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Pharam > Antiviral Therapy > Flashcards

Antiviral Therapy Flashcards

1
Q

DNA Viruses

A

Chicken Pox
Herpes
Cytomegalovirus
Hepatitis B

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2
Q

RNA Viruses

A

Influenzaa A,B,C
Resouratiry Syncytial Virus
Hepatitis C

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3
Q

RNA Retrovirsus

A

HIV-1/HIV-2

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4
Q

Infection Process

A 
Adsorption
Penetration/uncoating
Replication, transcription and translation
Assembly
Releaase of New virus
Secondary Infection
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5
Q

Inhibition of viral DNA Polymerase

A

Acyclovir
Ganciclovir

Resembles Base analogs

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6
Q

Inhibition of uncoating of RNA virsus

A

Amantidine/Rimantidine

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7
Q

Hepatitis C RNA polymerase inhibitor

A

Ribavirin

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8
Q

RNA Virus Budding Inhibitor

A

Zanamivir
Oseltamivir
Peramivir

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9
Q

RNA retrovirus (HIV) drug families

A

Adhesion inhibitors
Nucleaside/non-nucleoside RT inhibitors
Integrase inhibitors
Protease inhibitors

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10
Q

Immune activation against virus

A

Macrophage to APC
APC to CD4+ Th cell w/ IL-1
IL-2 Autocrine on CD4+ T helper -> Th1 and Th2
Th1 creates IFN

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11
Q

Interferon Functions

A

Activates killer cells

Induces resistance of other host cell to virus

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12
Q

Antibody effects on virus

A

Binds antigen = neutralization

Fc on antibody allows macrophage opsonization = phagocytosis

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13
Q

Active immunizaation

A

Vacination with antiviral vaccines = celluar and hemoral response
Cellular and humoral activated

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14
Q

Passive immunization

A

Inject antiviral antibodies
Use for treatment aand prophalyxis
Last 1-3 months

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15
Q

Interferon production

A

Specialized interferon producing cells have TLR7 and 9 that recognize viral DNA/RNA = type 1 secretion

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16
Q

Interferon Induced Genes Effects

A

Inhibit:

Viral penetration and uncoating
Viral transcription
Viral translation
Viral protein gylcosylation

Activate:
killer cells

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17
Q

Interferon Alpha Spectrum

A

Most rna and DNA viruses

Retroviruses

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18
Q

Drugs on DNAA virus class

A

Drugs may be best for Herpes and varicella or best on CMV

19
Q

Acyclovir Mechanism

A

Phosphorylated by viral thymidine kinase

  1. Selective metabolic activation in virus infected cells
  2. competitive inhibitor at Viral DNA poly
  3. Incorporation into DNA
  4. Causes chain termination/inhibits DNA poly
20
Q

Acyclovir Spectrum

A

Spectrum: HSV-1>HSV-2>VZV

21
Q

Ganciclovir Mechanism

A

CMV UL97 kinaase phosphorylates drug first then cellular kinases do di and triphosphate

Competitive inhibitor of dGTP = inhibits elongation

10x concentration in infected cells

22
Q

Ganciclovir Spectrum and use

A

CMV»HSV-1>HSV-2>VZV>EBV> HSV-6

Prophylaxis and treatment of CMV (especially for transplant patients)

23
Q

Lamivudine Mechanism and Use

A

Competes with dCTP to inhibit RT

Used against Hep B and HIV

24
Q

Docosanol Mechanism

A

Inhibits attachment of enveloped viruses to cells

25
Q

Docosanol Spectrum

A

DNA viruses - HSV1 and 2, human herpesvirus 6, CMV

RNA Virsues - Influenza and RSV

26
Q

Docosanol Use

A

Topical cream 10% for oral HSV if used within 12h of prodromal symptoms on face

27
Q

Attachment and penetration of influenza

A

By hemagglutinin/neuraminidase

Binds to sialic acid on ends of glycoprotein sugar chain s= conformation change in F that triggers fusion

28
Q

Influenza M2 protein

A

Allows Genome release within cells when virus enters acidic vesicle = M2 channels open

29
Q

Amantadine Mechanism and spectrrum

A

Prevents uncoating of influenza A virus only by inhibiting action of M2 protein ion channel = inhibition of acidification

30
Q

Amantadine use

A

Seasonal Prophylaxis

31
Q

Neuraminidase

A

Mediates release from host cells by hydrolizing terminal sialic acids

32
Q

Oseltamivir (Tamiflu) mechanism and spectrum

A

Inhibits Neuraminidase = virus aggregates on cell surface and fails to spread

Influenza A and B virus only

Used prophylactivally

33
Q

Hep C RNA virus infection mechanism (Causes hepatic cirrhosis and promotes cancer)

A
  1. Attaches to cells by glycoprotein E
  2. Transported to endosome for uncoating
  3. Genome copied by RNA dependent RNA poly
  4. mRNAs translated by host
  5. Assembly by protease processing
34
Q

NS3-4A Protease and Inhibition

A

Serine protease that cleaves HCV precursors for assembly

Inhibited by Simeprevir

HCV only

35
Q

NS5B and Inhibitors

A

An RNA-dependent RNA polymerase = copies RNA viral genome

Sofosbuvir (Sovaldi) = metabolite incorporated in RNA and terminates chain = inhibition of repliucation

36
Q

NS5A and Inhibitors

A

Required for HCV replication and assembly

Ledipasvir = disrupts replication and assembly by binding to domain 1 (which binds zinc and RNA)

37
Q

HIV GP41 (folds on itself) and GP120 (Attaches)

A

Binds to Host CD4+ T helpers -> CD4 (both needed) and CCR5 (both needed) and CXCR4

38
Q

CD4/CCR5 receptors on

A

Thelpers
Monocytes/macrophages
Neurons in CNS

39
Q

Long Terminal Repeats of HIV Fxns

A

Used for integration into host genome by viral integrase

In host DNA -> recognized by HIV tat protein and by host NFkB = transcription of HIV genome

40
Q

Nucleoside inhibitors of RT Class Properties

A

All resemble nucleosides (activated intracellularly to triphosphates)

Lack 3’OH necessary for continued poly of cDNA

Work on HIV1 and HIV 2

Can cause hepatic damage

41
Q

Zidovudine

A

Phosphorylated by Thymidine Kinase

A nucleoside inhibitor

42
Q

Lamivudine

A

Cytosine analog, incorporates into viral cDNA (nucleoside inhibitor)

Spectrum = Hep B and HIV

43
Q

Non-nucleoside RT inhibitor Class properties

A
  1. Don’t require intracellular phosphorylation
  2. Bind to RT adjacent to active site = confirmation change = inhibition
  3. Spectrum = HIV-1
  4. Cause rash
  5. Rapid resistance w/ monotherapy
44
Q

Class properties of Protease inhibitors

A

Prevents maturation of virus (HIV-1 and 2)

Used in combination w/ RT inhibitors

Resistance develops quickly when used alone

Pharam (2 decks)

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