Antiviral drugs are a class of medication used for treating viral infections. Most antivirals target specific viruses, while a broad-spectrum antiviral is effective against a wide range of viruses. Unlike most antibiotics, antiviral drugs do not destroy their target pathogen; instead they inhibit its development.

1. ANTIVIRAL
DRUGS
PRESENTED BY-
DR. BRATATI DEY
DEPT. OF OMR

2. CONTENTS
⁎ Introduction to virus
⁎ History
⁎ Classification
⁎ Mode of action
⁎ Pharmacokinetics
⁎ Uses
⁎ Doses
⁎ Adverse effect
⁎ Infection caused by virus
⁎ Conclusion
⁎ References

3. INTRODUCTION
⁂ Viruses have been defined as
submicroscopic entities
which reproduce within the
specific living cells.
⁂ Virus may contain either
ribonucleic acid (RNA) or
deoxyribonucleic acid
(DNA)

4. INTRODUCTION
⁂ Viruses are the ultimate expression of
parasitism.
⁂ They not only take nutrition from the host
cell, but also direct its machinery to
synthesize new virus particle.
⁂ In majority of acute infections viral
replication is already at its peak when
symptoms appear.
⁂ To be effective, therefore, therapy has to
be started in the incubation period, i.e. has
to be prophylactic.

6. HISTORY
From 1972 to date, >50 new viruses have been found as etiologic
agents of disease.
However, it took almost 60 years for antiviral development to reach
its current status of effectiveness.
In 1967, Kates and McAuslan described the first viral enzyme, pox
virus DNA-dependent RNA polymerase.

7. HISTORY
➢ In 1963, Iododeoxyuridine,
described earlier by Prusoff had
been shown to be active against
herpes simplex.
➢ Secondly, amantadine had been
shown not only to inhibit
influenza virus, but also to cause
resistance development.
➢ Finally, interferon were
extensively discussed as potential
antiviral drugs against several
viral infections.

8. HISTORY
➢ The field of antiviral drugs grew rapidly in the
herpes area with the development of acyclovir
(Schaffer et al., 1978) and other inhibitors.
➢ Development of drugs against hepatitis B virus
(HBV) has been successful and there is a large
effort to discover drugs against hepatitis C
virus.

9. CLASSIFICATION
Anti-herpes virus
Acyclovir, Famcyclovir
gancyclovir
Anti-retrovirus
Nucleoside reverse transcriptase
inhibitor
Zidovudine, Lamivudine, Abacavir
Nonnucleoside reverse
transcriptase inhibitors
Nevirapine
Protease inhibitors
Ritonavir, Indinavir
Anti influenza
virus
Amantadine
Nonselective
antiviral
Interferon α

10. Mechanism
Of Action Of
Antiviral
Drugs

11. ANTIHERPES VIRUS
Acyclovir
➢ It requires a viral specific enzyme for conversion to the active
metabolite that inhibit DNA synthesis.
Acyclovir
Herpes virus specific thymine kinase
Acyclovir monophosphate
Cellular kinase
Acyclovir Triphosphate
Inhibit herpes virus DNA
polymerase completely.
Gets incorporated in viral
DNA and stops lengthening of
DNA strand. The terminate
DNA inhibit DNA polymerase
irreversibly.

12. Mode of
action of
Acyclovir

13. • Acyclovir active against
H. simplex Type I
Herpes simplex type II
Varicella Zoster
Epstein-barr Virus
CytomegaloVirus (CMV)

14. Pharmacokinetics
➢ Only 20% of oral dose of acyclovir is
absorbed.
➢ Little plasma protein bound, and widely
distributed attending CSF conc. 50% of
plasma conc.
➢ It penetrate cornea well.
➢ Excreted in urine.
➢ Plasma t1/2 2-3hours.

15. Available as

16. Uses
Acyclovir is effective in patient with normal as well as
deficient immune status.
1. Genital Herpes simplex can be treated by topical, oral, or
parenteral acyclovir.
Primary disease Recurrent Disease Severe cases
5% ointment locally 6 times a
day for10 days. (effective only
in mild cases)
Late and more severe cases
should receive oral therapy
(1g/day in 5 divided dose).
Topical therapy is totally
ineffective.
Response to oral treatment is
slow & incomplete.
Treated parenterally 5mg/kg iv
infused 1 hour repeated 8 hourly
for 10 days.
Suppressive oral therapy with
200mg 4 times a day(later TDS
or even BD).
It is recommended to stop treatment after 1 year.

17. Uses
• Mucocutaneous Herpes
simplex- It is a type 1 virus
disease remain localize to lips
and gums. May be treated with
10 day oral acyclovir (200mg 5
times/ day).
• Chicken pox- Patient with
immunodeficiency and
neonates calls for specific
therapy.
Dose- Acyclovir 15mg/kg/day
i.v. for 7days.

18. Uses
Herpes simplex encephalitis (
type I virus)
Treatment –
10 mg/kg 8 hourly iv for 10
days. treatment is effective if
started early.
Herpes Zoster- Acyclovir
should be used only in
immunodeficient individuals
or in severe cases.
Dose –
5 mg/kg 8 hourly i.v. for 7
days. Early started oral
therapy is also beneficial.
complication- post herpetic
neuralgia

19. Adverse Effect
1. Topical- stinging and burning sensation
after each application.
2. Oral- well tolerated, headache, nausea,
malaise and some CNS effect.
3. Intravenous- rashes, sweating, fall in BP
occurs only in few patient.
4. Decrease in g.f.r is most dependent
toxicity.
5. Reversible neurological disturbances.
6. No teratogenic potential.

20. Famciclovir
➢ It has good oral bioavailability and prolonged
intracellular t1/2 of the active triphosphate
metabolite.
➢ Mode of action- like acyclovir it needs viral
thymidine kinase for generation of active DNA
polymerase inhibitor.

21. Uses
➢ Famciclovir inhibits H. simplex, H
zoster but not acyclovir resistance stains.
➢ Some activity against hepatitis B virus
(HBV).
➢ It is alternative to acyclovir for herpes
zoster.
Pharmacokinetics
➢ Plasma t1/2- 2 hours

22. Doses
➢ Genital herpes – 250mg TDS for 5 days.
➢ Recurrent cases – 250mg BD up to 1year.
➢ Herpes zoster – 500mg TDS for 7 days.

23. Adverse
Effect
Headache
Nausea
Loose
motion
Itching &
rashes
Mental
confusion

24. Anti Retroviral Drugs

25. HAART- Highly
Active Anti
Retroviral
Therapy
(A term coined in the late 1990s to describe the
effectiveness of combination drug therapies
used to treat HIV.)
➢ It causes suppression of HIV replication and
prolonging as well as improving the quality of
life of the patient.
➢ The drugs used are zidovudine, didanosine,
zalcitabine

26. HAART
Zidovudine – dose
200mg TDS or
300mg BD
Didanosine –
dose 200 mg BD
Zalcitabine – it used in
combination with
Zidovudine, (.75mg
TDS)

27. ANTIRETROVIRAL
AGENT
Zidovudine
➢ It is thymidine analogue
(Azidothymine).
Mode of action – After
phosphorylation in the host cell
Zidovudine triphosphate
selectively inhibit viral reverse
transcriptase in preference to
cellular DNA polymerase.

28. Zidovudine
ZDV-
monophosphate
ZDV-
diphosphate
ZDV-
triphosphate
Inhibit viral
replication
Binds reverse
transcriptase
Incorporated
into viral DNA
Premature
chain
termination

29. Pharmacokinetics
➢ Oral absorption is rapid.
➢ Bioavailability- 65%
➢ It is quickly cleared by hepatic
glucoronidase.
➢ T1/2- 1-4 hour
➢ 15-20% of unchanged drug excreted in
urine.
➢ It crosses placenta and found in milk.

30. Doses

31. Adverse effect
Anemia
Granulocytopenia
Myopathy
Pancreatitis
Lactic acidosis

32. Drug
Interactions
➢ Paracetamol increases azidothimidine toxicity, by
competing for glucoronidation.
➢ Azoles antifungal also inhibit azidothimidine
metabolism.
Uses
1) Used in HIV infected patients.
2) However, beneficial effect are limited from a few
months to a couple of year after which
progressively nonresponsiveness develops.

33. Lamivudine
Mechanism of action
➢ It inhibit HIV reverse
transcriptase as well as
hepatitis B virus (HBV)
DNA polymerase.
➢ Its incorporation in
DNA results in chain
termination.
➢ Most human DNA
polymerase are not
effected & low systemic
toxicity.

34. Uses
• Apart from HIV lamivudine is
also effective against hepatitis B
virus as it inhibit DNA
polymerase in the HBV.
• It requires long term treatment.
• It used in combination with other
anti-HIV drugs, and effective as
azidothimidine.

35. Adverse effect
➢ Lamivudine is
well absorbed and
well tolerated with
no serious adverse
effect in
therapeutic dose.
➢ It can cause
insomnia, fever,
headache,
diarrhea.
➢ Pancreatitis and
neuropathy are
rare .

36. Non Neucleoside
Reversetranscriptase
Inhibitor
(Nevirapine)
➢ The NNRT inhibitor bind to reverse
transcriptase (are not converted to
triphosphate derivatives) & bring about the
change in the enzyme thereby inactivating
the enzyme.
Mode of action- Directly inhibit HIV reverse
transcriptase without the need for
intracellular phosphorylation
Uses- effective only against HIV-1, but do not
inhibit HIV-2

37. Adverse effect
➢ It can cause GI disturbances.
➢ allergic reactions (stevens–johnson
syndrome)
Pharmacokinetics
➢ Well absorbed and extensively
bound to plasma protein.
➢ these drugs are metabolized by
cytochrome P450 enzyme.

38. Newer Anti
Retroviral Drugs
Fusion inhibitor
It block the entity of HIV into CD4
cell.
active only against HIV-1
Ex–Enfuvirtide (Fuzeon)
Integrase inhibitor
It disable the integrase protein that
HIV use to insert its genetic
material into CD4 cells
Ex – Raltgravir

39. Anti
Influenza
Virus Drugs
Amantadin
➢ Chemically it is tricyclicic amine,
unrelated to neucleic acid
precursor, but inhibit replication
of influenza A virus.
➢ A protein designated ‘M2’which
act as an ion channel has been
identified as one of its target of
action.
➢ Resistance to amantadine
developed by mutation causing
amino acid substitution in the M2
protein.

40. Adverse Effect
✓ Generally, well tolerated
– Nausea
– Anorexia
– Insomnia
– Dizziness
– Nightmare
– Lack of mental
concentration
– Postural hypertension
have been reported
– Amantadine is
contraindicated in
epileptic patients, as it
causes convulsion

41. Uses
1. Prophylaxis of influenza A2,
especially in high-risk patient
2. Treatment of influenza (A2): A
modest therapeutic effect
(reduction in fever)
3. Parkinsonism

42. Nonselective
antiviral
drugs/anti-
hepatitis virus
ANTI HEPATITIS
VIRUS
FOR HEPATITIS
B
LAMIVUDINE
ADEFOVIR
TENOFOVIR
FOR HEPATITIS
C
RIBAVIRIN
INTERFERON α

43. WHAT ARE
INTERFERON?
Interferon are chemical
signaling molecule belong
to cytokine.

44. Uses
1. Chronic hepatitis B and C
2. Aids related Kaposi’s Sarcoma (But not
to treat HIV as such)
3. H. simplex, H. zoster and CMV infection
in immunocompromised patients as
adjuvant to acyclovir/Gancyclovir

45. Adverse
effect
It is not effective orally. s.c. or i.m. injected
interferon is limited by substantial adverse
effects.
1. Flu like symptoms- Fatigue, pain,
malaise, fever, dizziness, anorexia, taste
and visual disturbances develops few
hours after injection
2. Neurotoxicity – numbness, neuropathy,
tremor.
3. Myelosuppression (dose limiting).

46. Classification of
Herpes Virus
Herpes simplex virus 1
Herpes simplex virus 2
Varicella zoster virus
Cytomegalo virus
Epstein-Barr virus
Human herpes virus – 6
Human herpes virus – 7
Human herpes virus – 8
Simian herpes virus B

47. Post-exposure prophylaxis to prevent HIV
infection
The recommended PEP regimens are

48. Treatment of COVID-19
₰ Ivermectin is a medication
used to treat many types of
parasite infestations.
₰ Although it is an anti-
parasitic drugs, now a days
Ivermectin is worldwide used
for the treatment of patient
infected with coronavirus.

49. CONCLUSION
❑ The application of antiviral drugs
in dentistry is restricted to
treatment of oropharyngeal herpes
simplex and herpes labialis that
occur particularly in
immunocompromised patients.
❑ Dentist run in the risk of
accidental exposure to HIV
infection and should be well
informed about its prophylaxis.

50. Herpes Labialis 1° Herpetic Gingivo
Stomatitis
Herpes Zoster Mumps
HSV – 1 HSV – 1 Varicella zoster Paramyxovirus
Topical – 5% acyclovir,
3% Penciclovir and 10%
Docosanol 4-6 times/day
at the first prodrome of
lesion
Acyclovir 200mg/kg
5times daily for 5 days
Treatment should be
start within 72 hours
of symptoms onset
for maximum
effectiveness.
Treatment of mumps is
symptomatic and may
involve the use of
analgesic and
antipyretics.
Systemic – Acyclovir
400mg BD for 5 – 10 days
Acyclovir / Valaciclovir /
Famciclovir
Prophylactic regimen –
Acyclovir 800mg/day
Valacyclovir 500mg or
famcyclovir 250mg
BD/Day for 5days
Systemic dose –
acyclovir 800mg 5
times a day,
Famcyclovir 500mg
TDS and
Valacyclovir 1gm
TDS
Vaccination –
prevention with live
attenuated vaccine.
(should be given in 12
– 15 months of life)

51. Viral Hepatitis Erythema multiforme Herpangina Infectious Mononucleosis
Hepatitis A HSV Coxsackievirus Epstein – Barr virus
Prevention measures to
reduce viral hepatitis
spread include aggressive
vaccination protocol
Supportive care, Electrolyte, a
liquid diet and nutritional
support
Supportive care,
including hydration
and topical
anesthesia
Symptomatic – topical
anesthetic gel, and
hydrogen peroxide rinse
Supportive- no antiviral
therapy during an acute
infection
Approved drug therapy
include- IFN-α, IFN-α2a,
Adefovir, Dipivoxil,
Lamivudine, entecavir,
Telbivudine.
Topical mouthwash or gel-
anesthetic agent
Systemic steroid- for minor E M
20 – 40 mg/day prednisolone
for 4 – 6 day
Major E M usually requires 40 –
80 mg/day with gradual tapering
over 2 -3 weeks
Acyclovir 400mg bd/day
indicated in some recurrent case
Specific antiviral
treatment is not
available
Specific therapy – Antiviral
drug Gancyclovir and α
interferon inhibit the
replication of virus
Corticosteroid – indicated
only in the presence of
complication like airway
obstruction, Hemolytic
anemia.

52. REFERENCES
❖ Essentials of medical pharmacology, K D Tripathi, 5th edition, 725-734
❖ P. N. bennett M. J. Brown, clinical pharmacology, 10th edition, 208-225
❖ Post-exposure prophylaxis to prevent HIV infection 1 December 2014
❖ Anil Ghom, textbook of oral medicinr and radiology, third edition 713-
739

53. T H A N K YO U