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Fungal/Virology > LEC 9 - Antiviral Agents + Targets > Flashcards

LEC 9 - Antiviral Agents + Targets Flashcards

1
Q

What is the conventional approach to control of viral diseases?

A

Vaccines

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2
Q

What is the objective of antiviral drug therapy?

A

Eradicate virus

Minimally impact the host

Prevent further viral invasion

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3
Q

What are the problems that people run into when developing anti-virals?

A

Need to penetrate host cells

Narrow therapeutic margin

Viral latency issues affect efficacy

Susceptibility testing is challenging/costly

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4
Q

What is the common way to classify antiviral drugs?

A

Through their mechanism of action

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5
Q

What are the five types of antivirals?

A

Immunomodulators

Ion channel blockers

Neuraminidase inhibitors

DNA/RNA synthesis inhibitors

Antiretroviral

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6
Q

What is the basic way that ion channel blockers work?

A

Block uncoating

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7
Q

What types of drugs are in the group of immunomodulators?

A

Interferons

Interleukins

Growth factors

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8
Q

What is the most dominant immunomodulator?

A

Type 1 interferon

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9
Q

What type of activity foes type 1 interferons have?

A

Antiviral activity

Immunomodulatory effects

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10
Q

What is Feline interferon-omega used for?

A

Cats - FeLV + FIV

Dogs - Parvo virus

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11
Q

What are the ion channel blockers?

A

Amantadines

(Amantadine + Rimantadine)

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12
Q

What are the amatadines used for?

A

Influenza A viruses

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13
Q

How does ion channel blockers work?

A

Block uncoating step of the life cycle

Insert into M2 protein channel - no H+ enters

No M1 protein dissociation

Keeps viral RNA within protein coat

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14
Q

Whats the normal steps in viral uncoating?

A

Endosomal acidification

Active viral M2 channel protein - H+ enters virion

Viral M1 matrix protein dissociates = viral uncoating

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15
Q

What causes resistance to ion channel blockers?

A

Mutations in M2 protein

Widespread, no longer recommended for use

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16
Q

What drugs are in the neuraminidase inhibitor family?

A

Oseltamivir + Zanamivir

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17
Q

What are the neuraminidase inhibitors used for?

A

Influenze A + B

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18
Q

How do the neuraminidase inhibitors work?

A

Block the release of Influenze A + B from host cell membrane

Sialic acid analods

Bind to NA and prevent enzymatic acitivty

Inhibits viral release - can’t infect new cells

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19
Q

What is the normal events that occur when Influenza A or B are released from the host cell?

A

replication occurs

Virus buds from host cell

remains bound to sialic acid on host cell membrane

Viral NA cleaves virus from salic acid

Virus released

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20
Q

How does resistance to NA inhibitors occur?

A

Sporadic cases

Mutation in NA

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21
Q

What infections has NA inhibitors been recommended for in dogs?

A

Canine parvo infection

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22
Q

What are the types of antiviral agents that are considered DNA/RNA synthesis inhibitors?

A

Nuceloside synthesis inhibitor

Nucleoside analogs - DNA

Nucleoside analogs - RNA

Nucleoside + Non-nucleoside reverse transcriptase inhibitors

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23
Q

How do nucleoside synthesis inhibitors work?

A

Directly inhibit DNA/RNA polymerase activity

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24
Q

What are the nucleoside synthesis inhibitors?

A

Foscarnet

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25
Q

What are the two types of nucleoside analogs for DNA syntesis?

A

Purine + Pyrimidine

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26
Q

What are the purine analogs?

A

Acyclovir

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27
Q

What are the pyrimidine analogs?

A

Cidofovir

Idoxuridine

Trifluridine

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28
Q

What drugs are nucleoside analogs that interfere with viral RNA synthesis?

A

Ribavirin

29
Q

How does foscarnet work?

A

Direct inhibition of DNA polymerase

Bind to pyrophosphate binding site

Prevent cleavage of pryophosphate

Halts DNA replication

30
Q

What viruses does foscarnet work for?

A

Wide range

Herpesvirus

– and –

Retrovirus

31
Q

What can cause resistance to foscarnet?

A

Mutations in viral DNA polymerase

32
Q

How do nucleoside analogs work?

A

Inhibit viral DNA polyermase

Chain termination activity

Converted to triphosphate nucleotides in host cell

33
Q

What viruses are the target for nucleoside analog treatment?

A

Herpesvirus

34
Q

What is Acyvlovir a analog of?

A

dGTP

35
Q

How does Acyclovir work?

A

Inhibits replication

ACV is converted to ACV-P by viral enzyme TK

Competitive inhibitor of viral polymerase

Higher affinity for DNA polymerase

36
Q

How is Acyclovir selective?

A

Uninfected cells will not change ACV into ACV-P

37
Q

How does resistance to Acyclovir occur?

A

Mutation in viral TK or DNA polymerase

38
Q

What are the prodrug derivatives of Acyclovir?

A

Valacylovir

Famicilovir

Valganciclovir

39
Q

What do all nucleoside analogs require?

A

Inital phosphorylation by virally-encoded enzymes

40
Q

What is ACV + PCV phosphorlylated by?

A

TK

41
Q

What is GCV phosphorylated by?

A

Viral Protein Kinase (PK)

42
Q

How does Vidarabine work?

A

Interferes with viral DNA polymerase activity

43
Q

How is vidarabine used in vet medicine?

A

FHV-1 ocular infections in cats

Topical use ONLY

44
Q

What is cidofovir an analog of?

A

Deoxycytosine

45
Q

How does Cidofovir work?

A

Inhibitiion of polymerase activity

Chain termination

46
Q

How do viruses become resistant to Cidofovir?

A

Mutations in DNA polymerase

47
Q

What does Cidofovir work against?

A

Herpes

Adeno

Poz

Papilloma

48
Q

How can Cidofovir be used opthalmically?

A

Herpes eye infections in cats

49
Q

What are the two forms of pyrimidine analogs?

A

Idoxuridine

Trifluridien

50
Q

What is the structure of Idoxuridine?

A

Iodine atom added to a uracil

51
Q

What is the structure of Trifluridine?

A

Contains -CF3 group added to Uracil

52
Q

How are Pyrimidine analogs used?

A

Feline herpes eye infectiosn

53
Q

What does Ribavirin resemble?

A

Purine analog

Resembles RNA nucleotides

54
Q

How does Ribavirin work?

A

Immunomodulator - promote Th1 development

Inhibits IMPDH enzyme - stops GTP synthesis

Inhibits RNA-dependent RNA polymerase - RNA replication

Promotes mutagenesis

Interferes with mRNA capping

55
Q

How does ribavirin promote mutagenesis?

A

Resemble both A + G bases

Incoporated into RNA

56
Q

What does ribavirin work against?

A

Both RNA + DNA viruses

Works best against RNA respiratory viruses + Herpes

57
Q

How does resistance to antiretroviral agents develope?

A

Mutations at or near drugs binding site

OR

Mutations that change the conformation of target protien

58
Q

What is the antiretroviral used to treat FIV + FeLV?

A

AZT

in combination with type I interferon

59
Q

How does Zifovudine work?

A

Selective inhibition of viral reverse transcriptase

60
Q

What are the non-nucleoside RT inhibitors?

A

Efavirenz

Nevirapine

Delavirdine

61
Q

How do the non-nucleoside RT inhibitors work?

A

Non-competively binding to reverse transcriptase + inhibiting its action

62
Q

What are the fusion/entry inhibitors?

A

maraviroc

– and –

Enfuvirtide

63
Q

How do the fusion/entry inhibitors work?

A

Interfere with receptor-mediated binding of virus to host

– or –

Prevent fusion of retroviral envelope with host cell membrane

64
Q

What are the integrase inhibitors?

A

Raltegravir

– and –

Elvitegravir

65
Q

How do integrase inhibitors work?

A

Inhibit integration of viral DNA into the host cell genome

66
Q

What are the protease inhibitors?

A

Saquinavir

Ritonavir

Indinavir

67
Q

How do the protease inhibitors function?

A

Binding to + inhibiting proteolytic activity of viral protease

Prevent cleavage of polypeptide into functional proteins

68
Q
A

Fungal/Virology (26 decks)

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