Antiviral drugs work by targeting specific parts of the viral replication cycle using mechanisms like inhibiting viral enzymes or incorporating into viral DNA to stop replication. They are classified based on the virus or viral enzyme they target, such as anti-herpes drugs like acyclovir that inhibit viral DNA polymerase, or anti-HIV drugs that include reverse transcriptase inhibitors, protease inhibitors, and integrase inhibitors. Developing effective antiviral drugs is challenging because viruses replicate inside cells and mutate rapidly, so they must target virus-specific processes without harming host cells.

1. Antiviral Drugs
Aasifa S
Sem2 Mpharmacology
SSR COLLEGE OF PHARMACY

2. Virus
Viruses have no cell wall and made up of nucleic acid components
They do not have a metabolic machinery of their own – uses host enzymes
Certain viruses multiply in the cytoplasm but others do in the nucleus
Most multiplication take place before diagnosis is made

3. Antiviral drug
Many antiviral drugs are Purine or Pyrimidine analogues.
Many antiviral drugs are Prodrugs.
o They must be phosphorylated by viral or cellular enzymes in order to become active.
Anti-viral agents inhibits active replication so the viral growth resumes after drug removal

4. Difficulties in production of Antiviral agents
Viruses live within human cell and they use process of these cells to multiply so they’re not readily
accessible
Have very sophisticated structures and not easy to kill
Before patient develop symptoms the virus have been duplicated already
Mutate rapidly and change they're defenses and shape.

5. Classification of antiviral drugs
A. ANTI-HERPES VIRUS AGENTS – Acyclovir, Ganciclovir, Valganciclovir
B. ANTI-INFLUENZA AGENTS- Amantadine, Rimantadine
C. ANTI-HEPATITIS VIRUS DRUGS-
a) Primarily for Hepatitis B - Lamivudine
b) Primarily for Hepatitis C - Ribavirin

6. D. ANTI-RETROVIRAL DRUGS-
a) Nucleoside reverse transcriptase inhibitors (NRTIs)-Zidovudine, Lamivudine
b) Non-nucleoside RTI (NNRTIs)- Nevirapine,
c) Protease Inhibitors (-navir)- Ritonavir, Lopinavir

7. E. Entry (fusion) inhibitors – Enfuvirtide
F. CCR5 ( Chemokine) receptor inhibitor- Maraviroc
G. Integrase inhibitors- Raltegravir

9. A- ANTI-HERPES VIRUS AGENTS

10. 1- Acyclovir (zovirax*)
[HSV and Chickenpox]
• Purine analogue
Mechanism of action
 inhibits the activity of viral DNA polymerase.
Effective against herpes viruses, once it entre the infected cell it changes to a powerful antiviral
agent.

11. Mechanism of action

12. How come it doesn’t work in some
cases?
• Deficient viral thymidine-kinase
• Mutations to viral thymidine-kinase or DNA polymerase

13. In what preparations do they
exist?
 Zovirax 3% ointment for 5 days to treat ulceration of cornea due to herpes simplex virus.
I.V for generalized herpes simplex infection.
Also prescribed in herpes zoster for 7 days it should be started within 48 hours from the onset of
symptoms.
Eg- 2-Famciclocir and valaciclovir: • Given 2-3 times daily.

14. Orally 5 times daily to treat genital herpes.
Tablet Acyclovir 200 mg / 400 mg

15. Which virus does it attack?
Herpes-simplex 1
Herpes-simplex 2
Varicella-zoster virus Most activity
Epstein-Barr virus
Cytomegalovirus

16. 2- Ganciclovir
• Synthetic guanosine analogue
• First antiviral approved for CMV treatment
• Mechanism of action: Similar to acyclovir
Mechanism of resistance:
Mutation of viral phosphokinase and/or viral DNA polymerase

18. When do we use Ganciclovir?
• 1. Herpes Epithelial Keratitis - Ganciclovir Gel 0.15% (Zirgan)
• 2. CMV Retinitis
• Initial: IV 5mg/kg BD for 14-21 days
• Maintenance:
IV 5mg/kg OD or
IV 6 mg/kg OD for 5 days/week

19. In what preparation do they exist
• Zirgan ointment 0.15% - ophthalmic gel
• Cytovene 500 mg

20. B- ANTI-INFLUENZA AGENTS

21. 1. Amantadine and rimantadine
Mechanism of action
inhibit the uncoating and replication of the viral RNA in infected cells.
Due to interruption function of the M2 protein, the drugs inhibit the acid (H+)-mediated dissociation of the
ribonucleoprotein (RNP) complex early in the process of replication.

22. • Treat influenza A infections when administered within the first 48 hours of symptoms
• For Prophylaxis during flu season
When do we use?

23. C -ANTI-HEPATITIS VIRUS DRUGS

24. Primarily for Hepatitis C -
Ribavirin
Prodrug, guanosine analogue , nucleoside inhibitor.
Mechanism of action
inhibit viral RNA polymerases and
interferes with RNA metabolism required for viral replication..

25. • Treat respiratory syncytial virus (RSV)
• Treat influenza A and B.
• HCV , HBV in combination with Interferon alpha
When do we use Ribavirin?

27. D - ANTI-RETROVIRAL DRUGS

28. a) Nucleoside analogues inhibitors(NRTI)
Eg : zidovudine, lamivudine
Acting as "false building blocks“, nucleoside analogues incorporate themselves, preventing DNA synthesis,
because normal bridges can no longer be built to build the double strand.
Thus they prevent the development of functional viral DNA

30. b) Non-nucleoside analogues
inhibitors(NNRTI):
Eg: Nevirapine,
• NNRTIs attach directly to the reverse transcriptase enzyme.
• Production of viral DNA from RNA is blocked
• Virus is unable to convert RNA into DNA, therefore unable to infect the cell and produce new virus
• Enzyme with NNRTI attached cannot function normally

32. c) Protease inhibitors
Eg: Ritonavir, Lopinavir
Mechanism of action
o Infected cell produces large viral proteins (polyproteins)
o Protease enzyme cleaves polyproteins into enzymes and structural proteins required to make new virus
o Protease inhibitors attach to and block protease enzyme
o The virus particles produced are defective and inactive and are unable to infect new cells

34. Eg: Enfuvirtide
Mechanism of action:
Competes with the gp41 subunit of the HIV-1 viral envelope and prevents fusion to the cell membrane CD4
receptors.
E- Fusion receptor protein
inhibitors

35. F- Integrase inhibitors-
Raltegravir.
Eg: Raltegravir
Mechanism of action :
• inhibit the viral enzyme integrase to prevent HIV replication and
viral integration into the host cell.

36. Overview - Life cycle Of HIV

37. Conclusion
• Selective toxicity for antiviral agents is achieved by targeting viral enzymes and virus specific steps
• Anti-viral agents are broadly classified into four groups depending upon their activity on viruses
• Idoxuridine and trifluridine are used only topically
• Variation in the sensitivity of anti-herpes agents to herpes family viruses is well recognised