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Antiviral Therapy

Chapter 33

TermDefinition
Difficulty of developing anti-virals Difficult to interfere with viral activity in the cell without adversely affectin the host. Viruses are dependent on the host cell's protein synthetic machinery
Prodrugs that target viral DNA polymerase (4) Acyclovir, Ganciclovir, Cidofovir and Foscarnet
Acyclovir mechanism 1 Acyclovir is phosphorylated by herpesvirus thymidine kinase and the monophosphate is then converted by cellular kinases to the triphosphate, which inhibits the herpesvirus DNA polymerase
Acyclovir mechanism 2 Acyclovir is also incorporated into the viral DNA --> chain termination
Acyclovir usage Acyclovir is used for the treatment of HSV and VSZ infection
Ganciclovir mechanism Ganciclovir gets monophosphorylated by virus UL97gene-specified kinase and then further phosphorylated by cellular kinases. The triphosphate than inhibits the CMV DNA polymerase
Ganciclovir usage Ganciclovir is used to treat CMV infection
Cidofovir mechanism Cidofovir is a chain terminator that targets the viral DNA polymerase. It is phosphorylated intracellularly to the diphosphate form and is then added to the 3' end of the viral DNA chain
Foscarnet mechanism Foscarnet is a compound that attaches to the pyrophosphate-binding site of the herpesvirus DNA polymerase, preventing nucleotide binding and therefore inhibiting viral replication
Nucleoside and nucleotide reverse transcriptase inhibitors (NRTIs) Zidovudine (azidothymine (AZT))
Nucleoside and nucleotide reverse transcriptase inhibitors mechanism Zidovudine is a analogue of thymine, that after conversion to the triphosphate by cellular enzymes acts as an inhibitor of, and substrate for, the viral reverse transcriptase. AZT triphosphate is also incorporated into the DNA --> chain termination
Non-nucleoside reverse transcriptors inhibitors classes Nevirapine, Efavirenz (EFV), Delavirdine and Etravirine
Non-nucleoside reverse transcriptors inhibitors mechanism These compounds act as non-competitive inhibitors of HIV-1 reverse transcriptase by binding to a hydrophobic pocket proximal to the enzyme catalytic site
Non-nucleoside reverse transcriptors inhibitors resistance A single mutation in the reverse transcriptase leads to resistance to these drugs
Protease inhibitors + mechanism Peptidomimetic inhibitors of the viral protease and prevents the cleavage of the gag and gag-pol polyproteins into functional structural proteins and enzymes. This produces immature, defective viral particles
Protease inhibitors resistance Resistance is well recognized and a number of protease mutations result in cross-resistance
Fusion inhibitors mechanism Peptides that block HIV before it enters the host cell by competitively binding to gp41, and blocking the post-fusion structure from forming
Integrase inhibitors mechanism Agents that inhibit the integration of the viral DNA into the host chromosome, by interacting with divalent cations of the catalytic core of the integrase
Antivirals targeting influenza virus mechanisms (3) 1. Inhibition of the penetration of virus into the cell, or its uncoating 2. inhibition of fusion of the virus envelope with cell membrane 3. Act on viral matrix proteins ion channels to inhibit the passage of hydrogen ion
Neuraminidase Inhibitors (NAI) mechanism NAIs are n-acetylneuraminic acid analogues and act as competitive reversible inhibitors of the neuraminidase enzyme active site. This prevents the release of virus and further spreading
Passive resistance Resistance is a consequence of general adaptive processes that are not necessary linked to a given class of anti-microbials
Active resistance Resistance is the result of a specific evolutionary pressure to develop a counterattack mechanism against an anti-microbial or class of anti-microbials so that bacteries previously sensitive become resistant
Created by: Beantha
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