Antiviral drugs are prescription medicines (pills, liquid, an inhaled powder, or an intravenous solution) that fight against flu viruses in your body. Antiviral drugs are not sold over-the-counter. You can only get them if you have a prescription from a health care provider. Antiviral drugs are different from antibiotics, which fight against bacterial infections.
If you get sick with flu, antiviral drugs are a treatment option. Check with your doctor promptly if you are at high risk of serious flu complications and you develop flu symptoms. Flu signs and symptoms can include feeling feverish or having a fever, cough, sore throat, runny or stuffy nose, body aches, headache, chills, and fatigue. Your doctor may prescribe antiviral drugs to treat your flu illness.
Benefits of Antiviral Drugs
Antiviral treatment works best when started soon after flu illness begins. When treatment is started within two days of becoming sick with flu symptoms, antiviral drugs can lessen fever and flu symptoms, and shorten the time you are sick by about one day. They also may reduce the risk of complications such as ear infections in children, respiratory complications requiring antibiotics, and hospitalization in adults. For people at high risk of serious flu complications, early treatment with an antiviral drug can mean having milder illness instead of more severe illness that might require a hospital stay. For adults hospitalized with flu illness, some studies have reported that early antiviral treatment can reduce their risk of death.
Classification of Antiviral Drugs
| Drug | Mechanism of Action | Therapeutic Uses | Key Notes |
| Neuraminidase Inhibitors Oseltamivir Zanamivir | -Prevent the release of new virions and their spread from cell to cell -Given prior to exposure they prevent infection -Given24-48 hours after onset of infection, they effect intensity and duration of symptoms | -Type A and B influenza viruses | -Orthomyxoviruses need neuraminidase for life cycle of the virus -Sialic acid analogs -Do not interfere with response immune response to influenza A vaccine -Zanamivir should be avoided in pts with severe reactive asthma or COPD |
| Amantadine Rimantadine | -Block the viral membrane matrix protein (M2) which is required for the fusion of viral membrane with cell membrane Preventing formation of endosome Interferes with viral uncoating -70 to 90% effective in preventing infection if tx begun at time of or prior to exposure to infection -Given w/in first 48 hours, they reduce duration and severity of systemic symptoms | -Influenza A viruses -Amantadine: Parkinson’s disease | -Do not impair the response of influenza A vaccine -Amantadine may accumulate to toxic levels in pts with renal failure -Cautious use in pregnant and nursing mothers (embryotoxic and teratogenic) -Cross-resistance occurs between the two drugs |
| Ribavirin | -Converted to 5’-phosphate derivative forming ribavirin-triphosphate Inhibits guanosine triphosphate formation Prevents viral mRNA capping, blocking RNA-dependent RNA polymerase | -Infants and young children: severe RSV infections -Chronic hepatitis C (w/ IFN) -Reduces mortality and viremia of Lassa fever | -Guanosine analogs -Contraindicated in pregnancy due |
| Interferon | -Interfere with ability of viruses to infect cells -Induce host cell enzymes that inhibit viral RNA translation Degradation of viral mRNA and tRNA | -IFN-α-2b: hepatitis B, C -Condylomata acuminate -Hairy cell leukemia -Kaposi’s sarcoma -IFN-β: MS | -Interferes with metabolism of THEOPHYLLINE -Potentiates the bone marrow suppression caused by other agents |
| Lamivudine | -Inhibitor of both HBV DNA polymerase and HIV reverse transcriptase -Must be phosphorylated by host cell enzymes to active form (triphosphate) | -HBV -HIV | -Cytosine analog -Chronic treatment reduces hepatic inflammation -Dose reductions required in moderate renal insufficiency |
| Adefovir dipivoxil | -Phosphorylated to adefovir diphosphate Incorporated into viral DNA Termination of further DNA synthesis and prevents viral replication -Causes decreased viral load and improved liver function | -Nucleotide analog -Cautious use in pts with existing renal disease | |
| Entecavir | -Intracellular phosphorylation to triphosphate Competes for viral reverse transcriptase | -LAMIVUDINE-resistant HBV | -Guanosine analog -Improves liver scarring and inflammation -Drugs that have renal toxicity should be avoided |
| Telbivudine | -Phosphorylated intracellularly to triphosphate Competes with endogenous thymidine triphosphate for incorporation into DNA Terminates further elongation of DNA | -HBV | -Thymidine analog -Dose should be adjusted in renal failure -Can be combined with LAMIVUDINE |
| Acyclovir | -Monophosphorylated in cell by thby thymidine kinase -Acyclovir triphosphate: competes with deoxyguanosine triphosphate as a substrate for viral DNA polymerase Incorporates into viral DNA Premature DNA-chain termination | -HSV 1 and 2 -Varicella-Zoster virus -EBV -DOC: HSV encephalitis -Prophylactic to sero+ pts before BM or heart transplant | Accumulates in pts with renal failure -Valacyclovir: hydrolyzed to Acyclovir -Resistance occurs due to altered or deficient to thymidine kinase and DNA polymerase -Cross-resistance to other cyclovirs occurs |
| Cidofovir | -Inhibits viral DNA synthesis | -CMV-induced retinitis in pts w/ AIDS | -Nucleotide analog -Eliminates the permanent venous access used for GANCICLOVIR therapy -CI in pts with renal impairment or taking nephrotoxic drugs -PROBENECID can be given to reduce risk of nephrotoxicity |
| Fomivirsen | -Directed against CMV mRNA | -CMV retinitis | -Antisense oligonucleotide -Should be used 2-4 weeks after CIDOFOVIR to reduce toxicity |
| Foscarnet | -Reversibly inhibits viral DNA and RNA polymerases Interferes with viral DNA and RNA synthesis | -CMV retinitis in immunocompromised pts -ACYCLOVIR-resistant HSV and Herpes Zoster infections | -Phosphonoformate |
| Ganciclovir | -Activated through conversion to nucleotide triphosphate Nucleotide competitively inhibits viral DNA polymerase | -CMV retinitis in immunocompromised pts -CMV prophylaxis in transplant pts | -Analog of ACYCLOVIR -Accumulates in pts with renal failure-Valganciclovir: rapid hydrolysis in intestine and liver |
| Peniciclovir | -Triphosphate inhibits HSV DNA polymerase -Pain and healing are shortened | -HSV 1 and 2 -Varicella Zoster | -Acyclic guanosine nucleoside |
| Famciclovir | -Prodrug metabolized to active PENCICLOVIR | -Acute herpes zoster | -In animals: increased mammary adenocarcinomas and testicular toxicity |
| Vidarabine (ara-A) | -Converted in cells to ara-ATP Inhibit viral DNA synthesis | -Tx of immunocompromised pts with herpetic and vaccinial keratitis -HSV kerato- conjunctivitis | -Adenosine analog |
| Trifluridine | -Converted to triphosphate Competitively inhibits incorporation of thymidine triphosphate into viral DNA Defective DNA -Irreversible inhibitor of viral thymidine | HSV 1 and 2 -Vaccina virus -DOC: HSV keratoconjunctivitis and recurrent epithelial keratitis | -Fluorinated pyrimidine nucleoside analog |
| NRTIs Zidovudine Stavudine Didanosine Tenofovir Lamivudine Emtricitabine Zalcitabine Abacavir | -After entering a cell, they are phosphorylated to corresponding triphosphate analog which gets incorporated into the viral DNA DNA chain elongation is terminated -Mitochondrial DNA polymerase γ is also susceptible at therapeutic doses | -HIV | -Analogs of native ribosides -All except Abacavir require dose adjustments in renally insufficient patients -Mutation at viral codon 184 causes resistance to Lamivudine but restores sensitivity to Zidovudine and Tenofovir -Concomitant use of agents in same class is contraindicated |
| Zidovudine (AZT) | Children and adults -Prevent prenatal infection in pregnancy | -Pyrimidine analog -STAVUDINE and RIBAVARIN should not be used with AZT -Drugs like PROBENECIDACETAMINOPHEN, LORAZEPAM, INDOMETHACIN, CIMETIDINE should be used cautiously | |
| Stavudine (d4T) | -Strong inhibitor of cellular enzymes such as β and γ DNA polymerases Reducing mitochondrial DNA synthesis | -HIV | -Thymidine analog -Renal impairment interferes with clearance |
| Didanosine (ddI) | -In host cell its transformed to ddATP Incorporation into DNA chain Termination of chain elongation | -HIV | -Should not be used with STAVUDINE |
| Tenofovir (TDF) | -Converted by cellular enzymes to diphosphate Inhibits HIV reverse transcriptase | HIV -AZT-resistant strains of HIV | -Nucleotide analog -Dose should be adjusted in renal insufficiency -Has significant drug interactins -If used with ddl, the dose of the drug needs to be decreased; not used together any longer -Decreases the concentration of ATAZANAVIR |
| Lamivudine (3TC) | -Terminates synthesis of proviral DNA chain -Inhibits reverse transcriptase of both HIV and HBV | -HIV (w/ AZT) | |
| Emtricitabine (FTC) | Inhibits both HIV and HBV reverse transcriptase | -HIV | -Derivative of LAMIVUDINE -Withdrawal in HBV-pts may lead to worsening of hepatitis |
| Abacavir (ABC) | -Guanosine analog -Sensitized pts should never be rechallenged because it may cause death -HLA genetic test can be done to screen pts | ||
| NNRTIs Nevirapine Delavirdine Efavirenz | -Highly selective, noncompetitive inhibitors of HIV-1 reverse transcriptase -Bind to enzyme adjacent to active site, causing conformational change, resulting in enzyme inhibition | -Lack of cross-resistance with NRTIs -Cross-resistance within the NNRTI | |
| Nevirapine (NVP) | -HIV-1 in adults and children | -Shouldn’t be used in women with CD4+ counts >250 or in men with counts >400 -14-dat titration period at ½ dose is mandatory to reduce risk of serious epidermal reactions | |
| Efavirenz (EFV) | -Treatment results in increases in CD4+ T cell counts and decrease in viral load | -Should not be given to pregnant women | |
| Etravirine | Active against 1st generation resistan | -2nd generation NNRTI | |
| HIV Protease Inhibitors Ritonavir Saquinavir Indinavir Nelfinavir Fosamprenavir Lopinavir Atazanavir Tipranavir Darunavir | -Reversible inhibitors of HIV aspartyl protease Prevents maturation of viral particles Production of non-infectious virions -Greater affinity for HIV-1 and 2 enzymes than human proteases, causing selective toxicity | HIV-1 and 2 -Naive pts: Protease Inhibitor + 2 NRTIs | -Drug interaction: Rhabdomyolysis: SIMVASTATIN, LOVASTATIN Excressive sedation: MIDAZOLAM, TRIZOLAM Respiratory depression: FENTANYL Others: WARFARIN, SILENDAFIL, PHENYTOIN -RIFAMPIN AND ST.JOHN’S WORT contraindicated with these drugs |
| Ritonavir (RTV) | -Allows for longer dosing of other protease inhibitors and also helps to prevent development of resistance | Enhancer/booster of other protease inhibitors | |
| Saquinavir (SQV) | Given with low dose of RITONAVIR -Increased levels of hepatic aminotransferases may be seen in pts with HBV or HCV | ||
| Indinavir (IDV) | -Dosage should be adjusted in pts with hepatic insufficiency -To avoid kidney stone formation, pts should drink 1.5 L of water per day | ||
| Nelfinavir (NFV) | -Non-peptide *Only protease inhibitor that can’t be boosted by RITONAVIR | ||
| Fosamprenavir (fAPV) | -Prodrug, metabolized to AMPRENAVIR | -Coadministered with RITONAVIR -Can inhibit the metabolism of other drugs | |
| Atazanavir (ATV) | -inhibits HIV protease -Competitive inhibitor of glucuronyl transferase | -Contraindicated with PROTON-PUMP INHIBITORS | |
| Tipranavir (TPV) | -Inhibits HIV protease in viruses that are resistant to other protease inhibitors | -Salvage regimens in pts with multidrug resistance | |
| Darunavir (DRV) | -Active against HIV protease that is resistant to other protease inhibitors | -Salvage regimens in pts with multidrug | -There may be decreased risk of hyperlipidemia |
| Enfuvirtide (Entry Inhibitor | -Fusion inhibitor -Binds to gp41 Prevents conformational change Preventing fusion of HIV membrane with host cell membrane | -Experienced pts with evidence of viral replication despite ongoing antiretroviral therapy | |
| Maraviroc (Entry Inhibitor) | -Blocks the CCR5 coreceptor that works together with gp41 to help HIV entry into cell | -Dose should be reduced when given with PROTEASE INHIBITORS | |
| Raltegravir (RAL) | -Integrase inhibitor -Inhibits the final step in integration of stand transfer of viral DNA into our own host cell | -Treatment-experienced pts with evidence of viral replication |