control of microorganisms: antivirals

prodrugs

prodrugs

only become pharmaceutically active once they are metabolized within the cell, and therefore exact mechanism of action is not always entirely clear

pleconaril

Attachment Antagonists

–Prevents attachment, exposure of RNA in picornaviruses

•Mainly Enterovirus and Rhinovirus, potentially Hepatitis A virus and Poliovirus

enfuvirtid

early inhibitors

–Binds to gp41 and inhibits HIV membrane fusion

amantadine and rimantadine

uncoating inhibitors

• interfere with Influenza virus protein M2 and prevent physiological changes needed to result in viral uncoating

arildone

–Binds to a stabilizes the Poliovirus capsid, preventing the uncoating, also effective against HSV-2 (mechanism unknown)

uncoating inhibitor

nucleic acid synthesis inhibitors

•Prodrugs converted into triphosphate nucleotide analogs and inhibits DNA Polymerase

Converted intracellularly by viral thymidine kinase, effective against EBV, CMV, HSV, VZV

Acyclovir

Valaciclovir (“esterfied” acyclovir)

Ganciclovir

Penciclovir

nucleic acid synthesis inhibitor

Converted intracellularly by cellular                                            kinases, effective against HSV and VZV

Adenosine arabinoside

nucleic acid synthesis inhibitor

sofosbuvir

–NS5B (RNA Polymerase) inhibitor in HCV that prevents viral RNA replication

nucleic acid synthesis inhibitors

ribavirin

–RNA analog that binds and prevents RNA synthesis in Hantavirus, HCV, and RSV

• nucleic acid synthesis inhibitors

NRTI

•__N__ucleoside analog __Reverse-T__ranscriptase __I__nhibitors

–Nucleoside analogs that prevent DNA synthesis via reverse transcriptase

effective against HIV

•Azidothymidine/Zidovudine

•Tenofovir

Nucleic acid synthesis inhibitors (NRTI)

effective against HBV

entecavir

nucleic acid synthesis inhibitors

NRTI

effective against both HIV and HBV

Lamivudine

Nucleic acid synthesis inhibitors

NTRI

Effective against HBV and HSV

adefovir

nucleic acid synthesis inhibitors

NRTI

fomivirsen

–Antisense nucleic acids that bind to mRNA and prevent translation in Cytomegalovirus

protein synthesis inhibitors

protein synthesis inhibitors

Some viruses translate many/all of their proteins at once and then utilize post-translational proteases to cleave the individual proteins apart from one another to make the mature viral proteins needed for assembly

•Darunavir and Fosamprenavir

–Protease inhibitors specific to enzymes in HIV that prevent formation of mature viral proteins

• protein synthesis inhibitors

•Boceprevir and Telaprevir

–Protease inhibitors specific to enzymes in HCV that prevent formation of mature viral proteins

• protein synthesis inhibitors

ledipasvir

–NS5A inhibitor in HCV that prevents assembly of the mature viral proteins

• assembly inhibitors

release inhibitors

In the Influenza virus, Hemagglutinin binds to siliac acid on the host cell to attach and Neuraminidase cleaves this bond to allow the virus to detach from the host cell

neuraminidase

• release inhibitors

• prevents the virus from being able to detach from the host cell and spread to new cells

•Oseltamivir (Tamiflu) and Zanamivir (Relenza)

–Neuarminidase inhibitors to prevent the spread of newly synthesized Influenza viruses

• release inhibitors

antiviral resistance

High viral loads with multiple strains, fast reproduction rates, and little to no proof-reading/repair leads to very high mutation rates in viruses, often making antiviral medication ineffective

combination treatment -HAART

Highly active antiretroviral therapy combines a “cocktail” of antiviral medication to combat HIV to prevent the rapidly-mutating HIV from developing resistance to the drugs

HAART

Highly active antiretroviral therapy

• antiretroviral drugs (ART), antiretrovirals (ARVs), or anti-HIV drugs, has proven to be effective at reducing the onset of AIDS and mortality rate of those affected with HIV