIV replication
B. Point Mutation inactivates the enzyme
C. Conserved/Odd substrates
D. Unique enzyme
E. The enzyme can be used in large quantity
F. Synergistic relationship

A

F. Synergetic relationship

29
Q

What is the main target for viral maturation?

A

HIV protease

30
Q

Ritonavir is an HIV protease inhibitor that affects?

A

Viral maturation

31
Q

Recall: Ritonavir is going to bind competitively and?

A

change the active site.

32
Q

Inhibition of viral gene expression involved which protease inhibitors?

A

HCV(Hepatitis C) NS3 /A4 protease inhibitors.

33
Q

Inhibtion of viral gene expression involved which protease inhibitors?

A

HCV(Hepatitis C) NS3 /A4 protease inhibitors.

34
Q

The HCV
polyprotein and
anti-HCV protease
inhibitors

A

Telaprevir, Boceprevir, Simeprevir, and Paritaprevir.

35
Q

Nirmatrelivir inhibits SARS-COVID2, what kind of inhibition is this for antivirals.

A

Viral gene expression

36
Q

Nirmatrelivir is a

A

Viral gene expression

37
Q

What are the modes of action for nucleoside analogs? 3

A

Inhibit nucleosides by competing for substrates
Terminate elongation if growing DNA/RNA chains
Form tight dead end complexes