Anti-Viral Drugs - Unit 2 Flashcards
Can antiretroviral kill the HIV virus?
No
What is the HIV infection process?
Virus bind and enter the cell—>HIV RNA is converted to DNA via reverse transcriptase—>integrates into host genome via integrase—>transcription—>protein is cleaved via protease—>bud off
What are the 5 major classes of antiretroviral drugs?
NRTI—>nucleoside reverse transcriptase inhibitorNNRTI—>non nucleoside reverse transcriptase inhibitor Protease inhibitor Entry inhibitor Integrase inhibitors
What is the mechanism of NRTI? and its major side effect?
DNA analogs (e.g. adenosine/guanine)—>termination of DNA chainLactic acidosis
What are the side effects of tenofovir/abacavir/zidovudine?
Tenofovir—>nephrotoxicity Abacavir—>hypersensitivity reactionZidovudine—>anemia
What is the mechanism of NNRTIs? and their common side effects?
Bind directly to reverse transcriptase—>inhibit its action Rash
What are the side effects for efavirenz
Efavirenz—>CNS symptoms (vivid dream etc.)/teratogen
What is the mechanism of protease inhibitors? and their side effects?
Bind to protease—>prevent it from cleaving proteins to function subunits Metabolic toxicities—->dyslipidemia/hyperglycemia/lipodystrophy
What is Ritonavir Boosting?
Ritonavir is a potent CYP450 inhibitor—>use in low dose with other drugs to increase their half life
What is the only HIV drug that is not orally administered? side effect? and when is it used?
Enfuvirtide—>entry inhibitor Increase rate of bacterial pneumonia When you ran out of other options
What is the only HIV drug that targets the host cell?
Maraviroc—>CCR5 antagonist
Why integrase inhibitors have become the first line treatment?
Very effective and low side effects
When and who should we start ART (antiretroviral therapy) to?
Everyone that has HIV
What is HAART and what is its concept?
HAART—>high active antiretroviral therapy (combo therapy)Combine at least 3 drugs with different mechanisms
What is the combo of HAART?
2 NRTIs + something else like integrase inhibitor/PI/NNRTIsPreferably with integrase inhibitor or PI
What are the HAART goals?
Reach undetectable viral load
If the resistance is developed against one of the NRTI, can you use another NRTI instead? and is the resistance permanent? and what is the best way to reduce resistance?
No because of cross resistance within classIt is permanentBest way is to adhere to drug treatments—>resistance only develop during replication—>low viral load—>low rate of resistance development
Most ppl who got Hep C clear it out or develop chronic Hep C? and is it curable?
Most people develop into chronic hep CIt is curable
How is Hep C infect cells?
Gain entry—>translate RNA into protein—>protease cleave protein into function subunits
What is the equivalent to viral cure for Hep C treatment? and what is the definition of SVR
SVR (sustained virologic response)—>Hep C remain undetectable 12 weeks after completion of the therapy
Why is interferon and ribavirin are no longer used for Hep C treatments?
Lower efficacy and a lot of side effects
What are the 3 new classes of drugs that treat Hep C? and how are they used?
NS (nucleoside) 5B polymerase inhibitorsNS5A inhibitors NS3/4A protease inhibitors Combo therapy like HIV
What are the mechanisms of NS5B polymerase inhibitor and NS5A inhibitor?
NS5B—>compete with nucleotide and cause RNA chain termination like NRTINS5A—>inhibit viral phosphoprotein
How does HSV replicate?
DNA virus enter cell—>use DNA polymerase to make mRNA
