Antiviral Drugs Flashcards
T/F: There is only one type of antiviral drug in use today?
FALSE: there are 4 types as of now - nucleoside analogs, non-nucleosides, protease inhibitors, entry inhibitors
How do antiviral drugs work?
they target essential virus functions, host cell intrinsic immunity, activate immune response
What essential virus functions do antivirals target?
1- viral entry 2- viral uncoating 3- Nucleic acid synthesis 4- assembly of viral particles 5- release of viral particles
What is the mechanism of the nucleoside analogs?
they compete for the enzymes in purine and pyrimidine synthesis pathways
T/F: Most antiviral drugs are effective against many different viruses?
FALSE: most drugs target functions of only one specific virus (viruses are each too unique for broad spectrum drugs to work)
What does “off target” effect mean in regard to antiviral drugs?
off target effects can harm host cells
What is one issue with “on target” drugs directed at viral enzymes?
They can be defeated by resistance mutations
T/F: most antiviral drugs have irreversible effects?
FALSE: most drugs are reversible = COMPETITIVE INHIBITORS
What does rebound mean in the context of antiviral drugs?
Rebound= virus replication resumes when drug is cleared
*because of this, many antiviral treatments are long-term or life-long
Why is drug resistance so prevalent among viruses?
high rate of virus replication
high mutation rate (RNA viruses»_space;> DNA viruses)
high selective drug pressure (long-term or multiple tx)
immunosuppressed host cannot clear virus-infected cells
T/F: resistance mutations often exist in a patient before drug treatment
TRUE!!
In order to fight resistance to antivirals the infected person may need immunosuppression alleviated, how is this done?
If they are on immunosuppressants then the doses may be lowered (ex. steroids, cyclosporin…)
T/F: In order to minimize antiviral resistance, antivirals given should all target the same viral functions?
FALSE: combine drugs with DIFFERENT targets:
all HIV pts treated this way
drugs with diff. MOA synergize
lower probability that multiple resistance mutations will be present
Why is it beneficial to target host functions when treating for a viral infection?
It is one method used to reduce the probability of antiviral resistance:
- infected cells may have a unique profile that can be targeted by a drug
- virus mutations don’t change cellular genes (no resistance possible)
- some cancer drugs target dividing cells and inhibit viruses
- MAY BE ASSOC. WITH TOXICITY
When do you treat someone for HSV1/2, or VZV?
- neonates infected with HSV
- frequent recurrences of HSV1/2
- complicated HSV infection (encephalitis, global dissemination)
- eye infection
- zoster infections w/i 3 days of rash (shingles)
Name this drug: nucleoside analog of guanosine, effective against HSV, inhibits DNA synthesis and viral replication by competing with deoxyguanosine triphosphate for viral DNA polymerase and being incorporated into viral DNA?
Acyclovir
Ganciclovir treats what?
CMV
How is ganciclovir similar and different from acyclovir?
both are nucleoside analogs of guanosine, similar MOA
-differences: highly toxic (suppresses BM, mutagenic, teratogenic, sever side effects)
Who should be treated with ganciclovir?
bone marrow and organ transplant pts
immunosuppressed people with active CMV
CMV retinitis
List the “broad spectrum” treatments for DNA viruses
foscaret
cidofovir
Name this drug: Trisodium phosphonoformate, inhibits viral DNA polymerase, effective against all herpesviruses, IV only, renal toxicity
foscarnet
Decsribe Cidofovir
nucleoside analog of cytosie
effective against DNA viruses: herpesvirus, adenovirus, papillomavirus, poxvirus
- IV only
-renal toxicity
Are there antivirals specifically designed to treat HBV?
No, HBV is treated with drugs designed for HCV and HIV
What are the current drug options for treating HBV?
- pegylated interferon alpha
- entecavir
- tenofovir disoproxil fumarate
