The viral enzymes are ideal targets because they differ from host enzymes and are much more likely to incorporate modified nucleosides due to their inaccuracy in genome synthesis.
Viral or cellular enzymes phosphorylate nucleoside analogs before their incorporation.
These agents exhibit their effect by preventing chain elongation in DNA synthesis or inducing mutations that lead to their early termination.
Commonly used nucleoside analogs include:
Acyclovir (ACV) – A guanosine analog that contains an acyclic, hydroxyethyl methyl side. The drug is effective against herpes viruses encoding a thymidine kinase, an enzyme that activates the prodrug form acyclovir. Thus, ACV is integral in treating clinical signs of all herpes simplex virus (HSV) and varicella-zoster virus (VZV) infections and may be administered as a prophylactic measure during epidemics due to its non-toxic nature.
Ganciclovir contains a single hydroxymethyl group in the acyclic side chain and shows significant activity against cytomegalovirus (CMV) infections through activation by a viral encoded protein kinase.
Cidofovir and adefovir are phosphate modified cytidine and adenosine analogs, respectively, and contain a phosphate attached to the sugar analog. The conjugated phosphate group eliminates the need for an additional phosphorylation step. Thus, cidofovir is integral in treatment regimens against cytomegalovirus (CMV) infections in acquired immunodeficiency syndrome (AIDS) patients.
The human immunodeficiency virus (HIV) is highly capable of gaining resistance against antiviral drugs. Physicians use combination therapy in which they prescribe multiple pharmaceuticals to avoid the phenomenon. Drugs usually include azidothymidine (AZT) and other nucleoside analogs such as zidovudine, dideoxyinosine, and lamivudine. The antiviral drugs inhibit the activity of reverse transcriptase.
Pyrophosphate analogs and non-nucleoside analogs drugs
Apart from nucleoside inhibitors, pyrophosphate analogs, such as phosphonoformic acid (PFA) and phosphonoacetic acid, interfere with the enzymatic activity of polymerases of some viruses. The drugs inhibit viral replication by binding to the pyrophosphate-binding site. PFA administration is an approved treatment method of cytomegalovirus (CMV) retinitis in HIV-infected patients.
Nevirapine and delavirdine are non-nucleoside analog drugs that target reverse transcriptase inhibitors. The mechanisms of action are through noncompetitive binding to sites on the reverse transcriptase apart from the substrate-binding site. Due to the unique mode of action, the drugs are beneficial in combination therapy for HIV-infected patients. Antiviral therapy may utilize several other targets other than viral polymerases.
Some enzymes, such as deoxyribonucleotide scavenging enzymes, are beneficial as targets for drug action. However, drugs targeting these enzymes limit the availability necessary for viral DNA replication.
Anti-influenza drugs attack the surface proteins of the virus, essential for their attachment to the host cell. Zanamivir and oseltamivir are effective against infections caused by influenza A and B through inhibiting neuraminidase.
Protease inhibitors and immunomodulators
The unique structure of the HIV protease and its function in producing infectious viral particles makes the enzyme an excellent target for therapeutic intervention. Antiviral drugs, such as saquinavir, indinavir, and other drugs, slip into the active site of HIV protease, thereby inhibiting its action. They are used in combination with nucleoside analogs, significantly reducing the blood levels of HIV infections. Interferons are at the forefront of host antiviral immune mechanisms. Commercially available interferons bind to cell surface receptors and stimulate the immune clearance of viral infection. However, they are not usually administered by themselves but rather in conjugation with other drugs.
Interferon-alpha (IFN-\alphaα) is a broad-spectrum antiviral immunomodulator effective against many viruses, including hepatitis viruses, herpes simplex virus (HSV), papillomavirus, and rhinovirus.
Imiquimod binds to Toll-like receptors and stimulates innate immune responses. Thus, the drug is particularly effective against papillomas, which are excellent evaders of the host immune system.
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