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Anti Influenza Agents

Influenza can be type A, B or C depending upon type. Influenza A and B are more common. Effective drugs have been discovered.

Life cycle

After binding host cell, fusion and entry occurs, gene is transferred, nucleic acid component is produced, leading to release of virus.

Two additional components are present:

1.      Heme agglutinin

Influenza virus binds heme agglutinin on host cell epithelial surface specifically respiratory tract.

2.      Neuraminidase on surface

Enzymes present within influenza virus on surface and enhance cleavage of newly formed mature virus components. These are cleaved and released to infect others, neuraminidase facilitates.

Mechanism of action

Basis of mechanism of action of most anti-influenzal agents are same, hemeagglutination, others neuraminidase.

A number of strains of humans and animals were endemic in 2003 and beyond resistant strains were discovered. H5, N1, swine flu and there is fear that transmission might occur.


Specifically for influenza A virus. Bind M2 proteins, necessary for fusion of viral membrane to cell membrane, as a result fusion does not take place.

Some effects are also seen against release of new virions.

Mechanism of Action:
  • Active against influenza A virus only.
  • These drugs block M2 proteins that act as an ion channel, and  necessary for fusion of viral membrane to the cell membrane.
  • Also interfere with release of new virions.
  • Orally, well absorbed .
  • Amantadine well distributed including CNS,  Rimantadine does not cross BBB to same extent.
  • Amantadine excreted unmetabolized in urine,  Rimantadine undergoes extensive metabolism by hydroxylation, conjugation, glucuronidation before urinary excretion.
  • T ½ = 12 – 18 hrs for Amantadine while it is 24 – 36 hrs for Rimantadine
Adverse effects


  1. Insomia,
  2. dizziness,
  3. ataxia,
  4. nervousness,
  5. light headedness.


  1. causes fewer CNS disturbances.
  2. contraindicated in pregnant and lactating women.
Amantadine Rimantidine
Half life 12-18 hours 36 hours
PPB 67% 14%
Metabolism Not metabolized Extensively metabolized
Excretion in urine Unchanged Metabolite form
ADRs As readily cross BBB, most troublesome CNS related:

  1. Insomnia
  2. Dizziness
  3. Ataxia
  4. Nervousness
  5. Light headedness
Cause fewer CNS disturbances

Zanamivir & Oseltamivir

Active against both influenza A & B.

Mechanism of Action:

They inhibit neuraminidase, that is essential for viral replication and release.


  • Oral/inhalation route and is approved for 7yrs and above.
  • Absence of significant metabolism
  • Rapid renal clearance
  • Nasal & throat discomfort
  • Bronchospasm in patients with reactive airway disease


  • Given orally and approved for one yr and above.
  • Prodrug activated in gut and liver
  • t ½ – 6 – 10 hrs
  • Excreted in urine
Adverse Effects:

Nausea and vomiting which decreases by administration with food.


  • Synthetic guanosine analog.
  • Effective against a broad spectrum of RNA & DNA viruses.
  • Orally, I/V, as an aerosol
  • Drug & metabolites excreted in urine.
Mechanism of Action:
  • Ribavirin inhibits viral mRNA by converting into ribavirin triphosphate (RTP).
  • Ribavirin triphophate inhibits replication of wide range of DNA, RNA viruses, including influenza A and B, Parainfluenza respiratory syncitial  and Paramyxovirurs, HCV and HIV
Therapeutic Uses
  1. Respiratory syncytial viral pneumonia and broncholitis.
  2. Aerosolized ribavirin used to treat influenza A & B infection.
  3. I/V Ribavirin decreases mortality in lassa fever & haemorrhagic fever if started.
  4. Severe measles pneumonitis.
Adverse Effects
  1. Dose dependent Anemia.
  2. Increased bilirubin levels
  3. Aerosolized ribavirin cause conjunctival or bronchial irritation.
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