4.44 Flashcards
• Inhibitors of viral replication
2
– every step in viral replication is potentially a target
– targeting host cell functions is generally not feasible (toxicity)
Enfuvirtide - (4)
HIV fusion inhibitor
Binds to gp41 region that folds back onto itself
Prevents fusion of membranes
Very specific to HIV
Maraviroc – (1)
CCR5 binding inhibitor
amantadine virus entry
• used to prevent
influenza
infections
amantadine virus entry
• blocks
penetration
and uncoating of
influenza A virus
Rimantadine =
analog of amantadine
Amantadine and rimantadine affect
M2’s function as an ion channel
Amantadine and rimantadine affect M2’s function as an ion channel
(3)
Following endocytosis, acidification of endosomes occurs
Then M2 can function as ion channel
Acidification within virion drives viral disassembly
mAb active against
original version of SARS CoV-2
mAb active against original version of SARS CoV-2
received — from the FDA
Emergency Use Authorization
Monoclonal antibody (mAb)
binds SARS-CoV-2 virions and
“—” them, which
means it
neutralizes
blocks the virus from interacting with ACE2 receptors and entering cells mAb was isolated from a recovered COVID-19 patient = a neutralizing IgG1 mAb directed against the SARS-CoV-2 spike (S) protein
Acyclovir - (3)
result of rational drug design (nucleoside analog)
target herpesviruses
Inhibits DNA synthesis
Viral genome replication
Acyclovir
Viral TK much more efficient than
cellular TK in this
reaction (so drug is specific to infected cells)
However, acyclovir has no effect on —
latency
Acyclovir is not effective against —
CMV
Ganciclovir is effective against
CMV
compared to acyclovir, although it is also
more toxic (cellular TK uses drug better too).
Gancicivir is — analog
nucleoside
foscarnet
Directly inhibits
herpesvirus and
cytomegalovirus
DNA polymerase
(nephrotoxicity issues)
Foscarnet is a
nonnucleoside inhibitor
Remdesivir is a nucleoside analog
interferes with the action of
viral RNA-dependent RNA polymerase
causes RNA synthesis termination after a few nucleotides