4.44 Flashcards

1
Q

• Inhibitors of viral replication

2

A

– every step in viral replication is potentially a target

– targeting host cell functions is generally not feasible (toxicity)

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2
Q

Enfuvirtide - (4)

A

HIV fusion inhibitor
Binds to gp41 region that folds back onto itself
Prevents fusion of membranes
Very specific to HIV

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3
Q

Maraviroc – (1)

A

CCR5 binding inhibitor

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4
Q

amantadine virus entry

• used to prevent

A

influenza

infections

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5
Q

amantadine virus entry

• blocks

A

penetration
and uncoating of
influenza A virus

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6
Q

Rimantadine =

A

analog of amantadine

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7
Q

Amantadine and rimantadine affect

A

M2’s function as an ion channel

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8
Q

Amantadine and rimantadine affect M2’s function as an ion channel
(3)

A

Following endocytosis, acidification of endosomes occurs
Then M2 can function as ion channel
Acidification within virion drives viral disassembly

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9
Q

mAb active against

A

original version of SARS CoV-2

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10
Q

mAb active against original version of SARS CoV-2

received — from the FDA

A

Emergency Use Authorization

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11
Q

Monoclonal antibody (mAb)
binds SARS-CoV-2 virions and
“—” them, which
means it

A

neutralizes

blocks the virus
from interacting with ACE2
receptors and entering cells
mAb was isolated from a recovered
COVID-19 patient = a neutralizing
IgG1 mAb directed against the
SARS-CoV-2 spike (S) protein
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12
Q

Acyclovir - (3)

A

result of rational drug design (nucleoside analog)
target herpesviruses
Inhibits DNA synthesis

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13
Q

Viral genome replication
Acyclovir
Viral TK much more efficient than

A

cellular TK in this

reaction (so drug is specific to infected cells)

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14
Q

However, acyclovir has no effect on —

A

latency

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15
Q

Acyclovir is not effective against —

A

CMV

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16
Q

Ganciclovir is effective against

A

CMV
compared to acyclovir, although it is also
more toxic (cellular TK uses drug better too).

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17
Q

Gancicivir is — analog

A

nucleoside

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18
Q

foscarnet

Directly inhibits

A

herpesvirus and
cytomegalovirus
DNA polymerase
(nephrotoxicity issues)

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19
Q

Foscarnet is a

A

nonnucleoside inhibitor

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20
Q

Remdesivir is a nucleoside analog

interferes with the action of

A

viral RNA-dependent RNA polymerase

causes RNA synthesis termination after a few nucleotides

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21
Q

Viral protease:

A

cleaves
viral proteins to their
final mature sizes

22
Q

Viral RNA-dependent RNA

polymerase:

A

viral genome

replication and transcription

23
Q

Hepatitis C virus treatments:

A

Newer 2-drug combination therapies

target specific HCV enzymes

24
Q

Other HCV treatments target

A

viral protease

25
Q

sofosbuvir

A

Inhibitor of RNA-dependent

RNA polymerase

26
Q

sofosbuvir

Inhibitor of

A

RNA-dependent

RNA polymerase

27
Q

Ledipasvir

Inhibitor of

A

RNA-dependent

RNA polymerase

28
Q

Paxlovid =

A

SARS-CoV-2
protease inhibitor: inhibits
production of mature
(cleaved) viral proteins

29
Q

Paxlovid

A — inhibitor

A

peptidomimetic

30
Q

Cidofovir is a relatively broad-spectrum

A

anti-DNA virus drug

31
Q

Cidofovir

inhibits

A

viral DNA

polymerase

32
Q

Cidofovir is a — analog

A

nucleoside

33
Q

Use is mainly limited toc

A
cytomegalovirus retinitis in
AIDS patients (toxicity limits dosage levels)
34
Q

Anti-HIV drugs:

nucleoside analog reverse transcriptase inhibitors (NRTI)

A

Need to be phosphorylated by cellular enzymes before being used by HIV reverse transcriptase (RT) (like acyclovir).
HIV RT uses these analogs and since they lack a 3’ –OH, DNA synthesis (reverse transcription) stops

35
Q

Anti-HIV drugs:

nucleotide analog reverse transcriptase inhibitors (NtRTI)

A

Act like NRTI but do not need to be phosphorylated (already contain phosphate)

36
Q

Anti-HIV drugs:

nonnucleoside reverse transcriptase inhibitors (NNRTI)

A

Bind sites on HIV RT enzyme that cause it to stop functioning, blocking reverse transcription

37
Q

Anti-HIV drugs: Protease inhibitors

A

HIV protease cleaves the initial HIV proteins to their final mature sizes
Protease inhibitors attempt to mimic an HIV protease cut site, competitively inhibiting HIV protease

Peptidomimetic inhibitors

38
Q

HAART =

A

highly active antiretroviral therapy

39
Q

HAART = highly active antiretroviral therapy
at least – drugs in combination
– nucleoside inhibitors plus a NNRTI or a protease inhibitor

A

3

2

40
Q

Anti-HIV drugs: Integrase inhibitors

A

Blocks integration of HIV dsDNA

into host cell chromosomal DNA

41
Q

Integrase inhibitors

interferes with the

A

strand transfer step

42
Q

Steps of HIV replication/infection that

are targeted by anti-viral therapies (4)

A

entry
reverse transcription
integration
maturation

43
Q

Virus release
Neuraminidase inhibitors - influenza virus
neuraminidase (NA)
(3)

A

release of virus from envelope
cleaves sialic acid (NA has enzymatic activity)
Inhibitors prevent efficient spread of virus from cell to cell

44
Q

Neuraminidase Inhibitors prevent

A

efficient spread of virus from cell to cell

45
Q

• Interferons

2

A

– natural products discovered in 1957

– Interferons assist the immune response

46
Q

• Interferons
– Interferons assist the immune response

  • inhibit
  • activate
  • increase
A

viral replication within host cells
natural killer cells and macrophages
antigen presentation to lymphocytes

47
Q

Effects of interferon therapy (3)

A
  • Fatigue
  • Fever
  • Myalgias
48
Q

Effects of interferon therapy

• Formerly (2)

A

main treatment
for hepatitis C Virus
(HCV) infection

used for HBV

49
Q

Ribavirin (2)

A

• Purine nucleoside analog
• Inhibits many RNA viruses
and some DNA viruses

50
Q

Ribavirin
• Inhibits many RNA viruses
and some DNA viruses
(3)

A

– Influenza A and B
– Measles
– Respiratory Syncytial Virus