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48 Cards in this Set
- Front
- Back
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what is the Rc for picorna
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ICAM-1
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where do viruses carry out protein synthesis and where does uncoating occur
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protein synthesis and uncoating carried out in cytoplasm
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how are enveloped viruses released from cell
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via exocytosis and take part of host cell membrane
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what is meant by the statement "viruses have to be doing something" in order for drug to work
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if the virus is sitting latent then the drug can't get to it and treat it this is why you have to treat herpes over and over due to it becoming latent
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what kind of cells are most important in fighting viruses
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T cells
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what kind of illness comes from epstein barr virus and cytomegalovirus (CMV)
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infectious mono which can also cause mental retardation and auditory deficit in fetus
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what are the characteristics of Herpesviridiae
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large dbl stranded DNA genome
1st infection is lytic, then latent infections afterwards enveloped virus |
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how are we able to exploit genes that are different from ours to target herpes infections
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due to their large dna genome that encodes for a lot of its genes
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which infection is above the waist
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HSV1
"fever blisters" |
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which infection is bellow the waist
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HSV2
genitals |
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is the herpes infection disseminated or localized in someone that is immunocompetent
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locallized, disseminated in immunocrompromised
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what are the therapeutic targets to fight herpes infections
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viral TK
viral DNA polymerase |
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what are the anti-HSV drugs
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acyclovir
valacyclovir penciclovir famciclovir ganciclovir valganciclovir cidofovir trifluridine foscarnet |
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how does acyclovir have specificity for the viral cell
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it only gets activated by viral thymidine kinase therefore an uninfected cell won't activate it w/ its thymidine kinase
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what are the properties of acyclovir and how does it work
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deoxyguanisine analog
taken up into cell phosphorylated by viral TK phosphorylated twice by cellular kinase competes w/ GTP(guanisine) for viral DNA due to lack of 3'OH it terminates viral DNA replication the terminated chain then inactivates the viral DNA polymerase |
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what is the MOA of acyclovir
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chain termination
inactivation of viral DNA polymerase |
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how does acyclovir accomplish chain termination
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due to its lack of 3'OH
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how does acyclovir halt herpes infection
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by inhibiting viral DNA polymerase
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what is the resistance to acyclovir
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mutation in viral DNA polymerase
mutation in viral thymidine kinase resulting in a decrease in affinity lack of thymidine kinase (most common) |
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what drugs are deoxyguanisine analogs, inhibit viral DNA polymerase and are prodrugs
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acyclovir (valacyclovir pro-prodrug)
penciclovir (famciclovir pro-prodrug) |
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what drug can be given to a pregnant woman w/ herpese
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acyclovir
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what are the properties of penciclovir and famciclovir
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deoxyguanisine analogs
require viral TK to activate don't cause chain termination due to having 3'OH |
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why do we need penciclovir when we already have acyclovir
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penciclovir is less potent
duration w/in infected cell is longer therefore less dosing frequency |
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what is the ADME of penciclovir and famciclovir
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penciclovir - topical or IV only
famciclovir - tablets only both renally excreted can't use in pregnancy due to teratogen effect |
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when must penciclovir be administered
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since topically only must be given prior to outbreak (prodromal stage)
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what is famciclovir used to treat
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oral dosing used to treat genital and mucocutaneous herpes
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how much time do you have to administer penciclovir and famciclovir after the herpes zoster outbreak to decrease the severity and duration of outbreak
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72 hrs
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what are the properties of Foscarnet
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not a neuclotide/side analog but a inorganic pyrophosphate
no TK required |
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what is the MOA of Foscarnet
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inhibits viral DNA polymerase
non competitively blocks the release of pyrophosphate from deoxynucleotide triphosphates that occurs during DNA chain elongation |
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what resistance is there for foscarnet
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mutation in viral DNA polymerase decreasing the affinity of drug
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what is a 1st line drug for serious CMV infections
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ganciclovir and valganciclovir
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what are the properties of ganciclovir and valganciclovir
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guanine analog
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what is the MOA of ganciclovir and valganciclovir
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competitively inhibits viral DNA polymerase and cellular polymerase (more selective for viral)
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what can ganciclovir and valganciclovir be used to treat
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Herpes and CMV
phosphorylated by viral TK in herpes phosphorylated in CMV specific enzyme (phosphotransferase) in CMV |
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what is the resistance to ganciclovir
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mutation in viral TK, UL97 (encodes CMV phosphotransferase), DNA polymerase
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what drug is given to treat CMV retinitis
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ganciclovir, valganciclovir, and foscarnet
used to stop further development of disease which may lead to blindness. can also be used to suppress other CMV complications. |
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what drugs come in an occular implant
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ganciclovir and valganciclovir
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what are the properties of Cidofovir
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cytadine analog
not exclusive to herpese (treats other DNA viruses) more stable since its a phosphonate and not phosphorylated doesn't require TK since its a phosphonate |
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what drugs can be used on TK RESISTANT STRAINS
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cidofovir
foscarnet |
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what drug is given to treat CMV retinitis in HIV pts
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cidofovir
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what is the MOA of cidofovir
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inhibits viral DNA polymerase thereby causing chain termination
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what is the resistance to cidofovir
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mutation in viral DNA polymerase resulting in decrease in affinity for drug
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why is cidofovir not a 1st line drug
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due to nephrotoxicity
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what is given w/ cidofovir to prevent nephrotoxicity
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probenecid and saline (a lot of fluids)
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how is cidofovir given
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via IV
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what are the propeties of trifluridine
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topically treats HSV 1 and 2 eye infections, can be used to treat CMV and cow pox as well
fluorinated pyrimidine analog gets phosphorylated by viral TK |
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what is the mechanism of action of trifluiridine
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inhibits thymidylate snythetase (monophosphate form does this)
inhibits viral DNA polymerase (triphosphate form does this) |
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what are the dosage forms for acyclovir and valacyclovir
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acyclovir = oral. topical, IV
valacyclovir = oral |
