What is the Classification of Antivirals?

October 9, 2025 •

3 min read

Antiviral drugs have become essential weapons against a wide range of viral infections, including HIV, influenza, and herpes. The complex and diverse life cycles of viruses mean that no single drug can effectively treat all infections, which is why understanding the classification of antivirals is critical for targeted therapy. These medications are typically categorized by the specific viral target, such as an enzyme or protein, or by the type of virus they are designed to combat.

Quick Summary

Antiviral drugs are categorized by their specific viral targets or mechanism of action. Classifications include inhibitors that block viral entry, replication, and release. This article details the different classes for viruses like HIV, influenza, and herpes, explaining how each type interrupts the viral life cycle and combating viral infections.

Key Points

Mechanism of Action-Based Classification: Antivirals are commonly classified by the specific stage of the viral life cycle they disrupt, such as entry, replication, or release.
Targeting Viral Entry: A class of antivirals prevents the virus from entering host cells. Examples include fusion inhibitors (e.g., Enfuvirtide for HIV) and CCR5 antagonists (e.g., Maraviroc for HIV).
Blocking Viral Replication: Many antivirals, including nucleoside analogs (e.g., Acyclovir for herpes) and reverse transcriptase inhibitors (e.g., Zidovudine for HIV), stop the virus from copying its genetic material.
Preventing Viral Release: Neuraminidase inhibitors (e.g., Oseltamivir for influenza) are a class of drugs that prevent newly formed viral particles from leaving the infected cell, limiting the spread of the infection.
Targeting Viral Maturation: Protease inhibitors, such as darunavir for HIV, prevent the production of mature, infectious viral particles by blocking an enzyme that processes viral proteins.
Host-Targeted Therapies: Some newer strategies focus on targeting host cell factors that viruses need for replication, a method that may result in broader efficacy and a lower risk of resistance.
Addressing Drug Resistance: Viral mutation can lead to resistance, a significant challenge in antiviral therapy. Combination therapies, as used for HIV (HAART), are a strategy to combat resistance.

The classification of antivirals is primarily based on their mechanism of action, disrupting various stages of a virus's life cycle. Unlike broad-spectrum antibiotics, antivirals must be specific to viral processes to minimize harm to host cells. This approach contrasts with the broader action of antibiotics. We will explore the main classes of antivirals based on where they interfere with the viral life cycle.

Inhibitors of Viral Entry and Uncoating

These antivirals prevent the initial steps of infection, either blocking attachment to or entry into a host cell, or preventing the virus from releasing its genetic material (uncoating).

Fusion and Entry Inhibitors

Fusion inhibitors stop the virus from merging with the host cell membrane. Enfuvirtide, an HIV drug, binds to a viral protein to block fusion. Maraviroc, another HIV medication, prevents the virus from interacting with a host cell co-receptor. Fostemsavir blocks HIV entry by targeting a viral protein.

Uncoating Inhibitors

Some antivirals target the uncoating process. M2 inhibitors like amantadine and rimantadine block a viral protein channel essential for influenza A virus uncoating. However, resistance is now common with this class.

Inhibitors of Viral Genome Replication and Expression

This is a common target for antivirals, focusing on the synthesis of viral genetic material.

Nucleoside/Nucleotide Analogs (NRTIs/NtRTIs)

These drugs mimic natural DNA and RNA building blocks. Incorporated by viral enzymes, they can halt replication by terminating the nucleic acid chain. Their selectivity often depends on viral enzymes having a higher affinity for the analog than host enzymes. Examples include acyclovir for herpesviruses, tenofovir and lamivudine for HIV and HBV, and sofosbuvir and remdesivir for HCV and SARS-CoV-2.

Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTIs)

NNRTIs bind to a non-active site on the HIV reverse transcriptase enzyme, changing its shape and preventing it from working. Efavirenz and nevirapine are examples.

Integrase Inhibitors

These drugs stop HIV from inserting its DNA into the host cell's genome. Raltegravir and dolutegravir are in this category.

Inhibitors of Viral Maturation and Release

These antivirals target the later stages, preventing the assembly of new viruses or their release.

Protease Inhibitors

Many viruses, including HIV and HCV, require a viral protease enzyme to cut long protein chains into functional proteins. Protease inhibitors block this enzyme, resulting in non-infectious viral particles. Examples include darunavir for HIV and glecaprevir for HCV.

Neuraminidase Inhibitors

Used for influenza, these inhibitors block the viral neuraminidase enzyme, which is needed to release new viruses from infected cells. Drugs like oseltamivir (Tamiflu) and zanamivir (Relenza) trap new viruses, preventing spread.

Host-Targeted and Immunomodulatory Antivirals

Some strategies focus on boosting host defenses or targeting host factors a virus uses. This can provide broader activity and reduce resistance.

Interferons: Host signaling proteins used to treat viral diseases like hepatitis B and C by inducing an antiviral state.
Host-Targeted Antivirals (HTAs): These drugs interfere with host cell pathways needed for viral replication. An advantage is a potentially higher barrier to resistance. Maraviroc is an example that targets the host CCR5 co-receptor.

Classification of Antivirals: Mechanism-Based Overview


Mechanism of Action	Drug Class	Viral Target(s)	Example Drugs	Key Target
Entry/Attachment	CCR5 Antagonists	HIV	Maraviroc	Host Cell CCR5 Receptor
	Fusion Inhibitors	HIV	Enfuvirtide	Viral gp41 Protein
	Attachment Inhibitors	HIV	Fostemsavir	Viral gp120 Protein
Uncoating	M2 Inhibitors	Influenza A	Amantadine, Rimantadine	Viral M2 Proton Channel
Genome Replication	NRTIs/NtRTIs	HIV, HBV, Herpesviruses	Acyclovir, Zidovudine, Tenofovir	Viral Reverse Transcriptase or Polymerase
	NNRTIs	HIV	Efavirenz, Nevirapine	Viral Reverse Transcriptase
	Integrase Inhibitors	HIV	Raltegravir, Dolutegravir	Viral Integrase Enzyme
	Polymerase Inhibitors	HCV, SARS-CoV-2, RSV	Sofosbuvir, Remdesivir, Ribavirin	Viral Polymerase (RNA or DNA)
Maturation/Release	Protease Inhibitors	HIV, HCV	Darunavir, Glecaprevir	Viral Protease Enzyme
	Neuraminidase Inhibitors	Influenza A and B	Oseltamivir, Zanamivir	Viral Neuraminidase Enzyme
Host Modulation	Interferons	HBV, HCV	Pegylated Interferon Alpha	Host's Immune Response
	Host-Targeted Antivirals (HTAs)	Various	Maraviroc (also Entry)	Host Cellular Pathways

Conclusion

The classification of antivirals, based on their targets and mechanisms, reflects the complexity of viral pathogens. By interfering with specific stages of the viral life cycle, pharmacology has developed effective treatments for viral infections. However, viral mutation and resistance, particularly in rapidly replicating viruses like HIV and influenza, necessitate ongoing drug development. Future efforts may focus on new host-targeted therapies, broad-spectrum agents, and drug combinations to address these challenges. Continued research into viral life cycles is vital for identifying new drug targets and expanding antiviral options.

Frequently Asked Questions

Antiviral drugs can be classified by the specific virus they target (e.g., HIV, influenza, herpes) or by their mechanism of action, such as inhibiting viral entry, replication, or release.

Antivirals for herpesviruses, like acyclovir and valacyclovir, work by inhibiting viral DNA polymerase. They are nucleoside analogs that act as a decoy, stopping viral DNA synthesis inside the infected cell.

Reverse transcriptase inhibitors are a major class of antivirals for retroviruses like HIV. They block the viral enzyme reverse transcriptase, which is needed to convert viral RNA into DNA for integration into the host cell's genome.

Yes, host-targeted antivirals (HTAs) work by modulating host cell pathways that viruses hijack for replication. This approach can be effective against multiple viruses and may have a higher barrier to resistance compared to direct-acting antivirals.

Influenza antivirals can be classified into M2 inhibitors, which block viral uncoating, and neuraminidase inhibitors (e.g., oseltamivir), which prevent the release of new virions from infected cells.

Viruses can develop resistance through genetic mutations, which is a significant challenge for antiviral effectiveness. This is especially common in viruses with high replication rates, such as HIV and influenza.

Combination therapy, or highly active antiretroviral therapy (HAART), is often used for HIV to target multiple stages of the viral life cycle simultaneously. This strategy increases treatment effectiveness and reduces the likelihood of viral resistance.