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Flashcards in Antiviral Agents Deck (15)
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What are the three outcomes of host cells that are virally infected?

1. Host cell is lysed (typically RNA virus-mediated i.e. influenza

2. Host cell is persistently infected = low levels of dz can be detected chronically and can recur

3. Host cell is latently infected = dz is undetectable and may recur. *These types of infections are not treatable with current antivirals


What are our primary means of viral control?

Public health measures

prophylactic vaccines


What are the 5 main stages of viral life cycle steps?

1. Viral attachment/entry/penetration
2. Uncoating (intracellular)
3. Protein synthesis and processing of virus (intracellular)
4. Packaging and assembly of virus (intracellular)
5. Viral release (intra/extracellular)


What is an endosome?

Viral hemagglutinin envelope + cell plasma membrane envelope

Viral envelope surrounded w/ hemagglutinin (extracellular) which is then endocytosed into cell and surrounded w/ cell plasma membrane


What do viral neuraminidases (NA) do?
What do NA inhibitors do?

Basically allow packaged virus at cell surface to be cleaved (i.e. released into extracellular environment)

Prevent the cleavage of viral packages at cell membrane. Also prevents entry of virus through mucin secretions of respiratory cells which reduces infection


What are some NA antivirals and how are they administered?

oseltamivir (Tamiflu) PO X 5d
zanamivir (Relenza) Inhalation BID X 5d
peramivir (Rapivab) IV single dose


What is a polymerase acidic (PA) endonuclease? Which antiviral drug is in this class?

Critical in translation of viral mRNA via "cap-snatching" mechanism. PA antivirals inhibit cap-dependent endonucleases

Xofluza (baloxavir) currently only one but,
favipiravir is under development


when do influenza antivirals need to be started?

Within first 48 hrs of symptom onset by either A or B

This decreases severity and duration by 1-2 days (80-90% effective)


How does a virus uncoat? What drugs are in this class?

Influenza A ONLY has virally encoded H+ ion channel (M2 protein) and this channel is what is blocked by antiviral drugs;
1. amantadine
2. rimantadine

*In 2014 most influenza A strains were resistant which is why we do not see this used much today


How is amantadine administered? Where does it accumulate and how is it excreted?

PO with accumulation in lungs
Kidneys as 90% unchanged drug
*Requires dosage adjustment for renal impairment


How is rimantadine excreted? Contraindications?

Hepatically eliminated
-half-life of 12 hrs i.e. 1-2 tabs daily
*Excreted in breast milk, contraindicated if breast feeding causes urinary retention, emesis, skin rash


How do viral DNA polymerase inhibitor drugs work?

1. They have 200X affinity for viral thymidine kinases (this is "on-switch" for replication)
2. Cellular (host cell) kinases convert acyclovir-MP (inactive) to acyclovir-TP making it active again
3. Acyclovir-TP also binds with greater affinity to viral DNA polymerase and is incorporated into viral DNA strands
4. These acyclovir incorporated strands stop DNA replication therefore strand elongation and these strands irreversibly bind VIRAL DNA polymerase inactivating them (suicide inactivation)


What are the names of some viral DNA polymerase inhibitors?



What are viral DNA polymerase inhibitor drugs used against?

HSV encephalitis
HSV keratoconjunctivitis (topical vidarabine and trifluridine)
Varicella Zoster Virus


Inhibitors of viral penetration drug name?

-needs to be applied in prodrome phase
-not therapeutic if applied during papular or later stages