L-28 Antiviral Agents and Viral Resistance

Antiviral drugs often target specific viral proteins to inhibit viral replication.

Mutations in viral proteins can lead to drug resistance, meaning the drug no longer effectively inhibits viral replication.

Antiviral drugs can stop viral replication, but often, when the drug is stopped, the virus can continue to replicate.

Effective host cell immunity is crucial for recovery from viral infections, even after using antiviral drugs.

Some antiviral drugs need to be phosphorylated to become active and inhibit viral replication.

The effectiveness of antiviral drugs in laboratory settings may not always translate directly to effectiveness in living organisms.

Reduced susceptibility of a virus to an antiviral drug, often due to mutations in the viral genome.

The concentration of a drug needed to inhibit viral growth by 50% or 90%.

Analogues are molecules that closely resemble the normal building blocks of DNA or RNA, like adenine or guanine. When a virus tries to use these analogues instead of the real deal, it fails to create its own DNA or RNA, leading to replication failure.

Amantadine and Rimantadine target the M2 channel, a protein critical for influenza virus entry into the host cell. Zanamivir and Oseltamivir are neuraminidase inhibitors, blocking the release of new virus particles from infected cells.

Ribavirin is a broad-spectrum antiviral drug that acts as a guanine analogue to interfere with viral RNA synthesis. Palivizumab is a monoclonal antibody that binds to and neutralizes the respiratory syncytial virus, preventing infection.

Remdesivir is a nucleoside analogue that interferes with viral RNA replication. Nirmatrelvir/Ritonavir is a protease inhibitor that blocks the necessary cleavage of viral proteins.

Interferons are naturally occurring proteins produced by the body to fight viral infections. They activate immune cells, suppress viral replication, and help restore normal cellular functions.

Interferons Alpha and Beta are produced by different cell types and have distinct antiviral activities. Alpha is produced by lymphocytes, while Beta is produced by fibroblasts.

A class of antiretroviral drugs that inhibit the reverse transcriptase enzyme, essential for HIV replication.

A class of antiretroviral drugs that bind to a different site on the reverse transcriptase enzyme, also preventing HIV replication.

These antiretroviral drugs target the HIV protease enzyme, which cleaves viral proteins for maturation.

A key enzyme that converts viral RNA into DNA, which is then integrated into the host cell's genome.

The site on the reverse transcriptase enzyme where NRTIs bind and block its activity.

The binding site on the reverse transcriptase enzyme where NNRTIs bind to inhibit its activity.

The difference between NRTIs and NNRTIs lies in their binding sites on the reverse transcriptase enzyme.

NRTIs are nucleoside analogs that lack a phosphate group, while NNRTIs are non-nucleosides that do not resemble any natural nucleotides.

A class of antiretroviral drugs that block HIV entry into host cells.

A class of antiretroviral drugs that inhibit the integration of HIV's DNA into the host cell's genome.

HCV, a type of RNA virus, replicates without needing to create DNA. It uses an enzyme called RNA polymerase to copy its RNA genome, allowing it to produce new copies of itself.

HSV-1 primarily causes infections in the mouth, face, skin, and esophagus, while HSV-2 is commonly found in the genitals, rectum, skin, and can sometimes infect the hands and brain.

Acyclovir is a drug that prevents viral DNA polymerase from working. It needs to be activated by cellular and viral kinases before it can stop the virus from replicating.

Foscarnet is an antiviral drug that directly blocks the activity of viral enzymes like DNA polymerase and RNA polymerase, preventing the virus from replicating. It's used to treat infections caused by the CMV virus, especially in people with weakened immune systems.

Trifluridine is effective in treating herpes simplex I keratitis, a type of eye infection, due to its ability to inhibit viral DNA synthesis and break DNA strands. It works ten times better than its predecessor, Idoxuridine, for this specific condition.

Enfuvirtide is a 33 amino acid peptide that binds to GP41, a protein on the surface of HIV. This prevents the virus from fusing with the host cell membrane, stopping infection.

Maraviroc is an entry inhibitor that blocks the CCR5 co-receptor on the surface of host cells, preventing HIV from binding and entering.

Raltegravir, Dolutegravir, and Elvitegravir are integrase strand transfer inhibitors. They prevent the HIV provirus from integrating into the host cell's DNA, stopping viral replication.

Emtricitabine is a nucleoside analog of cytidine, inhibiting HIV reverse transcriptase and blocking viral DNA synthesis.

Tenofovir disoproxil fumarate inhibits HIV reverse transcriptase, acting as a DNA chain terminator.

Pre-exposure prophylaxis (PrEP) is the use of antiretroviral drugs to prevent HIV infection in people at high risk. It's typically a combination of emtricitabine and tenofovir.

Telbivudine, Lamivudine, Entecavir, Adefovir, and Tenofovir are nucleoside analogs used to treat Hepatitis B. They inhibit HBV polymerase, preventing viral replication.

Imiquimod is an immune response modifier used to treat HPV infections. It stimulates the body's immune system to fight the virus.

Boceprevir, Telaprevir, and Simeprevir are protease inhibitors used to treat Hepatitis C. They block the NS3-4a protease, preventing the cleavage of the viral polyprotein into functional proteins.

Reverse transcriptase (RT) drugs are useful for treating HBV, a DNA virus, because HBV uses reverse transcriptase to convert its RNA genome into DNA. RT inhibitors block this process.