Antiviral drugs are a class of medication used specifically for treating viral infections. Unlike antibiotics which only work on bacterial infections, its target viruses with the goal of preventing or reducing the severity of illness. Some key facts about antiviral medications include:
- Antivirals work by interfering with the virus's ability to enter host cells, replicate its genetic material, assemble new virus particles, or leave infected cells. They have varying levels of effectiveness depending on the virus.
- Common drugs available treat infections caused by influenza viruses, herpesviruses, hepatitis viruses, HIV, and others. However, there are currently no approved drugs that cure chronic hepatitis C virus or HIV infections.
- Resistance to antiviral drugs occurs when viruses mutate and become less susceptible to the drug's effects over time. This makes ongoing research and development of new antivirals important.
- Antiviral medications are most effective when taken as prescribed as part of treatment initiated soon after symptoms start. Missing doses or stopping treatment early can allow a virus to replicate and develop resistance.
Classes of Antiviral Medications
There are several main classes of antiviral drugs that work through different mechanisms:
Nucleoside/Nucleotide Analog Reverse Transcriptase Inhibitors (NRTIs):
These Antiviral Drugs mimic the natural building blocks (nucleosides) that viruses use to make DNA and RNA. When the compounds are incorporated into the growing nucleic acid chain, they cause DNA/RNA synthesis to stop, inhibiting viral replication. Well-known NRTIs include AZT, 3TC, TDF, and FTC used to treat HIV.
Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTIs):
NNRTIs bind directly to and disable the reverse transcriptase enzyme that retroviruses like HIV rely on to transcribe their RNA into DNA. Examples are efavirenz, etravirine, and nevirapine.
Protease Inhibitors:
Protease inhibitors block the action of viral proteases, enzymes that cleave nascent proteins in nascent virus particles. In HIV, this final processing step is required for viral replication. Examples are ritonavir, saquinavir, and darunavir.
Adamantanes:
Adamantanes inhibit influenza A viruses by interfering with a viral membrane protein (M2 ion channel) required for uncoating the virus once inside the host cell. Amantadine and rimantadine are adamantane antivirals previously approved for flu but now have limited effectiveness due to resistance.
Fusion Inhibitors:
Fusion inhibitors prevent fusion of the viral envelope with host cell membranes, blocking entry. Enfuvirtide is a fusion inhibitor used against HIV-1.
Polymerase Inhibitors:
These target viral polymerases, enzymes that synthesize viral DNA or RNA. Favipiravir inhibits the RNA polymerase of influenza and other RNA viruses.
Treatment of Specific Viral Infections
Influenza:
Neuraminidase inhibitors oseltamivir (Tamiflu) and zanamivir (Relenza) are first-line treatments for both influenza A and B. They work by inhibiting the viral neuraminidase enzyme, preventing spread within the host. Amantadine and rimantadine may also be used but have high resistance rates. Treatment should begin within 48 hours for best effect. Vaccination is the best prevention strategy.
Herpesviruses:
For herpes simplex virus (HSV), nucleoside analogs such as acyclovir, valacyclovir, and famciclovir are frequently prescribed antivirals to treat outbreaks of cold sores or genital herpes. They disrupt HSV DNA replication. For Varicella zoster virus (VZV), the same drugs can shorten shingles outbreaks and reduce complications in immunocompromised patients. Long-term daily suppressive therapy may be used for recurrent HSV infections.
Hepatitis:
Entecavir and tenofovir are commonly used to treat chronic hepatitis B virus (HBV) infection. By mimicking natural building blocks, they interfere with HBV DNA polymerase activity and replication. Direct-acting antivirals (DAAs) such as glecaprevir, ledipasvir, sofosbuvir, and others can cure over 95% of patients with chronic genotype 1 hepatitis C virus (HCV) infection when given as part of combination therapy regimens.
HIV:
Highly active antiretroviral therapy (HAART) uses a combination of at least three drugs, typically including two NRTIs along with either a NNRTI, protease inhibitor, or integrase inhibitor. Strategically combining antivirals that target different stages of the viral lifecycle has transformed HIV from a fatal infection to a manageable chronic condition. Strict adherence is required to fully suppress the virus and prevent resistance. Pre-exposure prophylaxis (PrEP) with emtricitabine/tenofovir can also greatly reduce HIV transmission risk.
Antiviral Drug Resistance and Future Directions
Resistance emerges when viruses mutate genetic information encoding viral proteins that antiviral drugs target. This occurs through natural selection whenever drug levels fall below what is needed to stop all viral replication. Monitoring for resistance is important in optimizing treatment, particularly for long-term infections. Newer antivirals continue advancing to overcome resistance, target different points in viral life cycles, require less frequent dosing, and cause fewer side effects. Vaccines also remain a critical frontline antiviral strategy for preventing viral infections and spread in the first place. With ongoing research, better treatment and prevention options for viral diseases will hopefully continue improving disease management and outcomes worldwide.
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