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Yr3 CSP > Anti-Viral Therapy, September 8th > Flashcards

Anti-Viral Therapy, September 8th Flashcards

1
Q

Generally, how do Anti-virals work?

A

Some work by blocking the Ligand-Receptor binding

Done by either binding to the Ligand or the Receptor

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2
Q

Where can drugs interfere with the Viral Lifecycle

A
  1. Membrane Fusion
  2. DNA/RNA Replication
  3. Integrating DNA into Genome
  4. Translating Viral RNA to Proteins (Not always)
  5. Assembly/Maturation of Virions
  6. Escape from Host Cell
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3
Q

What diseases is Aciclovir effective against?

A

Herpes Simplex 1/2

Herpes Zoster

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4
Q

What is the composition of Aciclovir?

A 
Guanosine Analogue (Acyclo-Guanosine)
Partial Nucleoside Analogue
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5
Q

What is the MOA of Aciclovir?

A
  1. Converted by Viral Thymidine Kinase to Monophosphate Acyclo-GMP
  2. Converted to Triphosphate using a Cellular Enzyme
  3. Inhibits action of Viral DNAP by terminating chains
  4. High Therapeutic Ratio (Viral TK is 3000x more effective at converting A-G to Monophosphate, and Viral DNAP is better at incorporating Triphosphate into Growing DNA chain than Cellular DNAP)
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6
Q

How is Aciclovir/Valaciclovir administered?

A

Topically (To Cold Sores/Eyes)
Orally
IV

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7
Q

What are the main side effects of Aciclovir/Valaciclovir?

A

Psychiatric (Cotard’s Syndrome)

Toxicity in overdose (Lethargy, Confusion, Myoclonus)

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8
Q

How does Valaciclovir compare to Acyclovir?

A

Valaciclovir is Acyclovir that is ESTER-LINKED to Valine

Thus, Greater Oral Bioavailability

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9
Q

Why do viruses grow resistant to Aciclovir/Valaciclovir

A

Mutation of Viral Thymidine Kinase/DNAP

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10
Q

What is Idoxuridine?

A

NucleoSide Analogue

Modified form of Deoxyuridine containing Iodine

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11
Q

When is Idoxuridine used?

A

Topically for Herpes Keratitis

Too toxic for Systemic Use

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12
Q

What can Ganciclovir and Valganciclovir kill?

A

CMV

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13
Q

What is Ganciclovir made up of?

A

Synthetic Analogue of Deoxyguanine

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14
Q

What is the MOA of Ganciclovir?

A
  1. Phosphorylated to Monophosphate by CMV Thymidine Kinase
  2. Then made into Triphosphate by Cellular Kinases
  3. Inhibits Viral DNAP more than Cell DNAP
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15
Q

What is Valganciclovir compared to Ganciclovir?

A

Valganciclovir is a VALINE Ester with Greater Oral Bioavailability

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16
Q

What are the main side effects of Val/Ganciclovir

A

BM Suppression

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17
Q

What is Foscarnet?

A

Pyrophosphate Analogue

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18
Q

What is the MOA of Foscarnet?

A

Blocks Viral DNAP

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19
Q

What is Foscarnet used for?

A

Herpes Simplex Virus 1/2
Herpes Zoster
CMV (Especially Retinitis as an Intravitreous Injection, it can also be as an IV injection)

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20
Q

What are the main side effects of Foscarnet?

A
  1. Nephrotoxicity
  2. Electrolyte Disturbances (CaMg)
  3. Genital Ulceration
  4. CNS issues (Parasthesia, Irritability, Hallucinations)
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21
Q

What is Cidofovir used against?

A

DNA Viruses

  1. Herpes
  2. Papilloma
  3. Adenoviruses
  4. Poxviruses
  5. MOSTLY CMV
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22
Q

What is the MOA of Cidofovir?

A

Blocks Viral DNAP

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23
Q

What are the Adverse effects of Cidofovir?

A
  1. GI
  2. Haematological
  3. Iritis
  4. Headache
  5. Weakness
  6. Hair Loss
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24
Q

What is the MOA of Trifluridine?

A

Nucleoside Analogue from modified Deoxyuridine

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25
Q

What does Trifluridine kill?

A

Herpes Simplex

Zoster Keratitis

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26
Q

What are the adverse effects of Trifluridine?

A

Burning

Stinging Oedema

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27
Q

What is the MOA of Vidarabine?

A

Adenosine Analogue with Different sugar needing Triple Phosphorylation

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28
Q

What is Vidarabine used for?

A

Herpes Simplex

Herpes Zoster

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29
Q

What are the adverse effects of Vidarabine?

A

GI
Leukopenia
Thrombocytopenia

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30
Q

What drugs are generally effective against Retroviruses?

A

Reverse Transcriptase Inhibitors

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31
Q

What are the different types/analogues of RTI

A

Nucleoside and Nucleotide Analogues

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32
Q

What is the function of the NRTI analogues?

A

They inhibit Reverse Transcriptase by incorporating themselves into the growing DNA chain

This stops a linkage to the subsequent base

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33
Q

What are NucleoSide analogues?

A

They are molecules with a Ribose sugar and Base

Requires Three Phosphorylations to incorporate it

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34
Q

What are examples of NucleoSide analogues?

A

Lamivudine (Hep B)
Abacovir and Emtricitabine (first line)
Zidovudine (second line)

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35
Q

What are the side effects of Lamivudine?

A 
Nausea
Fatigue
Headaches
Diarrhoea
Cough
Pro-inflammatory response
Autoimmunity
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36
Q

What are examples of NucleoTide analogues?

A

Tenofovir (HepB) and Adefovir

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37
Q

What are the side effects of Tenofovir?

A

Renal Insufficiency

Fanconi syndrome

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38
Q

What is Fanconi Syndrome?

A

Condition where normally absorbed products are excreted in urine

39
Q

What is the MOA of NNRTIs?

A

They bind to RT away from the active site

Hampering its effect via distortion

40
Q

What are the first-line choices of NNRTIs?

A

Efavirenz and Rilpivirine

41
Q

What are the other less favourable NNRTIs?

A

Etravirine (Can cause CNS toxicity) and Doravirine

Nevirapine has more serious effects

42
Q

What is the MOA of PIs?

A

Bind to Viral Proteases responsible for the viral precursor proteins that usually make up Virions

43
Q

What are the main PIs?

A

Darunavir and Ritonavir

44
Q

What suffix underlies all Integrase Inhibitor drugs?

A

-tegraVir

45
Q

What suffix underlies most NNRTI drugs?

A

-INE or -VIRINE except Efavirenz

46
Q

What suffix underlies most HCV PI drugs?

A

-preVir

47
Q

What suffix underlies most NS5A inhibitor drugs?

A

-asVir

48
Q

What suffix underlies most NS5B drugs?

A

-buVir

49
Q

What suffix underlies most NRTI drugs?

A

-INE except Abacavir

50
Q

What two drugs make up Truvada?

A

Tenofovir and Emtricitabine

51
Q

What is the MOA of Integrase Inhibitors?

A

Inhibits Integrase which usually mediates integration of the HIV DNA (made by Reverse transcription) into the host genome

52
Q

What are some examples of Integrase Inhibitors?

A

Raltegravir
Dolutegravir
Bictegravir

53
Q

What is the MOA of Fusion Inhibitors?

A

Blocking GP41 on the surface of HIV Virions

GP41 usually mediates fusion between HIV envelope and Cell membrane?

54
Q

What is an example of Fusion Inhibitors

A

Enfuvirtide

55
Q

What is the MOA of Entry Inhibitors?

A

Blocking CCR5 on the Cell surface

Together with CD4 can enable GP120 to bind to HIV and allow Cellular entry

56
Q

What is an example of Entry Inhibitors?

A

Maraviroc

57
Q

What is the usual combination of Anti-retroviral therapies?

A

Two NRTI + something else

  1. Tenofovir + Emtricitabine
  2. Abacovir + Lamivudine

Either of these PLUS a Third

  • *3. Integrase Inhibitor (Raltegravir)
    4. Protease Inhibitor (Darunavir)
    5. NNRTI (Doravirine, Rilpivirine
58
Q

For Anti-retroviral therapy, what do you use if you cannot use Tenofovir or Abacovir?

A

Usually a combination of:

  1. Integrase + Protease
  2. Integrase + Lamivudine
  3. Boosted Protease + Lamivudine
59
Q

When is PrEP given?

A

To people with sexual practices that could expose them to HIV

Truvada into a single daily pill

60
Q

What do you do during a Post-exposure to body fluids/needlestick injury?

A

Wash with antiseptic/fluid on part

Truvada combo + Dolutegravir/Raltegravir for TWENTY EIGHT DAYS

61
Q

What is Ribavirin?

A

Guanosine Analogue

62
Q

What can Ribavirin do?

A

Inhibits Viral RNA-dependent RNAP

Incorporates to new RNA chain and terminates it

63
Q

What is Ribavirin effective against?

A 
Hepatitic C
Viral Haemorrhagic Fever
RSV
Flu (Sometimes)
Herpes (Mystery but true)
64
Q

What are the adverse effects of Ribavirin?

A

Haemolytic Anaemia
BM Suppression
Psychiatric effects (Depression)
Cough

65
Q

What are the main classes of drugs to treat Influenza?

A
  1. Neuraminidase Inhibitors
  2. M2 Inhibitors
  3. Ribavirin
66
Q

What does Neuraminidase do and how do Neuraminidase Inhibitors stop this?

A
  1. Viral Neuominidase cleaves Sialic Acid from Glycoprotein
  2. This will release Virions from the host
  3. Virions will stop aggregating
  4. Reduction of inactivation of Virions by Host mucus
  • NI will stop all of this lol
67
Q

What are examples of Neuraminidase Inhibitors?

A

OseltAMIVIR

ZanAMIVIR

68
Q

What is the suffix that underlies Neuraminidase inhibitors

A

-AMIVIR

69
Q

What is the MOA of M2 Inhibitors?

A

Inhibits M2 protein of the Virus from decreasing H+ influx

This will STOP uncoating/recoating

70
Q

What are the main drugs of the M2 Inhibitor class?

A

Amantidine

Rimantidine (Less neuro side effects)

71
Q

What is the suffix that underlies M2 inhibitors?

A

-TIDINE

72
Q

What drugs do we usually use to treat Hepatitis C?

A 
Ribavirin
Pegylated IFN (Though usually B)
73
Q

What is Pegylated IFN?

A

Alpha or Beta
Cytokines enhancing immune response

Pegylated so they are linked to Polyethylene-Glycol to prolong Half Life

Given by Injection

74
Q

What are the side effects of Pegylated IFN?

A

Malaise

Fever

75
Q

What are the new Treatments for Hepatitis C?

A 
Direct Acting Agents (DAAs)
-------------------------------
Protease Inhibitors
NS (Non-structural) inhibitors
- NS5A, NS5B
76
Q

Give examples for Protease Inhibitors against Hepatitis C

A

Glecaprevir
Grazoprevir
Tenofovir (Not active against Hep C Protease but boosts the drugs via blocking metabolism)

77
Q

What is the function of Protease inhibitors?

A

Inhibition of Viral NS3/4A serine protease

78
Q

What is the function of NS5A inhibitors?

A

Inhibits NS5A which is a viral protein promoting Assembly

79
Q

Give examples of NS5A inhibitor drugs

A

Daclatasvir
Elbeasvir
Ledipasvir

80
Q

What is the function of NS5B inhibitors?

A

Inhibits NS5B which is a viral RNA-dependent RNA polymerase

81
Q

Give examples of NS5B inhibitors

A

Sofosbuvir (NucleoT/Side analogue)

Dasabuvir (Non-NucleoT/Side analogue)

82
Q

Can Hepatitis C be cured?

A

Yes

It is an RNA virus so it cannot integrate itself into the genome

83
Q

What is SVR?

A

Relating to Hep C, Cure

After Antiretroviral therapy, it is defined as the presence of no HCV RNA in the blood after 6 months

84
Q

When do we typically give Ribavirin for Hep C cases?

A

When first line fails

85
Q

How many different genotypes of Hep C are there?

A

6 (1 and 3 are the most common)

86
Q

What is the main disadvantage of DAA

A

Expensive and takes a 12 week course

87
Q

When considering elimination therapy for Hep C, what must you consider?

A
  1. Liver damage? (Cirrhosis/Fibrosis/Carcinoma)
  2. Transplant or Consideration?
  3. Manifestations OUTSIDE Liver (Cryoglobulinemia, Glomulonephritis)
  4. Positive for HepB/HIV
  5. Alcohol/Recreational Drugs
  6. Which Genotype
  7. Previous failed treatment with other drugs?
88
Q

What types of drug types are commonly used to treat against Hep B?

A

RTIs (Lamivudine and Tenofovir)

Interferon (Peg IFN)

89
Q

What is Hepatitis B?

A

Hepadnavirus: DNA virus using RT to integrate its genome into host cell cycles

90
Q

What is the big issue regarding Hep B for relapsing?

A

Patients with both Hep B and C whilst being treated for C may cause relapsing of Hep B

91
Q

How is RSV usually treated?

A

Palivizumab: mAb against RSV Fusion glycoprotein

Ribavirine via inhalation

92
Q

How is Ebola usually treated?

A

mAb blocking the docking

93
Q

How is Coronavirus generally treated?

A

Remdesavir: Inhibitor of RNA-dependent RNAP

Yr3 CSP (4 decks)

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