This presentation gives you an idea about the pharmacology of Anti Viral agents.

2. Introduction
 Antiviral drugs are one class of antimicrobials.
 Antiviral drugs are a class of medication used specifically
for treating viral infections.
 These aren't used for the bacterial infections.
 Unlike most antibiotics, antiviral drugs do not destroy
their target pathogen instead, they inhibit their
development.
 Most antiviral are considered relatively harmless to the
host, and therefore can be used to treat infections.

3.  Natural anti viral are produced by some plants such as
eucalyptus and Australian tea trees.
 Most of the antiviral drugs now available are designed to
help deal with HIV, herpes viruses, the hepatitis B and C
viruses, and influenza A and B viruses.
 The viruses not only take the nutrition from the host cell
but also replicate itself in the host by using its
metabolism.
 The drugs which have been developed they target the
specific steps of the virus multiplication.

4. Virus
 The virus cannot replicate on its own
 They needs a host cell.
 It utilize the host cell energy to replicate and form
DNA , RNA, and synthesize protein.
 Viruses are difficult to kill as they live inside the host
cell.
 By killing them the host cells are also killed.

6.  The drugs which have been developed they target the
specific steps of the virus multiplication.
 The steps such as:
cell penetration,
uncoating,
reverse transcription,
virus assembly,
maturation,
release from the host cell.
 The viral replication is already reaches its peak when
the symptoms appear.
 To be effective the therapy should be started in the
incubation period (the period between the exposure
to an infection and the appearance of the first
symptoms).

8. Classification
Antiviral drugs
(Non-
retroviral)
Anti-
Hepatitis
Virus Drugs
Ribavirin
Interferon α
Sofosbuvir
Simeprevir
Declatasvir
Ledipasvir
velpatasvir
Lamivudine
Entecavir
Adefovir
dipivoxil
Tenofovir
telbivudine
Anti-
Influenza
Virus Drugs
Amatadine
Rimantadine
Oseltamivir
Zanamivir
peramivir
Anti- Herpes
Virus drugs
Idoxuridine
Trifluridine
Acyclovir
Valacyclovir
Famcicyclovir
Gancicyclovir
Valagancicyclovir
Cidofovir
foscarnet

9. Drugs
A. Acyclovir
It is an anti- herpes virus drug.
It has to react with the virus specific enzyme for its
conversion into an active metabolite.
It inhibits the DNA synthesis & viral replication.
Acyclovir
Herpes virus specific thymidine kinase
Acyclovir mono phosphate
Cellular kinases
Acyclovir tri phosphate
Inhibits herpes virus DNA gets incorporated in viral DNA
polymerase activity and stops lengthning of DNA strand.
Terminated DNA inhibits DNA
polymerase activity

10. The acyclovir is active only against herpes group of viruses.
HSV-1 , HSV-2 while CMV is not affected.
During therapy HSV and VZV have been found to develop
resistance to acyclovir.
 Pharmacokinetics:
Only about 20% of an oral plasma dose of acyclovir is absorbed.
On topical application the absorption is negligible.
It penetrates cornea well.
It is primarily excreted unchanged in urine.
Plasma t 1/2 is 2-3 hours.

11.  Uses
Genital herpes simplex
Mucocutaneous H. simplex
H. Simplex encephalitis
H. Simplex (type 1)keratitis
Herpes zoster
Chicken pox
Adverse effects
CNS: Nausea, Headache, convulsions, coma, lethargy,
hallucinations, Malaise.
Dermis: Rashes, sweating, Stinging & Burning sensation
in the skin.
Fall of BP.

12. Drug Interaction results
Acyclovir +NSAID’s Cause kidney problems
Acyclovir +Warfarin Decreases metabolism of
warfarin
Acyclovir +
Chlorotheophylline
Decrease metabolism of
chlorotheophylline
Acyclovir +Abacavir Excretion rate of Abacavir
decreased.

13. B. Gancicyclovir
It is the analogue of acyclovir which is most active against CMV.
It also inhibits other herpes viruses.
Due to poor oral absorption, bioavailability it is very low(<10%).
{Its prodrug is valgancicyclovir which is better absorbed orally. 60%
bioavailability orally}
The plasma t1/2 of gancicyclovir is 2-4 hrs.
It is mostly excreted unchanged in the urine.
Its systemic toxicity is high.
This may cause serious adverse effects like- depression, rash, fever, vomiting,
neuro psychiatric disturbances.

14. Drug Interaction result
Gancicyclovir + Zidovudine Potentiate myelosuppresion
Gancicyclovir + Cyclosporin May promote nephrotoxicity
Gancicyclovir + Didanosine Increase levels of didanosine
Gancicyclovir + Probenecid Increase levels of gancicyclovir in
serum

15. Mechanism of action
Ganciclovir triphosphate is a competitive inhibitor of
deoxyguanosine triphosphate (dGTP)
Incorporation into DNA and preferentially inhibits viral
DNA polymerases more than cellular DNA polymerases.
It serves as a poor substrate for chain elongation,
thereby disrupting viral DNA synthesis.

16. Anti herpes virus drug.
First pyrimidine metabolite to be used as antiviral drug.
It was synthesized by William Prusoff in the late 1950s.
It is used only topically due to cardio-toxicity.
It enters the viral DNA to break it.
C. Idoxuridine

17. D. Amantadine
It is an anti- influenza virus drug.
Available in the form of hydrochloride salt (amantadine
hydrochloride).
This medication used to treat dyskinesia associated
with parkinsonism and influenza caused by type A
influenza virus.
MOA : It acts by inhibiting the viral M2 protein and
prevents the uncoating of the viral genome within the
infected cell.

18. E. Ribavirin
Ribavirin, also known as tribavirin.
It has broad range anti viral activity.
It acts against HCV, Influenza A & B and many other DNA and
double stranded RNA viruses.
Its oral bioavailability is 50%.
It is partly metabolized and eliminated mainly by the kidney.
It accumulates in the body on daily dosing and persists for month
after discontinuation.
Long term half life is >10 days.
The most common therapeutic use of oral Ribavirin is in chronic
hepatitis C.

19.  Mechanism Of Action:
It is a guanosine (ribonucleic) analogue used to stop viral
RNA synthesis and viral mRNA capping.
Ribavirin is a prodrug.
which when metabolized resembles purine RNA
nucleotides.
In this form, it interferes with RNA metabolism required
for viral replication.

20. F. Interferon
α and β interferon are released by all the cells against the
viral infections.
Interferon inhibit many RNA and DNA viruses.
Interferon receptors are JAK-STAT tyrosine protein kinase
receptors.
After i.m. or s.c. injection, interferon is distributed into the
tissues
It is degraded in the kidney and to some extent in liver.
It remains detectable in the plasma for <24 hrs.
IFN are administered thrice a week.

21. Uses
Chronic hepatitis B.
Chronic hepatitis C.
AIDS related Kaposi's sarcoma
H.Simplex , H. zoster
Follicular lymphoma, chronic myeloid leukemia.
Adverse effects
Flu like symptoms: fatigue, aches, pains, fever, dizziness, anorexia,
visual disturbances, nausea.
Neurotoxicity : numbness, neuropathy, altered behavior, mental
depression, sleepiness, rarely convulsions.
Thyroid dysfunction.
Hypotension, arrhythmias, alopecia and reversible liver
dysfunction.