Antiviral II Flashcards

(37 cards)

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.

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

19
Q

Similar to herpesviruses, What infections does HIV form ?

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
To inhibit both viral DNA and RNA polymerase this drug does not require the activation of viral or cellular TK What drug is this?
Foscarnet
26
Efavirenz, nevirapine and delavirdine all inhibit
HIV RT.
27
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
Yes, it works great with Azidothymidine.
28
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
F. Synergetic relationship
29
What is the main target for viral maturation?
HIV protease
30
Ritonavir is an HIV protease inhibitor that affects?
Viral maturation
31
Recall: Ritonavir is going to bind competitively and?
change the active site.
32
Inhibition of viral gene expression involved which protease inhibitors?
HCV(Hepatitis C) NS3 /A4 protease inhibitors.
33
Inhibtion of viral gene expression involved which protease inhibitors?
HCV(Hepatitis C) NS3 /A4 protease inhibitors.
34
The HCV polyprotein and anti-HCV protease inhibitors
Telaprevir, Boceprevir, Simeprevir, and Paritaprevir.
35
Nirmatrelivir inhibits SARS-COVID2, what kind of inhibition is this for antivirals.
Viral gene expression
36
Nirmatrelivir is a
Viral gene expression
37
What are the modes of action for nucleoside analogs? 3
Inhibit nucleosides by competing for substrates Terminate elongation if growing DNA/RNA chains Form tight dead end complexes