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antivirals Flashcards

1
Q

Capsid

A

Capsid: protein coat surrounding genetic material of a virus

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2
Q
  • DNA polymerase:
A
  • DNA polymerase: an enzyme which catalyzes the process of DNA
    replication
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3
Q
  • Endocytosis:
A
  • Endocytosis: ingestion/engulfing of materials (e.g. a virus) via the
    cell membrane
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4
Q
  • Envelope:
A
  • Envelope: outermost lipid (fatty) layer which protects genetic
    material when traveling between host cells; only present on some
    viruses
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5
Q
  • Incubation period:
A
  • Incubation period: time duration between exposure to the virus and
    the appearance of symptoms
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6
Q
  • Latency:
A
  • Latency: the ability a pathogenic virus to lie dormant within a cell
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7
Q
  • Neuraminidase:
A
  • Neuraminidase: an enzyme found on the surface of influenza virus
    which enables the virus to be released from the host cell
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8
Q
  • Nucleocapsid:
A
  • Nucleocapsid: core of a virus, made up of the genetic material and
    the capsid
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9
Q
  • Reverse transcriptase:
A
  • Reverse transcriptase: an enzyme used to generate
    complementary DNA (cDNA) from an RNA template (reverse
    transcription)
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10
Q
  • RNA polymerase:
A
  • RNA polymerase: the enzyme which catalyzes the process of
    transcription
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11
Q
  • Transcription:
A
  • Transcription: the synthesis of RNA from a DNA template
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12
Q
  • Translation:
A
  • Translation: the synthesis of protein from RNA
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13
Q
  • Virion:
A
  • Virion: a complete and free-living virus particle outside of its host;
    the vehicle for transmission of the genome to the next host cell or
    organism
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14
Q

What is a Virus?
* genomes?
* Viral genomes direct their own?
* metabolic machinery
* alive?
* Can infect all ?
* Reproduction rate?
* tx dif?

A

What is a Virus?
* “Virus” in Latin means “poison”
* Small, obligate parasites with DNA or RNA genomes
* Viral genomes direct their own replication and the synthesis of other
viral components, using host cell machinery
* No metabolic machinery of their own
* Not “alive” themselves
* Can infect all living organisms; commonly cause disease in humans
* Reproduces much faster than bacteria
* Much more difficult to treat than bacteria
Pellett PE, et al. Basics of virology. Handb Clin Neurol. 2014.

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15
Q

viral structures?

A
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16
Q

DNA viruses for this class

A
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17
Q

RNA viruses for this class

A
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18
Q

DNA vs RNA life cycles

A
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19
Q

Virus Life Cycle General Steps:
1. Attachment:
2. Entry:
3. Replication:

A
  1. Attachment: Polypeptide binding sites (on envelope or capsid) interact with host cell receptors
  2. Entry: receptor-virus complex enters host cell (e.g. endocytosis)
  3. Replication: utilizing host cell metabolic processes, nucleic acids and proteins are synthesized and assembled into viral particles
    * Process varies (DNA vs RNA)
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20
Q

DNA Viruses life cycle
* Viral DNA enters?
* Host cell’s enzyme used?
* Translation?
* what is made?
* Release of?
* end resullts

A
  • Viral DNA enters host cell nucleus
  • Host cell’s RNA polymerasem catalyzes transcription into mRNA
  • Translation of mRNA into virus- specific proteins: Enzymes for further synthesis of
    viral DNA and Structural proteins comprising viral coat and envelope
  • Release of complete virions
  • Via budding or host cell lysis
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21
Q

RNA Viruses life cycle
* mRNA production?
* Translation into?
* Assembly of and release?
* NOTE:

A
  • Enzymes within virion synthesize
    mRNA from the viral RNA template
    OR viral RNA serves as its own
    mRNA
  • Translation into enzymes
    (including RNA polymerase,
    structural proteins)
  • Assembly of and release similar to
    DNA viruses
  • NOTE: host cell nucleus usually
    NOT involved in viral replication
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22
Q

Retroviruses (RNA)
* Virion contains ?
* DNA copy?
* Provirus DNA is?
* Completed viruses released?
* NOTE:

A

Retroviruses (RNA)
* Virion contains reverse
transcriptase enzyme (RNA-
dependent DNA polymerase) 
complementary DNA
* DNA copy integrated into host cell
genome (“provirus”)
* Provirus DNA is transcribed into
new viral genome RNA and mRNA
for translation into viral proteins
* Completed viruses released via
budding
* NOTE: retroviruses often replicate
without killing host cell

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23
Q

Common Viral Drug Targets

A
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24
Q

Herpesviruses
* genome?
* Responsible for?
* Eight Types Can Infect Humans:

A
  • DNA viruses
  • Responsible for cold sores, genital ulceration, chickenpox, shingles,
    etc.
  • Eight Types Can Infect Humans:
  • Herpes simplex viruses (HSV-1 and HSV-2)
  • Varicella-zoster virus (VZV/HHV-3)
  • Epstein-Barr virus (EBV/HHV-4)
  • Cytomegalovirus (CMV/HHV-5)
  • Herpesvirus type 6 (HBLV/HHV-6)
  • Herpesvirus type 7 (HHV-7)
  • Kaposi’s sarcoma herpesvirus (KSHV/HHV-8)
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25
Q

Herpes Simplex Viruses (HSV-1 &
HSV-2)
* *Manifestations

A
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26
Q

hsv 1 and 2 spread

A

Highly Contagious:
* Transmission via direct contact
* Sharing food utensils/drinks
* Oral-genital contact

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27
Q

hsv development cycle

A
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28
Q

hsv exposure

A
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29
Q

hsv primary infection

A
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30
Q

hsv latency

A
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31
Q

hsv reactivation

A
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32
Q

hsv triggers for reactivation

A
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33
Q

prodromal symptoms of hsv reactivation

A

pain, tingling, burning

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34
Q

hsv tx agents

A
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35
Q

hsv Therapeutic management considerations:

A
  • Primary vs reactivated infection
  • Severity
  • Site of infection
  • Frequency of recurrences
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36
Q

acyclovir preps for hsv
oral cap, tablet, suspension and ointment

A
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37
Q

acyclovir moa

A

Converted to acyclovir monophosphate (via thymidine kinase) and
triphosphate (via other enzymes) to target viral DNA synthesis
Monophosphate: incorporates into viral DNA = chain termination
Triphosphate: competitive inhibition and inactivation of viral DNA
polymerase

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38
Q

acyclovir rx for adults (recurrent and primary infections)

adjusted for?

A
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39
Q

acyclovir interactions

A

tizanidine

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40
Q

acyclovir adrs

A

GI upset, malaise; Local pain (topical)

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41
Q

valcyclovir preps

A

Oral: tablets (500 mg or 1000 mg)

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42
Q

valcyclovir moa

A

Prodrug which is rapidly converted to acyclovir
[See acyclovir MOA]

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43
Q

valcyclovir dosing (primary and recurrent infections)

adjust for?

A
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44
Q

valcyclovir interaction

A

tizanidine

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45
Q

valcyclovir Adverse Effects

A

GI upset, headache

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46
Q

maternal use of valcyclovir

A

Following maternal administration of valacyclovir, acyclovir is detectable in cord
blood and amniotic fluid; Pregnancy Category B
Higher than serum concentrations present in breast milk (caution)

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47
Q

DDIs: Acyclovir and Valacyclovir

A
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48
Q

penciclovir prep

A

1% external cream

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49
Q

penciclovir moa

A
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50
Q

penciclovir dosing

A
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51
Q

penciclovir ddi

A

minimal

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52
Q

penciclovir adr

A

Erythema, headache

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53
Q

maternal penciclovir

A

not used

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54
Q

famciclovir preps

A

Oral: tablets (125, 250, and 500 mg)
*Tablets contain lactose

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55
Q

famciclovir moa

A

Prodrug which is rapidly converted to active penciclovir
[See Penciclovir MOA]

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56
Q

famciclovir dosing (primary and recurrent infections)

adjust for?

A
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57
Q

famciclovir ddis

A

minimal

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58
Q

famiciclovir adrs

A

Nausea, headache

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59
Q

famciclovir in pregnancy

A
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60
Q

Docosanol preps

A

10% external cream

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61
Q

docosanol moa

A
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62
Q

docosanol dosing

A
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63
Q

docosanol ddi

A

none

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64
Q

docosanol adrs

A

well tolerated

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65
Q

Thymidine Kinase role and selectivity with rx

A
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66
Q

Penciclovir: Efficacy

A

Penciclovir: Efficacy
* Penciclovir 1% cream vs. matching
placebo cream
* 3,057 immunocompetent patients
initiated treatment
* Penciclovir: n = 1,516
* Placebo: n = 1,541
* Penciclovir recipients’ lesions healed
31% faster than placebo patients
* HR 1.31; 95% CI (1.20 to 1.42); P=
0.0001)
* Significant benefit when initiated in
both early (p = 0.001) and later (p =
0.0055) stages
* Effective at speeding healing and
pain relief by ~1 day

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67
Q

acyclovr suspensionexample rx

A
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68
Q

valacyclovir recurrence example rx

A
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69
Q

penciclovir example rx

A
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70
Q

famciclovir recurrence example rx

A
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71
Q

Orthomyxoviruses
* genome
* Responsible for?
* Four generates

A
  • RNA viruses
  • Responsible for causing influenza
  • Four generate infect vertebrates
  • Influenza A (most virulent, “seasonal flu”)
  • Influenza B (“seasonal flu”)
  • Influenza C (milder)
  • Influenza D (infect swine, cattle, sheep – NOT humans)
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72
Q

Influenza A
* Divided into subtypes based on?
* Subtypes known to infect humans:
* Known to cause ?

A
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73
Q

Influenza A and B
* Cause?
* Affect who?
* transmission?
* Incubation period:

A
  • Cause acute viral respiratory disease or “seasonal flu”
  • Affect individuals of all ages worldwide
  • Primarily respiratory droplet transmission person-to-person
    (sneezing, coughing, etc.)
  • Some airborne and indirect contact transmission
  • Incubation period: average ~2 days (range 1-4 days)
74
Q

Influenza A and B
* Manifestations (not comprehensive):

A
  • Fever, nonproductive cough, myalgia, malaise, chills, sore
    throat, nausea, congestion, headache, fatigue
  • Varies based on infecting strain and severity
75
Q

flu A and B drugs

A
  • Oseltamivir (Tamiflu)
  • Baloxivir marboxil (Xofluza)
76
Q

Therapeutic management considerations of flu A and B:

A
  • Treatment vs. post-exposure prophylaxis
  • Severity
  • Onset of symptoms (48-hour window)
77
Q

Oseltamivir prep

oral ans suspension

78
Q

Oseltamivir dosing

tx and prevention,adjust for?

79
Q

Oseltamivir moa

80
Q

Oseltamivir ddi

81
Q

Oseltamivir adr

A

gi, headache

82
Q

Oseltamivir maternal

A

Oseltamivir phosphate and its active metabolite oseltamivir carboxylate cross the
placenta. Use during pregnancy and breastfeeding is acceptable.
Limited excretion into breast milk

83
Q

Neuraminidase Inhibitors diagrammed

84
Q

Baloxavir marboxil prep

A

single tablet pack (40 or 80 mg)

85
Q

Baloxavir marboxil moa

86
Q

Baloxavir marboxil dosage

tx and prophy

87
Q

Baloxavir marboxil ddi

88
Q

Baloxavir marboxil adrs

89
Q

Baloxavir marboxil pregnancy

A

Pregnancy: No adverse events in animal reproduction studies; minimal data; not
recommended
Unknown if excreted in breast milk

90
Q

endonuclease inhibitors diagrammed

91
Q

oseltamavir example rx

92
Q

Baloxavir marboxil example rx

93
Q

Retroviruses

A
  • RNA viruses
  • Responsible for causing acquired immunodeficiency syndrome
    (AIDS), T-cell leukemia
  • Retroviruses with implications in Dentistry
  • HIV-1: Most common; higher rate of transmission, Worldwide
  • HIV-2: Also causes immune suppression; less virulent, Endemic in West Africa
94
Q

Human Immunodeficiency Virus
(HIV)

95
Q

Oral Care challenges for the HIV Patient

96
Q

Oral Complications of HIV

what is seen with low cd4 counts

97
Q

Opportunistic Infections of HIV

cd4 levels for prophy, preffered agents

98
Q

HIV Transmission

A
  • Anal or vaginal intercourse
  • Oral sexual activity
  • Exposure to infected blood
  • Sharing of needles or syringes (injecting drugs,
    tattooing, etc)
  • Accidental percutaneous injury
  • Pregnancy, childbirth, or breastfeeding
99
Q

HIV Post-Exposure Prophylaxis (PEP)

timeframe

100
Q

HIV PEP regimens

101
Q

HIV PrEP

pre tx testing

A

Preventative strategy to prevent transmission of HIV for those who are at high risk but are currently HIV negative
Pre-treatment evaluation and testing:
* HIV, HBV, STI testing
* Renal function, osteoporosis, lipid testing

102
Q

HIV PrEP regimens

A
  • Tenofovir disoproxil fumarate-emtricitabine
  • Tenofovir alafenamide-emtricitabine
103
Q

Reduction of HIV Transmission strategies

104
Q

undetectable HIV means?

A

untransmissable

105
Q

HIV Life Cycle steps

A
  1. Binding
  2. Fusion
  3. Reverse Transcription
  4. Integration
  5. Replication
  6. Assembly
  7. Budding
106
Q

binding anf fusion of hiv

what rx’s stop these stages

107
Q

reverse transcription of hiv

108
Q

integration hiv

109
Q

replication, assembly, and budding of hiv

inhibitory rx?

110
Q

Antiretroviral Therapy
The routine use of a combination of HIV medication classes to?
* Recommended for?
*cure?
* Potential for?

A

The routine use of a combination of HIV medication classes to
treat or prevent HIV
* Recommended for all patients with HIV, regardless of CD4
count
* NOT a cure
* Potential for resistance; adherence is KEY

111
Q

goals of ART

A
  • Reduce morbidity and mortality associated with HIV
  • Restore and preserve immunologic function
  • Suppress plasma HIV viral load
  • Prevent HIV transmission
112
Q

HIV Drug Classes

A

* Nucleoside Reverse Transcriptase Inhibitors (NRTI)
* Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTI)
* Protease Inhibitors (PI)
* Integrase Strand Transfer Inhibitors (INSTI)
* Fusion Inhibitors
* CCR5 Antagonists
* Attachment Inhibitors
* Post-Attachment Inhibitors
* Capsid Inhibitors

113
Q

NRTIs and NNRTIs moa diagrammed

114
Q

NRTIs
* Nucleoside reverse Transcriptase Inhibitors names

A
  • Abacavir (Ziagen)
  • Abacavir-Lamivudine (Epzicom)
    * Abacavir-Lamivudine-Zidovudine (Trizivir)
  • Didanosine (Videx)
  • Emtricitabine (Emtriva)
  • Lamivudine (Epivir)
  • Stavudine (Zerit)
    * Tenofovir alafenamide-Emtricitabine (Descovy)
  • Tenofovir disoproxil fumarate (Viread)
    * Tenofvoir disoproxil fumarate-Emtricitabine (Truvada)
  • Zidovudine (Retrovir)
  • Zidovudine-Lamivudine (Combivir)
115
Q

NRTI moa

A

block and prevent reverse transcriptase enzyme from accurately
copying its RNA into complementary DNA( cDNA

116
Q

Abacavir-Lamivudine-Zidovudine (Trizivir) moa

A

block and prevent reverse transcriptase enzyme from accurately
copying its RNA into complementary DNA( cDNA

117
Q

Tenofovir alafenamide-Emtricitabine (Descovy) moa

A

block and prevent reverse transcriptase enzyme from accurately
copying its RNA into complementary DNA( cDNA

118
Q

Tenofvoir disoproxil fumarate-Emtricitabine (Truvada) moa

A

block and prevent reverse transcriptase enzyme from accurately
copying its RNA into complementary DNA( cDNA)

119
Q

NRTI adrs

common and serious adrs

A
  • Common: N/V/D, upset stomach, headache
  • Serious: bone marrow suppression (and associated increased risk of bleeding or oral ulcers), peripheral neuropathy, pancreatitis, lipoatrophy, hepatic steatosis, lactic acidosis
120
Q

NRTI contraindications

A
  • Abacavir and moderate or severe hepatic insufficiency
121
Q

NRTI ddi

A

minimal
* Tenofovir products and high-dose or multiple NSAIDs  May enhance nephrotoxic effects of tenofovir
* Category D: Consider Therapy Modification

122
Q

NNRTIs
* Non-nucleoside reverse transcriptase inhibitors names

A
  • Doravirine (Pifeltro)
    * Efavirenz (Sustiva)
  • Etravirine (Intelence)
  • Nevirapine (Viramune)
    * Rilpivirine (Edurant)
123
Q

NNRTIs moa

A

block and prevent reverse transcriptase enzyme from accurately
copying its RNA into complementary DNA (cDNA)
* Binding occurs in a pocket further away from active site

124
Q

Efavirenz (Sustiva) moa

A

block and prevent reverse transcriptase enzyme from accurately
copying its RNA into complementary DNA (cDNA)
* Binding occurs in a pocket further away from active site

125
Q

Rilpivirine (Edurant) moa

A

block and prevent reverse transcriptase enzyme from accurately
copying its RNA into complementary DNA (cDNA)
* Binding occurs in a pocket further away from active site

126
Q

nnrtis adr

common ones, sedation? serious adr?

127
Q

Rilpivirine must be administered with?

A

Rilpivirine must be administered with a full meal to increase absorption
(better absorbed with acids)

128
Q

Rilpivirine*
PLUS ddi

129
Q

Efavirenz or Etravirine ddi

130
Q

Protease Inhibitors (PIs) diagrammed

131
Q

Protease Inhibitors (PIs)
* MOA:

A
  • MOA: block protease enzyme to prevent new (immature) HIV from
    becoming a mature virus that can infect other CD4 cells
132
Q

Protease Inhibitors and P450

A
  • CYP3A4 substrates
  • Often “boosted” by pharmacokinetic enhancers
133
Q

protease inhibitors adrs

134
Q

oral adverse effects of :
* Atazanavir, Ritonavir, Fosamprenavir

A
  • Fosamprenavir - Perioral numbness (lips), taste changes
  • Atazanavir - Dental (tooth) pain, taste changes
  • Ritonavir - Taste changes
135
Q

Protease Inhibitors
* Examples:

A

-vir suffix
* Atazanavir (Reyataz)
* Atazanavir-Cobicistat (Evotaz)
* Darunavir (Prezista)
* Darunavir-Cobicistat (Prezcobix)
* Fosamprenavir (Lexiva)
* Indinavir (Crixivan)
* Lopinavir-Ritonavir (Kaletra)
* Nelfinavir (Viracept)
* Saquinavir (Invirase)
* Tipranavir (Aptivus)

136
Q

Atazanavir (Reyataz) moa

A

block protease enzyme to prevent new (immature) HIV from
becoming a mature virus that can infect other CD4 cells

137
Q

Atazanavir-Cobicistat (Evotaz) moa

A

block protease enzyme to prevent new (immature) HIV from
becoming a mature virus that can infect other CD4 cells

138
Q

Darunavir (Prezista) moa

A

block protease enzyme to prevent new (immature) HIV from
becoming a mature virus that can infect other CD4 cells

139
Q

Darunavir-Cobicistat (Prezcobix) moa

A

block protease enzyme to prevent new (immature) HIV from
becoming a mature virus that can infect other CD4 cells

140
Q

Fosamprenavir (Lexiva) moa

A

block protease enzyme to prevent new (immature) HIV from
becoming a mature virus that can infect other CD4 cells

141
Q

Darunavir ddi with:

142
Q

Atazanavir ddi with:

143
Q

Fosamprenavir ddi with:

144
Q

INSTIs moa diagrammed

145
Q

Integrase stand transfer inhibitors

INSTIs moa

A

block integrase enzyme, preventing insertion of HIV viral DNA into the
DNA of the host CD4 cell, thus preventing replication

146
Q

INSTIs general adrs

A
  • Generally well tolerated
  • Increased weight gain, insomnia, dizziness
147
Q

INSTIs adrs for dentistry

A
  • Osteopenia/osteoporosis
  • Xerostomia (dry mouth)
  • Oral ulcers, mucosal irritation
  • Altered taste
  • Increased risk of bleeding
148
Q

INSTIs: DDIs
* Raltegravir PLUS:

A
  • Proton pump inhibitors= may increase concentrations of raltegravir
  • Category B: No Action Needed
149
Q

INSTIs
* Examples:
* suffix?

A

-gravir suffix
* * Cabotegravir (Apretude)
* Dolutegravir (Tivicay)
* Raltegravir (Isentress)
* Elvitegravir (within combination products)
* Bictegravir (within combination products)

150
Q

Dolutegravir (Tivicay) moa

A

block integrase enzyme, preventing insertion of HIV viral DNA into the
DNA of the host CD4 cell, thus preventing replication

151
Q

Bictegravir (within combination products) moa

A

block integrase enzyme, preventing insertion of HIV viral DNA into the
DNA of the host CD4 cell, thus preventing replication

152
Q

backbone hiv therapy

153
Q

Other Drug Classes for HIV

A
  • CCR5 Antagonists
  • Attachment Inhibitors
  • Post-Attachment Inhibitors
  • Capsid Inhibitors
154
Q

Pharmacokinetic Enhancers moa

155
Q

Pharmacokinetic Enhancers general adrs

156
Q

Pharmacokinetic Enhancers dentistry related adrs

which specific PK enhancer?

A
  • Ritonavir: Metallic or bitter taste, oral ulcers or inflammation, perioral numbness/tingling, increased bleeding risk (if DDI with anticoagulants)
  • Dry mouth
157
Q

Pharmacokinetic Enhancers examples

A
  • Ritonavir (Norvir)
  • Cobicistat (Tybost)
158
Q

Ritonavir (Norvir) moa

A

block CYP3A4, increase rx concentration (decreases amoutn rx used= lower toxiciity)

159
Q
  • Cobicistat (Tybost) moa
A

block CYP3A4, increase rx concentration (decreases amoutn rx used= lower toxiciity)

160
Q

Pharmacokinetic Enhancers diagrammed

161
Q

Ritonavir ddis with:

162
Q

Cobicistat ddis with:

163
Q

most common signle tab regimens for HIV

164
Q

Bictegravir-TAF-Emtricitabine MOA’s

A

Bictegravir: INSTI
TAF-Emtricitabine: NRTI

165
Q

Dolutegravir-Abacavir-Lamivudine moa’s

A

Dolutegravir- INSTI
Abacavir- NRTI
Lamivudine- NRTI

166
Q

Dolutegravir-Lamivudine moa’s

A

Dolutegravir- INSTI
Lamivudine- NRTI

167
Q
A

hsv tx agents

168
Q
  • Oseltamivir (Tamiflu)
  • Baloxivir marboxil (Xofluza)
A

flu A and B drugs

169
Q
  • Abacavir (Ziagen)
  • Abacavir-Lamivudine (Epzicom)
    * Abacavir-Lamivudine-Zidovudine (Trizivir)
  • Didanosine (Videx)
  • Emtricitabine (Emtriva)
  • Lamivudine (Epivir)
  • Stavudine (Zerit)
    * Tenofovir alafenamide-Emtricitabine (Descovy)
  • Tenofovir disoproxil fumarate (Viread)
    * Tenofvoir disoproxil fumarate-Emtricitabine (Truvada)
  • Zidovudine (Retrovir)
  • Zidovudine-Lamivudine (Combivir)
A

NRTIs
* Nucleoside reverse Transcriptase Inhibitors names

170
Q
  • Doravirine (Pifeltro)
    * Efavirenz (Sustiva)
  • Etravirine (Intelence)
  • Nevirapine (Viramune)
    * Rilpivirine (Edurant)
A

NNRTIs
* Non-nucleoside reverse transcriptase inhibitors names

171
Q

* Atazanavir (Reyataz)
* Atazanavir-Cobicistat (Evotaz)
* Darunavir (Prezista)
* Darunavir-Cobicistat (Prezcobix)
* Fosamprenavir (Lexiva)
* Indinavir (Crixivan)
* Lopinavir-Ritonavir (Kaletra)
* Nelfinavir (Viracept)
* Saquinavir (Invirase)
* Tipranavir (Aptivus)

A

Protease Inhibitors
* Examples:

172
Q
  • Cabotegravir (Apretude)
    * Dolutegravir (Tivicay)
  • Raltegravir (Isentress)
  • Elvitegravir (within combination products)
  • Bictegravir (within combination products)
A

INSTIs
* Examples:

173
Q
  • Ritonavir (Norvir)
  • Cobicistat (Tybost)
A

Pharmacokinetic Enhancers examples

174
Q

what can these formulations be used for?

A

HIV PEP regimens

175
Q

mechanism of what rx?

block and prevent reverse transcriptase enzyme from accurately
copying its RNA into complementary DNA( cDNA

176
Q

block and prevent reverse transcriptase enzyme from accurately
copying its RNA into complementary DNA (cDNA)
* Binding occurs in a pocket further away from active site

A

NNRTIs moa

177
Q
  • MOA: block protease enzyme to prevent new (immature) HIV from
    becoming a mature virus that can infect other CD4 cells
A

Protease Inhibitors (PIs)
* MOA:

178
Q

block integrase enzyme, preventing insertion of HIV viral DNA into the
DNA of the host CD4 cell, thus preventing replication

A

Integrase stand transfer inhibitors

INSTIs moa

179
Q
A

Pharmacokinetic Enhancers moa

180
Q

what HIV rx is both a PI and a PK enhancer?

pharm 2 (20 decks)

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