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7/18/2019 2012,UHN PHARMACOLOGY OF ANTIVIRAL.ppt
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Introduction to viruses
• Obligate parasites
• Specific to type of cells they target
-poliomylelitis virus attacks nerve cells-hepatitis virus attacks liver cells
• Reproduction is their only truecharacteristic of being alive
• Much smaller than bacteria (20-300nm
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General principles
• = Viruses are parasitic, i.e. they utilize:
- Host metabolic enzymes
- Host ribosome for protein synthesis
• = Structure of viruses
- Nucleic acid core: N! or "N! - #ften contain crucial virus-speci$c
enzymes
-Surrounded by protein: %capsid&
- ' and sometimes an outer lipid%envelope&
• = (omplete viral particle: %virion&
• = #ften visible by electron microscopy:
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Viral Structure
• !ot a cell"
• DNA or RNA (retrovirus)
• Surrounded by protective protein coat(capsid
• Genetic material carries information for
multiplication• Hijacs bioc!emical mac!inery of !ost
cell to carry t!ese processes out
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Virion Structure
Nucleic Acid
Spike
Projections
Protein
Capsid
Lipid Envelope
Virion
Associated
Polymerase
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Invasion of a cell by a virus
• Virus can lie dormant for many years until itcomes into contact "it! a suitable !ost cell
• #inds "it! molecules on surface of !ost cell
• Herpes$"!ole virus enters cell
• #acteriop!a%e$viral DNA injected via !ollo" tail
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Viruses
• Steps for Viral Replication
– )* adsorption and penetration intocell
– +* uncoatin of viral nucleic acid
– * synthesis of reulatory proteins
– * synthesis of "N! or N!
– /* synthesis of structural proteins – 0* assembly of viral particles
– 1* release from host cell
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1. Herpesviridae - Double Stranded DNA viruses
2. Respiratory Syncytial Virus
RSV - Causes lung infection in infants. A double-stranded RNA
virus.
. !nfluen"a Virus#ypes A $ % - Single-stranded RNA viruses t&at cause t&e flu.
'. Hepatitis %
Double stranded DNA virus t&at causes &epatitis. (ic)ed up
fro* blood. Very &ardy virus t&at +ill survive drying. C&ronic
infection is co**on and can lead to &epatocellular carcino*a.
,. Hepatitis C
Single stranded RNA virus t&at causes &epatitis. !nitial infection
is often asy*pto*atic. any /,0 go on to c&ronic &epatitis
+it& a ris) of developing cirr&osis.
3. Hu*an !**unodeficiency Virus
H!V -A single-stranded RNA retrovirus.
Co**on Viral (at&ogens
for +&ic& +e &ave antiviral drugs
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Virus Classifications
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Therapeutic Overview for Treatment of Viral Infections
). 2loc3 viral attachment to cells 4fusioninhibitors*
+. 2loc3 uncoatin of virus 4ion channel
bloc3ers*. 5nhibit viral N!6"N! synthesis 47olymerase
inhibitors*
. 5nhibit viral protein synthesis 47rotease
inhibitors*/. 5nhibit viral release 4Neuraminidase
inhibitors*
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8echanisms of !ction of!ntiviral drus
• !vailable antiviral drus ,e9ective speci$c typeof virus:
– None eliminate latent virus
• arets include:
= Viral entry
= Viral uncoatin
=Nucleoside analos:
=Non-nucleoside polymerase
inhibitors
=Non-nucleoside reverse ; transcriptase inhibitors
= 7rotease inhibitors
= Neuraminidase inhibitors
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Sites of Drug Action
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).5nhibition of Viral!ttachment < ntry
• Fusion inhibitors eg. Enfuvirtide• !nti H5V peptide ; structurally similar to asement of p)
– H5V binds to cellular receptors trierin aconformational chane in p) e>posin a
fusion peptide – p) then refolds and if fusion peptide is
properly inserted into the host cell membrane,the refoldin brins the virion envelope and cellmembrane into close pro>imity permittin
fusion• nfuvirtide binds to p) causin steric hindrance
of protein refoldin
– virus-host cell interaction trapped at bindinstae
– No membrane fusion or viral entry
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fusion/attachment inhibitors
• ?usion inhibitors andattachment inhibitorsare drus that stopH5V from ettin into
(6-cells.• 5f H5V cannot fuse or
attach to the healthy(6-cell, it cannotbein ma3in moreof itself .
?usion orattachment
inhibitor
(6-cell
H5V
N45 Viral 6usion !n&ibitors
7 4nfuvintide 6u"eon 8
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araviroc Sel"entry9 binds to CCR,9 preventing an interaction +it&
gp120. !t is a :c&e*o)ine receptor antagonist.: Ne+ agent approved
in 200;. !ndicated for treat*ent-e<perienced adult patients infected+it& only CCR,-tropic H!V-1 detectable9 +&o &ave evidence of viral
replication and H!V-1 strains resistant to *ultiple antiretroviral
agents. =iven orally
Maraviroc
Ne+ 4ntry !n&ibitor
+ 5 hibiti f i l ti
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+.5nhibition of viral uncoatin:5on (hannel 5nhibitors :
4!mantadine , "imantadine*
!nfluen"a A virus
M! proton c"annel
#A! "aema$$lutinin
NA! neuraminidase
Virus enters %y receptor
mediated endocytosis
events!
p# induced
con&ormational c"an$e
in "aema$$lutinin
permits &usion 'it"
endosomal mem%rane
M c"annel opens and
virion matri( protein
dissociates – releasin$
ri%onucleoprotein
hibi i f i l
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.5nhibition of viral enomereplication 4H5V*
Nucleoside !naloues 4N"5s*
• All nucleoside analogues reuire phosphor!lation totriphosphate for activit!
• "ost viruses encode their own pol!merases
#potential target for selectivit!$
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"everse ranscriptase5nhibitors 4"5*
• !ll are +, dideo>ynucleosides.
• !ll competitively inhibit N! dependent"N! polymerase 4reverse transcriptase*.
• !ll bloc3 early events in virusreplication.
• !ll are chain terminators 4li3e !cylcovir*.
• #nce viral N! is interated into hostcell enome, they don@t Aor3.
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"everse ranscriptase 5nhibitors4"5* #cont.$
• "esistance develops due to chanesin enzyme. Hih virus load resultsin mutants that are resistant. (ross
resistance is not complete so cansAitch from one inhibitor to anotheror use in combination to decreaseresistance. 2B donCt use tAo drustoether Aith same adverse e9ect
The high rate of RT mutation and resistanceto the nucleoside inhibitors led to the
development of non-nucleoside inhibitors
" i 5 hibi
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"everse ranscriptase 5nhibitors4"5*
• hese drus are non-competitiveinhibitors of reverse transcriptase
• he idea is that mutations in " leadin toresistance to nucleoside inhibitors Aouldbe di9erent than those leadin toresistance of the non-nucleoside inhibitors
• hus, the nucleoside and non-nucleoside" inhibitors could be used in combinationtherapy.
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Nucleoside "everseranscriptase 5nhibitors 4N"5s*
• Didovudine 4!D*: thymidine analoue – >cellent substrate for cellular thymidine
3inase 4H5V no E* – No selectivity at activation, accumulates in
most dividin cells
– No @ #H roup, contains N obliatory chainterminator – ppp!D more potent competitive inhibitor of
H5V reverse transcriptase than cellular "• Famivudine 4(*: cytidine analoue
– F-stereoisomer Ahich contains a S atom – chain terminator < competitive inhibitor of " – ppp( inhibits H5V " cellular " – !lso used in chronic Hep2 Ahere evidence of
viral replication
– Feast to>ic of N"5s
n v ra rus
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n v ra rusNucleoside and Nucleotide
!nalos
Figure 20.16a
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N"5s < NN"5s
• N"5s 4nu3es* and NN"5s 4non-nu3es* are drus that stopreverse transcriptase fromAor3in.
• "everse transcriptase is the
enzyme 4helper* that helps H5Vive (6-cells the instructionsneeded to ma3e more H5V.
• 5f the (6-cell does not etthe instructions, it cannot ma3emore H5V.
N"5 or NN"5
H5V instructions"everse
transcriptaseenzyme
N)*+,nucleoside reverse transcriptase in"i%itors- NN)*+,nonnucleoside reverse transcriptase in"i%itors.
!cyclovir: 5nhibition of Viral N!
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!cyclovir: 5nhibition of Viral N!
synthesis% Steps
). (ompetitively inhibits N! polymerase+. erminates N! elonation 4no @ hydro>yl*. 5rreversible bindin betAeen N! polymerase and interrupted N!
chainN2: viral N! polymerase more sensitive to ppp!(V than cellular N!polymerase
N l id "
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Non-nucleoside "everseranscriptase 5nhibitors 4NN"5s* ;
!nti H5V• favirenz, Nevirapine• &&'TIs bind near the catal!tic site of the
reverse transcriptase• (ermit 'T to bind d&T( and primer)
template* but inhibit the +oining of the two
Structurally different
to NR#!s
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'everse TranscriptaseInhibitors
• Didovudine 4!D*
• idanosine- causes pancreatitis,
• Famivudine- causes pancreatitis
• Dalcitabine- causes peripheral
neuropath!,
• Stavudine- causes peripheral neuropath!,
• !bacavir
hibi i f i l
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.5nhibition of viralmaturation
• H5V 7rotease inhibitors: "itonavir, sauinavir
• 5nhibit cleavae of the a6pol H5V polyprotein
• herefore, viral particles Ahich bud frominfected cells are immature and non-infectious
• 5nteraction Aith 7/I 4(J7!*
– 5nhibitors of 7/I enhance S of protease inhibitors
– 7/I inducers can loAer plasma levels of 75s andencourae viral resistance
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7rotease 5nhibitors
• he protease enzyme cleavesprecursor molecules to producemature, infectious virions
• these aents inhibit protease and
prevent the spread of infection
• hese aents cause a syndrome ofaltered body fat distribution, insulin
resistance, and hyperlipidemia
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7rotease 5nhibitors
• The protease en-!me cleaves precursormolecules to produce mature* infectiousvirions
• these agents inhibit protease andprevent the spread of infection
• These agents cause a s!ndrome ofaltered bod! fat distribution* insulin
resistance* and h!perlipidemia>t&er agents?
7 Nelfinavir
7 A*prenavir
7 @opinavir
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7rotease 5nhibitors
• he protease enzyme cleavesprecursor molecules to producemature, infectious virions
• these aents inhibit protease andprevent the spread of infection
• hese aents cause a syndrome of
altered body fat distribution,insulin resistance, andhyperlipidemia
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Viral (rotease !n&ibitors
#&is approac& &as resulted in useful H!V treat*ent.
#&e protease cleaves a &uge protein called :gag-pol: based ont&e gene seg*ent coding for it into capsid9 reverse
transcriptase9 integrase.
olecular *odeling of t&e en"y*es active site &as lead to
several in&ibitors. All of t&ese drugs *i*ic t&e peptide
substrates for t&e en"y*e.
Several are approved no+ approved via a fast trac) process.
Resistance is a proble* +&en agents are used alone.
5&en co*bined +it& a R#!9 &ave t+o different *ec&anis*s ofactivity and decreased resistance and en&anced antiviral effect.
#&ey bloc) cell to cell spread of H!V.
4<? - Sauinavir /S01
2 )itonavir
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proteaseinhibitors
• 7rotease inhibitorsare drus thatbloc3 the protease
enzyme 4helper* sothat the (6-cellcannot $nishma3in neA H5V.
7rotease inhibitor
NeA H5V material
7rotease enzyme
3t"er a$ents!
2 Nel&inavir2 Amprenavir
2 Lopinavir
2 +ndinavir
/ 5nhibition of viral release
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/.5nhibition of viral release 45nKuenza Virus*
•Danamivir• !naloue of Sialic !cid
• 5nhibits neuraminidases – "ationale: Normally virus
attaches via interactionbetAeen haemalutinin
and sialic acid moietiespresent on cell membraneG7s.
– #n viral eresshaemalutinin present onnascent virions also bind tosialic acid moietiespreventin release.
– viral neuraminidase4envelope bound enzyme*cleaves sialic acid frommembrane G7s, freeinvirions.
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•
any drug options are available for people living+it& H!V.
• 4ac& type of drug fig&ts H!V in its o+n +ay to stop
t&e virus fro* *a)ing *ore of itself reproducing.• Bsually9 a co*bination of or *ore drugs ta)en
toget&er a drug regi*en is needed to fig&t H!V .
• #+V,"uman immunode&iciency virus
+&at )inds of *edications are available
for people living +it& H!V
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Hu*an !**unodeficiency Virus H!V
!nfection +it& H!V is associated +it& a disease
)no+n as Acquired Immuno Deficiency Syndrome AIDS
H!V is a typical retrovirus
#&e nucleocapsid contains
t+o copies of t&e RNA
geno*e capped and polyadenlyated
Viral Fife (ycle: H5V
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Viral Fife (ycle: H5V4retrovirus*Notes
• Gp)+I binds to cellse>pressin ( orchemo3ine receptors e(("/
• Viral entry depends on p)Ahich folds resultin infusion of H5V and taret cellmembranes
• (ellular "N! polymerases
copy N! into m"N! andenomic viral "N!
• 7roteases cleave viralpolyproteins 4maturation* toyield 3ey viral proteins:
– Ga: proteins thatdetermine viral core
4matri> proteins* – 7ol: reverse
transcriptase <interase
– nv: envelope proteinthat determines viraltropism 4speci$city for
host*
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H5V Fife (ycle
From The Immunodecienc! linic ) 0niversit! 1ealth &etwor2 3ebsite* www.tthhivclinic.com
(roteas
einhibitors #(Is$
&'TIs and&&'TI
FusionInhibitors
'4Inhibitors
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)eproduced 'it" permission &rom Adis +nternation Ltd.4
Ne' 5ealand &rom ori$inal article %y M. 6arry in Clinical
P"armacokinetics 78894 :/:1!78;2<8.
#&e life cycle of H!V and t&e site of action of Anti H!V agents
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!ntiviral rus
nzyme 5nhibitors
• 5nterferons prevent spread ofviruses to neA cells 4Viralhepatitis*
• Natural products of the immune
system in viral infections
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5nterferon
• 3hat is interferon5• = iscovered in )L/1
• = 7roteins produced naturally by cells inimmune system after e>posure to viruses
• = 8ay be a %natural anti-viral factor&
• = General classes of interferon:
• = !lpha, beta, amma
• = secreted from di9erent types of cells• = 7harmaceutical use:
• = Not practical as a pharmaceutical until massrecombinant production 4M)LIs*
• = Still considered a %dru of the future&
5nterferon mechanism of
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5nterferon, mechanism ofaction:
• 6$ binds to cell surface receptors
• 7$ induces e8pression of translation inhibitor!protein #TI($
• 9$ TI( binds to ribosome* inhibits host e8pressionof viral proteins
5nterferon has broad spectrum anti-viral
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5nterferon has broad spectrum anti-viralactivity
• 4N! viruses*:• - herpes simple> ) and +O herpes zoster - human papillomavirus 4enital Aarts*• 4"N! viruses*:
- inKuenzaO chronic hepatitisO common cold• 4also*: - breast cancerO lun cancerO - Earposi@s sarcoma 4cancer associated Aith
!5S*
7harmaco3inetics: = Not orally bioavailable = ypically routes: intramuscular, subcutaneous,
topical 4nasal spray*
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are there other Aays totreat H5VP
•
Jes. 5nterase inhibitors $ht H5Vin a di9erent Aay.
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interase inhibitors
• 5nterase inhibitors aredrus that prevent H5Vfrom usin the interaseenzyme to interate
4combine* its instructionsinto the (6-cell@sinstructions.
• 2y stoppin the use ofthe interase enzyme,interase inhibitors
prevent H5V from ma3inmore of itself.
5nterase enzyme
5nterase inhibitor
(6-cell@s instructio
H5V instructions
A ti t l i
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Anti)!tomegalovirusAgents
• Gancyclovir
• Valancyclovir
• (idofovir
• ?oscarnet
• ?omivirsen
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!nti-Hepatitis !ents
• Famivudine )&ucleoside 'everse
Transcriptase Inhibitor #&'TI$
• !defovir )&ucleotide Inhibitor
• 5nterferon !lfa
• 7eylated 5nterferon !lfa
•"ibavirin
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!nti-5nKuenza !ents
• !mantadine
• "imantadine
• Danamivir
Summary:
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Summary:Virus "eplication < 7harmacoloical
5ntervention