Antiviral & Antifungal Drugs PDF

Antiviral drugs &Antifungal drugs  Anti-Viral drugs 1- Inhibition of attach or penetration of the virus into the host cell: 2- Inhibition of viral nucleic acid synthesis 3- Inhibition of viral protein integration 4- Immunomodulators: ◻ Some drugs stimulate the body’s immune...

Antiviral drugs &Antifungal drugs  Anti-Viral drugs 1- Inhibition of attach or penetration of the virus into the host cell: 2- Inhibition of viral nucleic acid synthesis 3- Inhibition of viral protein integration 4- Immunomodulators: ◻ Some drugs stimulate the body’s immune system ◻ Best responses to antiviral drugs are in patients with competent immune systems ◻ A healthy immune system works synergistically with the drug to eliminate or suppress viral activity 1- Inhibition of attach or penetration of the virus into the host cell: 1)gamma globulins, 2)Amantadine, remantadine, 3)interferon 1-gamma globulins: -from pooled plasma -given I.M. during viral incubation period -active against (measles, polio, rabies)  2- Amantadine, remantadine: -mechanism of action: inhibit M2 proton ion channel needed uncoating of influenza virus -given orally as a prophylaxis of influenza A - can be used in treatment of Parkinsonism as it inhibit dopamine reuptake -side effects: nausea, vomiting, dizziness N.B.: Remantadine is better than amantadine 2- Inhibition of viral nucleic acid synthesis a- inhibition of viral DNA polymerase: b- inhibition of reverse transcriptase c- inhibition of viral mRNA  a- inhibition of viral DNA polymerase *-- viral DNA replication *effective against DNA viruses(herpes, cytomegalovirus, hepatitis B) *they need intracellular activation ( acyclovir, gancyclovir) ✔ acyclovir : -topical -systemic: oral or IV in immunocomperimized -S.E: nephrotoxicity ✔ Gancyclovir -more toxic -against cytomegalovirus -given oral or IV -SE: bone marrow depression  b- inhibition of reverse transcriptase (abacavir, tenofovir) Act by competitive inhibition of HIV-1 transcriptase Incorporation of wrong nucleoside into growing DNA resulting in immature chain They need in tracellular phosphrylation for activation SE: nausea, vomiting, diarrhea, hypersensitivity  c)Inhibition of viral mRNA (ribavirin) *-- synthesis of triphosphate capsule of viral mRNA *need intracellular activation *broad spectrum antiviral drug DNA, RNA vituses *kinetics: -poor GIT absorption -widely distributed(pass BBB) *SE: N, V, fatigue, rash *CI: end stage RF, IHD, pregnancy  3- Inhibition of viral protein integration -- protease ( ritonavir, saquenavir) *act by – processing of immature viral proteins into functional conformations *advantages: -effective against HIV-1, HIV-2 -not need intracellular activation *SE:- bleeding tendency as – of clotting factors - Insulin resistance so hyperglycemia & lipid redistribution 3- Immunomodulators (interferon) ✔ Interferon: - Glycoproteins secreted from host cells in response to viral or parasitic infection - Interfere with viral: penetration, transcription, maturation, protein processing & release - Increase phagocytic activity of macrophages - Increase proliferation of cytotoxic T cell Used in treatment of hepatitis B, C: s.c or IM Antifungal drugs  Antifungal drugs: *Alter cell membrane permeability: A- azole: ketoconazole,fluconazole, itraconazole voriconazole B- polynes: amphotericin B C-terbinafine *block nucleic acid synthesis:flucytosine *disrupt microtubule function: griseofulvin  Treatment of lung aspergillosis: Voriconazole, amphotericin B is another option Voriconazole: binds and inhibits ergosterol synthesis which is the principle sterol in fungal cytoplasmic membrane Kinetics: absorbed orally, metabolized and eliminated mainly by liver Side effects: GIT upset, sever skin reaction, vision changes and swelling in hand, foot and joint. Treatment of pulmonary candidiasis Amphotericin B along with flucytosine Azole: ketoconazole, fluconazole and itraconazole Treatment of pulmonary histoplasmosis