The various target sites and/or mode of action of antiviral agents are briefly highlighted in this section.
- Viral attachment inhibition: Viral attachment to host cells is often the first prerequisite to their entry into infected cells. Once they attach to specific receptors on their target host cell, viruses penetrate the outer cell structure and start to uncoat within the host cell. Viral attachment, penetration and uncoating are often the first step in the replication of viruses within living host cells. Amantadines, rimantadine and enfuvirtide are examples of antiviral agents that inhibit or interfere with viral penetration and uncoating.
- Viral nucleic acid synthesis: Viruses as earlier said only have one type of nucleic acid. It is either the virus contains DNA, and is called a DNA virus or its nucleic acid is RNA, and is called an RNA virus. Both DNA and RNA (found separately in each viral particle or virion) are critical in the life cycle of viruses; and they play important roles in the entire replication processes of viruses because these macromolecules direct the activities of the agent. Antiviral agents that interfere with the synthesis of viral nucleic acids (either DNA or RNA) act as nucleoside analogues i.e. they resemble the nucleoside molecules (inclusive of guanosine, adenosine, cytidine and thymidine) required by potential viral particles for the synthesis of their own nucleic acids (DNA or RNA). Antiviral agents in this category specifically interfere with the activities of enzymes (e.g. polymerases) that direct viral DNA or RNA synthesis; and their inclusion or incorporation into viral nucleic acids automatically inhibit or obstruct the biosynthesis of DNA or RNA in the virion. A wide variety of antiviral agents are nucleoside analogues or inhibitors of viral nucleic acid synthesis. Examples of antiviral agents that are nucleoside analogues include acyclovir, zidovudine or azidothymidine (AZT), cidofovir, ribavirin, lamivudine, and zalcitabine or dideoxycytidine amongst others. AZT, a reverse-transcriptase (RT) inhibitor is used to manage HIV/AIDS patients. The drug (i.e. zidovudine) interferes with RT in retroviruses (e.g. HIV) in order to inhibit their activity in viruses; and it is selectively toxic in action because the human cell lacks reverse transcriptase enzymes. RT is an RNA-dependent-DNA-polymerase enzyme that is mainly responsible for the synthesis of viral DNA from viral RNA (which serves as a template for this purpose) in retroviruses (particularly HIV).
- Other antiviral agents: Nelfinavir, saquinavir, indinavir and ritonavir are viral protease synthesis inhibitors. Antiviral agents that are in this category (i.e. protease inhibitors) are novel antiviral agents; and they inhibit viral assemblage and release from infected host cells which is the primary function of protease enzymes in viruses. Viral particles easily develop resistance to protease inhibitors, thus they should be used in combination with other antiviral agents (e.g. AZT) especially in HIV/AIDS patients.
Denyer S.P., Hodges N.A and Gorman S.P (2004). Hugo & Russell’s Pharmaceutical Microbiology. 7th ed. Blackwell Publishing Company, USA. Pp.152-172.
Drusano G.L (2007). Pharmacokinetics and pharmacodynamics of antimicrobials. Clin Infect Dis, 45(suppl):89–95.
Ashutosh Kar (2008). Pharmaceutical Microbiology, 1st edition. New Age International Publishers: New Delhi, India.
Axelsen P. H (2002). Essentials of Antimicrobial Pharmacology. Humana Press, Totowa, NJ.