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MD3001resp > mechanism of antiviral drugs > Flashcards

mechanism of antiviral drugs Flashcards

1
Q

what are the main viruses one that’s effects the brain?

A

HSV
HIV

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2
Q

what are the main viruses that effects the mouth?

A

HSV

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3
Q

what are the main viruses that effects the liver?

A

Hepatitis B and C
CMV

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4
Q

3 aims of therapy for anti-virals?

A

viral eradication = hepatitis C and influenza

long term suppression = HIV and hepatitis B

management of flares/reactiveness of disease = herpesviruses

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5
Q

what are viruses

A

sub microscopic infectious agents (80-1400 nm)

  • they are obligate parasites = this means that they fully rely on the metabolic processes of host cells
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6
Q

how do we classify viruses?

A
  • route of transmission (arbovirus= viruses by insects)
  • the disease they cause
  • size/shape
  • appearance of the capsid
  • presence or absence of a lipid environment.
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7
Q

what is the Baltimore classification system?

A

based on the mechanism of mRNA production

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8
Q

Baltimore classification of system:

what are retroviruses?

what do DNA viruses require?

A

they are ‘reverse transcribed’ to DNA and integrated to the host genome.

DNA viruses transcription.

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9
Q

Baltimore classification system:

what is the positive sense RNA virus?

what are tiger negative sense RNA virus?

A

positive = contain RNA in 5’-3’ orientation which can be directly used as mRNA for translation into proteins.

negative= contain RNA in 3’-5’orientation which requires conversion to 5-3’ before translation into proteins.

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10
Q

what is an example of:
I
II
III

A

I = ds-DNA = adenovirus, Herpes virus

II= ss-DNA = parvoviruses

III = ds-RNA = reoviruses

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11
Q

what is an example of:
IV
V

A

IV= +ss RNA
V= - ss RNA

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12
Q

WHAT are the 3 main mechanisms of action of anti-viral therapy?

A

-Virucides
- Anti viral drugs
- immunomodulators

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13
Q

mechanisms of actions of the anti-viral therapy?

A

virucides= detergents, organic solvents, UV light

Antiviral drugs = inneffective vs non replicating /latent virus

immunomodulators = it will replace the deficient host immune response, enhance the endogeous response (reduces the harmful host immune response)

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14
Q

what stage does the antiviral drugs hat are the 8 stages of viral life cycle?

at which pint does antiviral drugs target?

A

1) attachment
2) penetration
3) disassembly
4) transcription
5) translation
6) replication
7) assembly
8) release

they can target any of these stage.

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15
Q

what is special about positive ssRNA viruses?

A

they don’t need to be transcribed - they can undergo direct translation in the host cell cytoplasm.

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16
Q

how do nucleoside analogues work as antiviral drugs?

how is this done?

A
  • these prevent viral replication by interfering with nucleic acid replication, transcription and translation
  • this is done using ‘analogue’ compounds which compete with essential nucleotides for binding sites
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17
Q

what is given to treat Herpes Simplex virus DNA replication?

A

acyclovir
- this will swap guanosine which acyclovir to bind with cytosine on the nucleotide chain.

  • this prevents the reading of th viral DNA= can’t transcribe.
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18
Q

what are the 4 considerations for antiviral therapy?

A
  • effectiveness and aim of therapy
  • toxicity and side effects
  • drug/drug interactions
  • emergencies of resistance
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19
Q

what does antiviral drug resistance result from?

A
  • resistance result from mutation within viral genomes
  • there is selective drug pressure = resistant viral population
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20
Q

what is the development of resistance favour by?

A
  • development of resiatnce favoured by:
  • high viral load
  • high intrinsic viral mutation rate
  • degree of selective pressure
  • resistance barrier of drug class/ individual agent
  • antiviral target that can mutate without effecting fitness
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21
Q

basic virology of HIV:

-what type of virus is it?
- what does it contain?
- where is the integrated?
- what will it be transcribed into?
- what will the CD4 cell be killed by?

A
  • it is a (+)ss RNA-RT retroviruses
  • contains reverse transcriptase - an RNA dependant DNA polymerase, which makes a copy of the viral RNA
  • the DNA copy is integrated into the genome of the host cell (often CD4 cells)
  • this provirus DNA is transcribed into both new genomic RNA and mRNA for translation into viral proteins using the host cell machinery.

CD4 cell are killed by invading virus and host becomes dangerously immune suppressed.

over time HIV will kill out white blood cells, immune system weakens, this makes you more susceptible to other infections.

22
Q

HIV:
history and clinical summery

what is the main rout of transmission?

what is the prevalence?

A

main route of transmission= sexual, parenteral, vertical

around 38 million people currently live with hIV

23
Q

HIV:
What parts of the viral life cycle with hIV drugs taregt?

A
  • blocks cell entry using
  • blocks RNA -> DNA (targeting reverse transcriptase)
  • blocks integration of provirus DNA into the host genome (targets integrase)
  • blocks the cleavage initially translates polypeptides into functional viral proteins (targeting proteases )
24
Q

what are the 2 classes of reverse transcriptase inhibitors?

what part of the cycle are they blocking?

A
  • they are blocking RNA -> DNA

1) nucleoside reverse transcriptase inhibitors NRTI’s
2) non nucleotide reverse transcriptase inhibitors NNRTI’s

25
Q

action of NRTI’S

A

nuceoside analogues which compete with reverse transcription preventing viral pro-DNA synthesis

  • also effects host cell DNA synthesis causing toxicity.
26
Q

what are the main drugs in NRTI’S?

A
  • tenofovir (analogue of adenosine)
  • lamivudine (analogue of cytosine)
27
Q

mechanism of action of NNRTI’S?

A

these are drugs which directly bind to RT causing conformational change. which stops the enzyme from working.

28
Q

example of drugs of nnrti’S?

A
  • EFAVIRENZ
  • it is well tolerated but sometimes causes a neuro-psychiatric side effects
  • low barrier to generation resistance.
29
Q

action of HIV integrase … action of the integrase inhibitor

A

HIV integrase mediates two critical reactions which allow viral DNA to join with host chromosomal DNA

(stops the viral DNA from integrating with the host chromosome DNA)

30
Q

main drugs in use as INTEGGRASE INHIBITORS?

A
  • dolutegravir
31
Q

action of proteases… protease inhibitors?

A
  • cleaves long polypeptides into essential proteins for viral muturation
  • does not occur in the host, so a good selective toxicity target.
32
Q

examples of PI?

side effects?

A
  • Darunavir
  • high barrier to resistance, drug interactions are frequent
  • diarrhoea is common.
33
Q

describe antiviral therapy?

A

typically give 3 drugs: often 2 NRTI’s and an additional drug from another class (NNRT, PI or integrase inhibitor)

more recently consideration of fear drugs from newer, more effective drug classes.

34
Q

when should people be put on antivirals?

A
  • previously doctors waited to put patients on antivirals when they has a low CD4 count.
  • but now, early ART initiation improves long term outcomes.
35
Q

long term adverse effects of NRTI drugs

Abacavir?
Tenofovir?

A

Abacavir = ischamic heart disease

tenofovir =
- decreased bone density, osteomalacia, increased risk of fracture
- decreased glomerular filtration, Fanconi syndrome.

36
Q

long term adverse effects of NNRTI drugs:

Efavirenz

A

depression, sleep disturbance, headache, suicidal thoughts

37
Q

long term adverse effects of PI drug:

Darunavir
Lopinavir

A

Darunavir = ischeamic heart disease

lopinavir = incheamic heart disease

38
Q

long term adverse effects of INSTI drugs:

Dolutegravir

A

weight gain

39
Q

Hepatitis C:
what family of viruses is it from?
what type of virus is it?
how is it transmitted?
what will it cause?

A
  • it is from the Flaviviridae family
  • (+) ss RNA virus
  • primarily transmitted through parenteral rotate, sexual transmission
  • causes acute and chronic hepatitis, cirrhosis and hepatocellular carcinoma.
40
Q

what type of virus id Hepatitis B?
what is it structure?
how does replication occur?

what does it cause?

A

1- hepatitis B virus is a HepaDNA virus

dsDNA virus, genome maintained on circular confirmation.

  • replication will occur by RNA intermediates
41
Q

what are the 2 treatments for chronic HBV?

A

1) immunomodulatory - pegylated IFNa

2) nucleoside therapies

42
Q
A
43
Q

what will aciclovir be used against?

A

HSV-1
HSV-2
VZV

44
Q

what other 3 other herpesvirus antivirals?

A

1) valaciclovir
2) ganciclovir/valganciclovir
3) Foscarnet

45
Q

valaciclovir

A

prodrug of aciclovir (has a high oral bioavailability)

46
Q

ganciclovir/ valganciclovir

A

= deoxyguanosine analogue (differes from aciclovir in its additional hydromethyl group on the side chain)

  • potent inhibitor of CMV replication

side effects = myelosupression, CN toxicity

47
Q

foscarnet

A

directly inhibited herpesvirus DNA polymerase or HIV RT

side effects = nephrotoxicity, electrolyte abnormalities

48
Q

influenza:
what type of virus is it?

what are the different types?

what does are examples of its varying severity?

who is at high risk

A
  • it is enveloped - ssRNA virus
  • there are 3 distinct types: A, B and C
  • seasonal epidemics and sporadic pandemics
  • mild coryza= life threatening pneumonia
  • elderly and immune comprised are at high risk
49
Q

describe the action of neuraminidase and neuraminidase inhibitors?

what are examples?

A

NA= cleaves a silica acid receptor on host cell enabling viral release

NA inhibitor = competitively bind the NA binding site, preventing viral release

eg) - oseltamavir = oral
zanamavir = inhalation

50
Q

SARS-CoV-2:
what type of virus is it?
what does it look like?
management?

A

(+) ssRNA cirus
- it has 4 structural proteins
- spike protein facilitates host cell entry via ACE2 receptor
- nucleocapsid protein contains viral genome

  • oxygen and ventilatory support is key in severe disease
51
Q

3 approaches to treatment of covid?

A
  • antivirals
  • anti-inflammatories (dexamethasone)
  • antibody treatment

MD3001resp (41 decks)

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