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1. replicate in host nuclei, via virus encoded DNA polymerase. Transcribed and trnaslted via host proteins. |
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1. replicate in host nuclei, via virus encoded DNA polymerase. Transcribed and trnaslted via host proteins. |
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DNAvirus, but replicated nad transcriped by viral proteins |
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DNA virus replciated via RNA intermediate. |
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RNA virus, genome serves as both mrna and tempalte for more RNA. Virus RNA polyemerase |
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RNA virus, genome serves as both mrna and tempalte for more RNA. Virus RNA polyemerase |
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RNA virus, genome serves as both mrna and tempalte for more RNA. Virus RNA polyemerase |
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inhibit viral dna replciation 2. compete with natural nucletoides for viral dna polyermase, and chain terminate. Converted to triphos via viral and host enzymes |
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guanosine derivative. Dna replication inhibition. first phosphate via viral thymidine kinase (hsvtk), second one via cellular one.this allows for drug to accumulate mostly in infected cells only. 3. Resistance- mutations in hsvtk and viral dna polymerase. 4. pharmdynamics- available oral topical andiv formulation. 5. adverse rxns- wellt olerated generally, some host dna polymerase use of the drug- some renal insufficiency and cns effects- in iv acyclocivr. |
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nucleotide analog- taken up by infected nad noninfected cells. Starts as monop and converted to dip via host enzymes. Competes w dCTP, and is chain terminator. Resistance- viral dna polymerase mutation. Pharmacodynamics- very long half life (17-65 hours). because is monop, has low bioavailability. Adverse effects- neprotoxicity, probenecid (used to increase peniciclin halflife by reducing clearance) will increase renal toxicity. |
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guanosine derivative. No chain termniation. Avoid dur\g pregnancy |
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guanosine derivative , competes with dGTP and chain termniator. Val- icnreases biovailability. Many adverse effects i.e. teratogenic, carcinogenic, mutagenic, but needed for hiv and immunocompromised patients. |
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topical, too toxic for anything other than opthalmic use |
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topical, too toxic for anything other than opthalmic use |
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moa: antisense mechanism- phosphotioates replace normal phophate linkages to prevent celsl from chewing up the foreign dna. binds early CMV transcript blockin\ translation and subsequent replication. No cross resistance (unlike nucleoside/nucleodtime analogs) because is specific to each viral dna strand. |
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moa: blocks viral dna polymerase, viral rna polymeraseand hiv rt directly. Binds in pocket reserved for triphosphates, prevetns cleavage. Resistance: Mutations in viral DNA polymerase, but is useable in viruses that have becoem resistant to some of the nucleoside analogs .Adverse effects: neprotoxicity with altered calcium and phosphate levels, penile ulcerations, and cns toxicities. |
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anti flu: virus enters via endocytosis, endosome are acidified. Acidifcation causes cleavage of hemagglutinin, on viral surfaces and activation of M2 ion channel. Amanditdine and rimantidine bind to this m2 channel, inhibiting unsheatihing process. Resistance: mutation of M2. Pharmacodynamics: well absorbed by oral administration. Amantidine excreted unmetabolzied in urine.adverse effects: CNS disturbances. Uses: can be used in prophylaxis and decreasing duration of syptoms |
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anti flu : virus enters via endocytosis, endosome are acidified. Acidifcation causes cleavage of hemagglutinin, on viral surfaces and activation of M2 ion channel. Amanditdine and rimantidine bind to this m2 channel, inhibiting unsheatihing process. Resistance: mutation of M2. Pharmacodynamics: well absorbed by oral administration. Rimantidine- several metabolic steps before excretion. adverse effects: CNS disturbances. Uses: can be used in prophylaxis and decreasing duration of syptoms |
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anti flu: Viral neuramidase is requried tro cleave sialic residues on surface of virus and host cells. Uncleaved sialic acid residues will bind to viral hmeagglutin and cause viral particelto aggregate, reducing viral escape from ifnected cells. This drug is a sialic acid analog that inhibits viral neuraminidase activity. Resistance= mutations in hmeaglutin or neuraminidase. pharmacodynamics zanamvir- dry powder. |
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anti flu: Viral neuramidase is requried tro cleave sialic residues on surface of virus and host cells. Uncleaved sialic acid residues will bind to viral hmeagglutin and cause viral particelto aggregate, reducing viral escape from ifnected cells. This drug is a sialic acid analog that inhibits viral neuraminidase activity. Resistance= mutations in hmeaglutin or neuraminidase. Oseltavir- taken oraly |
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Hepatitis B/C : Host proteins- exert antiviral, immunomdoulating and antiprolif effects. Interferon binds to jak-stat activators, resutls in activation of gene products that contribute to antiviral defesnse. Enhances immune resposnes - by increasing lytic effects of cytotoxic t lymphs and histocompatibility antigens. mechanisms of interferon mediated inhibtion: transcritpipon, translation, protein processing, viral maturation . Pharmacodynamics- PEG - increased half life from 2-3 hours to54 hours. Oligo A synt. Adverse events - alot- influenza symptoms at first myelosupression, neurotoxicity, autoimmuen disorders, hepatoxocity. p450 metabolism. can be used for treatmetn of Hep b and C ( HCV patietns get ribavarin as well (only works in 50 percent of patients)) |
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HCV Guanosine analog works on several steps: lower cellular GTP levels, inhibtion of viral MRNA capping and RNA virus replciation. Adverse effects: hemolyticanemia, psychiatric, and teratogenic. A lot of contraindications for many pateitns. |
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targets HCV ns3 protease. Telaprivir plus ribavarin plus IFN looks promisig . Adverse affects: only adiditonal one is rash. Resistance emerges rapidly alone. |
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HBV usage Guanosine analog. Blocks binding of dGTP on HBV RT. Blocks reverse transcriptase activity. Long half life. Drug supresses virus only, quick reboudn once treatment stops. Resistance: requires two mutations, not much resistance yet, hoewr priot treatment wit lamivudine accelerates cross resistance. |
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HBV? dgtp prodrug, chain terminator. Efective even after lamivudine resistance and entecavir cross resistance. |
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HBV . can be used for HBV. |
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HBV. synthetic thymidine analog, better than limuvdine, however lamivudine resistance causes cross restance. |
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