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Fusion inhibitors Block ATTACHMENT: Maraviroc Block PENETRATION: Enfuvirtide
Integrase inhibitors Raltegravir
Protease inhibitors (-navir): Lopinavir, Atazanavir, Darunavir, Fosamprenavir, Saquinavir, Ritonavir, lndinavir
Reverse transcriptase inhibitors 1. NRTI´s 2. NNRTI´s
NRTI´s (Nucleoside Reverse Transcriptase Inhibitors) Tenofovir (TDF) Emtricitabine (FTC) Abacavir (ABC) Lamivudine (3TC) Zidovudine (ZDV,formerly AZT) Didanosine (ddl) Stavudine (d4T)
NNRTI´s (Non-Nucleoside Reverse Transcriptase Inhibitors) END E= Efavirenz N= Nevirapine D= Delavirdine
Prevent maturation of new viruses Protease inhibitors
Protease inhibitor that can "boost" other drug concentrations by inhibiting cytochrome P-450. Ritonavir
Protease inhibitors; TOXICITY 1. Hyperglycemia 2. GI intolerance (nausea, diarrhea) 3. Lipodystrophy. 4. Nephropathy 5. Hematuria (indinavir).
NRTI that´s a nucleotide analog and does NOT have to be ACTIVATED Tenofovir
NRTI used for general prophylaxis and during pregnancy to reduce risk of fetal transmission. Zidovudine (ZDV)
NRTI´s (Nucleoside Reverse Transcriptase Inhibitors); TOXICITY 1. Bone marrow suppression 2. Peripheral neuropathy 3. Lactic acidosis (nucleosides) 4. Rash (non-nucleosides) 5. Anemia (ZDV). 6. Pancreatitis (Didanosine)
Bone marrow suppression caused by NRTI´s can be reversed with Granulocyte colony stimulating factor (G-CSF) and erythropoietin
Reversibly inhibiting HIV integrase. Raltegravir (Integrase inhibitors)
Raltegravir (Integrase inhibitors); TOXICITY Hypercholesterolemia
Binds gp41, inhibiting viral entry Enfurvitide
Skin reaction at injection site Enfurvitide
Binds CCR-5 on surface of T cells/monocytes, inhibiting interaction with gp120 Maraviroc
Inhibit influenza neuraminidase, decreasing the release of progeny virus. Zanamivir, Oseltamivir
Zanamivir, Oseltamivir; CLINICAL USE BOTH Inlfuenza A and B
Inhibits synthesis of guanine nucleotides by competitively inhibiting IMP dehydrogenase Ribavirin
RSV, Chronic Hepatitis C Ribavirin
Ribavirin; CLINICAL USE RSV, Chronic Hepatitis C
Ribavirin; TOXICITY 1. Hemolytic anemia 2. Severe Teratogen
Acyclovir (Nucleoside analog); MOA Inhibits viral DNA polymerase by chain termination.
Acyclovir; CLINICAL USE 1. HSV and VZV 2. HSV­ encephalitis; Prophylaxis in immunocompromised patients.
Prodrug of acyclovir, has better oral bioavailability. Valacyclovir
Herpes zoster Famciclovir
Acyclovir; TOXICITY Obstructive crystalline nephropathy and acute renal failure if NOT adequately HYDRATED!!!
Acyclovir; MECHANISM OF RESISTANCE Mutated viral thymidine kinase
CMV Ganciclovir, Foscarnet
Ganciclovir; TOXICITY MORE toxic to host enzymes than Acyclovir 1. Leukopenia 2. Neutropenia 3. Thrombocytopenia 4. Renal toxicity
MORE toxic to host enzymes than Acyclovir Ganciclovir
Foscarnet; MOA Pyrophosphate analog
Inhibit viral Nucleic Acid synthesis 1. Guanine nucleotide synthesis: -Ribavirin (RSV, HCV) 2. Viral DNA Polymerase inhibitors: -Foscarnet (CMV) -Cidofovir (HSV Acyclovir resistant) 3. Guanosine analogs: -Acyclovir (HSV, VZV) -Ganciclovir (CMV)
Foscarnet; CLINICAL USE 1. CMV retinitis in immunocompromised patients when ganciclovir fails 2. Acyclovir-resistant HSV.
Foscarnet; MECHANISM OF RESISTANCE Mutated DNA polymerase
What decreases Cidofovir toxicity Coadminister with Probenecid and IV saline
Glycoproteins synthesized by virus-infected cells Interferons
Interferons; MOA block replication of both RNA and DNA viruses.
IFN-Alpha 1. Chronic Hepatitis B and C 2. Kaposi sarcoma 3. Hairy cell leukemia 4. Condyloma acuminatum 5. Renal cell carcinoma 6. Malignant melanoma
IFN-Beta Multiple sclerosis
IFN-Gamma Chronic granulomatous disease
Created by: heidy39