Anti-HIV Drugs

Antiretroviral therapy (ART) targets the replication cycle of the human immunodeficiency virus (HIV) and is classified based on the viral enzyme or mechanism that is inhibited. The goal of therapy is to suppress viral replication to reach the outcome of undetected viral load. Currently, reverse transcriptase, protease, integrase, and entry inhibitors are used in combined ART (cART) regimens. Combination therapy (3-drug regimen) is used to prevent drug resistance and cross-resistance, which develop through genetic mutations.

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Antiretroviral drugs

  • Classified based on the phase of the retrovirus life cycle that the drug inhibits
  • Goal: suppress viral replication in human immunodeficiency virus (HIV) infection
  • Standard of care: at least 3 drugs taken simultaneously

Virion structure of HIV

  • Virion envelope contains 2 membrane glycoproteins:
    • gp41 (transmembrane)
    • gp120 (surface/docking protein)
  • Matrix protein p17: surrounds the virus core
  • Virus core: 
    • Capsid protein p24
    • 2 single-stranded, enveloped positive-sense ribonucleic acid (RNA) coated with nucleocapsid protein
    • Enzymes (reverse transcriptase, integrase, protease)

Replication cycle of HIV

  • Target cells: CD4+ T cells, macrophages, and dendritic cells
  • HIV cell entry: 
    • The virion first enters via a break in the mucous membrane. 
    • The virion crosses the mucosal barrier and seeks target cells.
  • HIV replication:
    1. Membrane fusion and binding of receptors (entry): the virion (carrying viral RNA, reverse transcriptase, integrase, and other proteins) initiates entry into the host cell. 
      • Virion binds the CD4 receptor and a chemokine receptor (CCR5 on macrophages, CXCR4 on T cells). 
        • Macrophage tropic viruses: R5 strains
        • T cell tropic viruses: X4 strains
      • Binding of gp120 with CD4 and the chemokine receptors leads to a conformational change, exposing the fusion domain at gp41.
      • This process pulls the viral and cellular membranes together, fusing them. 
    2. The capsid protein shell (surrounding the viral RNA and proteins) is uncoated as the virion traverses the cytoplasm.
    3. Reverse transcription: Reverse transcriptase-mediated synthesis of proviral deoxyribonucleic acid or DNA (from the viral RNA) occurs.
    4. Integration: Viral DNA is transported across the nucleus and integrated into the host DNA, facilitated by integrase.
    5. Replication: Viral DNA is transcribed and multiple copies of new HIV RNA are formed, which are transported to the cytoplasm. 
      • New HIV RNA becomes the genome of the new virus. 
      • Other copies of the RNA are used to make new HIV proteins.
    6. Assembly: New viral RNA + proteins + enzymes move to the cell surface and form noninfectious particles.
    7. Budding and maturation: 
      • Particles (viral RNA + proteins) eventually bud out of the host cell with the immature HIV.
      • Viral protein protease then cleaves the newly synthesized polyproteins, producing mature HIV.
HIV replication cycle

HIV replication cycle:
1. Virion binds the CD4 receptor and a chemokine receptor, followed by a conformational change that facilitates fusion of the virion and the host cell.
2. A capsid protein shell (surrounding the viral RNA and proteins) is uncoated as the virion traverses the cytoplasm.
3. Reverse transcriptase-mediated synthesis of proviral DNA occurs.
4. Viral DNA is transported across the nucleus and integrated into the host DNA, facilitated by integrase.
5. Viral DNA is transcribed, and multiple copies of new HIV RNA form and are transported to the cytoplasm. New HIV RNA becomes the genome of a new virus. Cytokine activation of the cell also occurs.
6. New viral RNA + proteins + enzymes move to the cell surface and form a noninfectious particle.
7. Particle (viral RNA + proteins) eventually buds out of the host cell with the immature HIV. Viral protein protease (enzyme) then cleaves newly synthesized polyproteins producing a mature HIV.

Image by Lecturio.

Major classes of antiretroviral drugs

Table: Major classes of antiretroviral drugs
Type of drugMechanism of action
Reverse transcriptase inhibitors
  • NRTIs: nucleoside reverse transcriptase inhibitors
  • NtRTIs: nucleotide reverse transcriptase inhibitors
  • NNRTIs: non-nucleoside reverse transcriptase inhibitors
  • Interfere with the translation of viral RNA into DNA
  • Affect reverse transcription
Integrase strand transfer inhibitors (INSTIs)
  • Prevent the insertion of the viral genome into the host DNA
  • Affect integration
Protease inhibitors (PIs)
  • Block the cleavage of protein precursors (by protease) necessary to produce mature infectious viral particles
  • Affect budding and maturation
Entry inhibitors:
  • CCR5 antagonists
  • Fusion inhibitors
  • Attachment inhibitors
  • Inhibit virion binding via gp120 (attachment inhibitor) or CCR5 receptor (CCR5 antagonist), and virion-host cell fusion (fusion inhibitor)
  • Affect viral entry
Post-attachment inhibitorBinds CD4 molecule, blocking entry but not the attachment
HIV drug classes

Schematic description of the mechanism of 4 classes of antiretroviral drugs against HIV:
Fusion or entry inhibitors: interfere with the binding, fusion, or entry of the HIV virion
Reverse transcriptase inhibitors: interfere with the translation of viral RNA into DNA
Integrase inhibitors: prevent the insertion of the viral genome into the host DNA
Protease inhibitors: block cleavage of the protein precursors necessary for the production of infectious viral particles

Image: “HIV-drug-classes” by Thomas Splettstoesser. License: CC BY 3.0, edited by Lecturio.

Failure of an antiretroviral regimen

  • Persistently elevated plasma HIV RNA levels in patients with previously undetectable virus, even with continued treatment 
  • Indicates resistance to 1 or more drugs in the regimen 
  • Requires change in regimen (need to implement a completely new combination of drugs)

Nucleoside Reverse Transcriptase Inhibitors and Nucleotide Reverse Transcriptase Inhibitors


  • NRTIs:
    • Zidovudine (ZDV) or azidothymidine (AZT): representative NRTI
    • Lamivudine (3TC)
    • Abacavir (ABC)
    • Emtricitabine (FTC)
    • Entecavir (ETV)
    • Truvada (emtricitabine/tenofovir)
    • Zalcitabine (ddC): discontinued
  • NtRTI (tenofovir, the only nucleotide analog):
    • Tenofovir alafenamide (TAF) 
    • Tenofovir disoproxil fumarate (TDF)
  • NRTIs no longer recommended for use (United States Department of Health and Human Services (HHS), 2019):
    • Didanosine (ddI): lactic acidosis, pancreatitis
    • Stavudine (d4T): lactic acidosis, pancreatitis

Mechanism of action

  • Act as chain terminators of the proviral DNA (lack 3′-hydroxy group, so other nucleotides cannot continue attaching)
  • Competitively bind to the deoxynucleotide triphosphate (dNTP)-binding site of reverse transcriptase, terminating elongation

Side effects

  • Mitochondrial toxicity:
    • Intracellular triphosphates for NRTIs do not affect human DNA polymerase α and polymerase β. 
    • Some intracellular triphosphates for NRTIs inhibit human DNA polymerase γ (mitochondrial enzyme), resulting in toxicities related to the inhibition of mitochondrial DNA synthesis.
    • Seen as: 
      • Lipodystrophy: abnormal distribution of fat, “buffalo hump”
      • Hepatic steatosis
      • Peripheral neuropathy
      • Pancreatitis
      • Lactic acidosis
    • Didanosine, stavudine: ↑ risk of mitochondrial toxicity
    • Phosphorylated emtricitabine, lamivudine, and tenofovir do not affect human DNA polymerase γ (no mitochondrial toxicity).
  • Bone marrow suppression: anemia, neutropenia, thrombocytopenia
  • Gastrointestinal (GI): nausea, vomiting, diarrhea, acute cholestatic hepatitis
  • Agitation, headaches, myalgia, and insomnia

Important features

  • NRTIs: for HIV-1 and HIV-2 infections
  • NRTIs are prodrugs: should be triphosphorylated to be active
  • NtRTI (tenofovir): should be diphosphorylated to be active
  • Metabolism and elimination:
    • Tenofovir: long elimination half-life (17 hours)
    • Emtricitabine, lamivudine, tenofovir: renal excretion of parent drug
    • Zidovudine, abacavir: hepatic (glucuronidation)
  • Resistance: rapid, especially when used as single agent

Summary of NRTI and NtRTI drugs

Table: NRTIs and NtRTIs
DrugAdverse effectsInteractions/contraindications
Zidovudine (AZT):
  • First ARV drug for HIV
  • Crosses the placenta (prevents mother-to-child transmission)
  • Lactic acidosis, hepatomegaly, hepatic steatosis
  • Bone-marrow suppression: anemia and neutropenia
  • GI: vomiting, diarrhea
  • Headache, myopathy, insomnia, nail hyperpigmentation
  • Diabetes, acute cholestatic hepatitis
  • Azole antifungals, valproic acid, atovaquone increase plasma levels
  • Caution in anemia, neutropenia, liver dysfunction (requires dose adjustment)
Emtricitabine: structurally similar to lamivudine
  • Minimal toxicity
  • Palmoplantar hyperpigmentation, headache, diarrhea, rash
  • Severe hepatitis in those infected with HBV, if medication is discontinued
Do not combine with lamivudine (the drugs compete with intracellular phosphorylation).
Lamivudine: active against the hepatitis B virus
  • Generally well tolerated
  • Pancreatitis in children
  • Severe hepatitis in those with HBV, if medication is discontinued
Do not combine with emtricitabine (the drugs compete with intracellular phosphorylation).
AbacavirHypersensitivity reaction (potentially fatal): fever, rash, abdominal pain, vomiting, dyspnea
  • Contraindicated in patients who are HLAB*5701 positive (risk of hypersensitivity reaction)
  • Associated with CV events
Tenofovir (NtRTI): TAF and TDF (TAF: active against the hepatitis B virus)
  • GI symptoms
  • Renal injury (TDF > TAF), Fanconi syndrome, bone loss (TDF > TAF)
  • Severe hepatitis in those infected with HBV, if medication is discontinued
  • Concurrent use of didanosine contraindicated
  • Decreases serum atazanavir levels
ARV: antiretroviral
CV: cardiovascular
GI: gastrointestinal
HBV: hepatitis B virus
HIV: human immunodeficiency virus
TAF: tenofovir alafenamide
TDF: tenofovir disoproxil fumarate

Non-nucleoside Reverse Transcriptase Inhibitors


  • 1st generation:
    • Efavirenz (EFV)
    • Nevirapine (NVP): not for initial treatment of HIV
  • 2nd generation:
    • Etravirine (ETV)
    • Rilpivirine (RPV)
    • Doravirine (DOR)
  • Delavirdine (DLV): no longer recommended for use (United States HHS, 2019)

Mechanism of action

Non-competitive inhibitors of reverse transcriptase: 

  • Bind directly to reverse transcriptase and inhibit viral DNA synthesis
  • Induce conformational changes in the enzyme structure, making it inactive
Antivirals Anti-HIV-drugs

Diagram of the mechanism of action of NRTIs and NNRTIs:
A: Note how NRTIs block the growing viral DNA genome by substituting the naturally occurring nucleosides and functioning as chain terminators.
B: On the other hand, NNRTIs bind directly to the reverse transcriptase enzyme, directly preventing viral DNA synthesis.
NRTI: nucleoside reverse transcriptase inhibitor
NNRTI: non-nucleoside reverse transcriptase inhibitor
RNAseH: ribonuclease H

Image by Lecturio.

Side effects

  • Rash, GI symptoms, headache, fever
  • Hepatotoxicity (increase in liver enzymes)

Important features

  • For HIV-1 infection
  • No effect on host-cell DNA polymerase
  • Metabolism: hepatic (by cytochrome P450 (CYP))
  • Concomitant use of potent CYP inducers or inhibitors should be avoided.
  • Resistance: 
    • Drug-resistance rate: 2%–8%
    • 1st-generation drugs have different resistance profiles than 2nd-generation drugs.
    • Do not use as monotherapy; should be combined with other agents to avoid resistance.

Summary of NNRTI drugs

Table: NNRTI drugs
DrugAdverse effectsInteractions/contraindications
Etravirine: most commonly used NNRTI in resistant HIV cases
  • Rash
  • Nausea
Can interact with other antiretroviral drugs (e.g., if in combination, dose of maraviroc should be doubled)
  • CNS/psychiatric effects: ↓ concentration, dizziness, dysphoria
  • Rash
  • QT prolongation
  • Hepatitis
Avoid in long QT syndrome, liver disease, psychiatric illness
DoravirineCNS/psychiatric effects similar to efavirenz (but much less common)Use with rifampin contraindicated (↓ doravirine exposure)
  • QT prolongation
  • Rash
  • Depression, insomnia, headache
  • Absorption is pH dependent, so, it should not be administered with PPIs, H2 inhibitors/antacids.
  • Avoid in long QT syndrome
Nevirapine: not initial treatment of treatment-naive patients (↑ toxicity)
  • Hepatic necrosis
  • Rash, serious cutaneous reactions
  • If considered, avoid in patients in moderate to severe hepatic disease.
  • If considered, avoid in women with CD4 count > 250 cells/mL or in men with CD4 count > 400 cells/mL (threshold for hepatotoxicity).
CNS: central nervous system

Protease Inhibitors


  • Darunavir (DRV)
  • Atazanavir (ATV)
  • Ritonavir (RTV)
  • Lopinavir (LPV): not for initial treatment of HIV
  • Fosamprenavir (FPV): not for initial treatment of HIV
  • Tipranavir (TPV): not for initial treatment of HIV
  • No longer recommended for use (United States HHS, 2019): 
    • Indinavir (IDV)
    • Nelfinavir (NFV)
    • Saquinavir (SQV): discontinued in the United States

Mechanism of action

  • Attachment to HIV aspartyl protease enzyme, preventing cleavage of Gag-Pol polyproteins and making the newly created virions immature/non-infectious
  • Boosting protease inhibitors (PIs):
    • Goal: inhibit metabolic clearance of HIV PIs (to improve oral bioavailability and prolong elimination half-life)
    • Medications/boosting agents used:
      • Ritonavir
      • Cobicistat (a ritonavir analog): better tolerated 
    • Effects:
      • Allows for reduction in drug dose and dosing frequency 
      • Increases drug concentration

Side effects

  • GI symptoms: nausea, vomiting, and diarrhea
  • Dyslipidemias, fat deposition, or metabolic syndrome
  • Lipodystrophy
  • Hepatotoxicity
  • Hyperglycemia, diabetes
  • Nephrolithiasis
  • Bleeding in hemophilia
  • PR prolongation

Important features

  • Active against:
    • HIV-1 and HIV-2
    • Hepatitis C 
  • Metabolism: 
    • Extensively metabolized by CYP 3A4 (except nelfinavir: CYP 2C19)
    • Concomitant administration of other potent CYP inducers or inhibitors should be avoided.
  • Resistance uncommon

Summary of protease inhibitors

Table: Protease inhibitors
DrugAdverse effectsInteractions/contraindications
  • Hyperbilirubinemia (indirect), cholestasis/cholecystitis, abnormal LFTs
  • ↑ Risk of kidney stones
  • Lower risk of hyperlipidemia than other protease inhibitors
  • Food increases absorption and bioavailability.
  • Avoid PPIs, antacids (reduce atazanavir concentration)
  • GI symptoms
  • Hepatotoxicity
  • Rash
  • Given with low-dose ritonavir/cobicistat; combination drug increases maraviroc levels (the dose of which needs to be reduced)
  • Avoid in severe liver disease
Ritonavir: booster
  • GI symptoms
  • Paresthesias
  • Lipid abnormalities
One of the most potent known inhibitors of CYP3A4; avoid taking drugs with narrow therapeutic index.
Lopinavir: coformulated with ritonavir
  • GI symptoms
  • Lipid abnormalities
Not for initial treatment (related to potency and toxicity)
CYP: cytochrome P450
GI: gastrointestinal
LFTs: liver function tests
PPIs: proton pump inhibitors

Integrase Strand Transfer Inhibitors


  • Raltegravir (RAL)
  • Elvitegravir (EVG)
  • Dolutegravir (DTG)
  • Bictegravir (BIC)

Mechanism of action

  • Binds to viral integrase enzyme, responsible for integration of viral DNA into host DNA of the infected cell 
  • Inhibits binding of the preintegration complex

Side effects

  • Usually well tolerated
  • Weight gain
  • GI symptoms, dizziness, fatigue
  • Increases creatine kinase (potential myopathy or rhabdomyolysis)
  • Depression (suicidal ideations)

Important features

  • Effective against both HIV-1 and HIV-2
  • Considered preferred 3rd agent for treatment-naïve patients
  • Neutral effect on lipids; option for patients with coronary artery disease
  • Metabolism:
    • Raltegravir and dolutegravir: glucuronidation
    • Bictegravir: cleared by glucuronidation and CYP
    • Elvitegravir: formulated with cobicistat (which is metabolized by CYP); thus, associated with ↑ drug-drug interactions 
  • Resistance to raltegravir or elvitegravir increases risk of integrase resistance.
  • Resistance uncommon with dolutegravir, bictegravir

Summary of integrase strand transfer inhibitors

Table: Integrase strand transfer inhibitors
DrugAdverse effectsInteractions/contraindications
  • Usually well tolerated
  • GI symptoms most common
  • Dizziness, headache, potential myopathy, depression (suicidal ideation)
  • Rash
Enzyme inducers (e.g., rifampin) increase its metabolism by inducing UDP-glucuronosyltransferase.
DolutegravirMild reversible creatinine elevation (inhibits the renal transporter, OCT2)
  • Contraindicated in patients with Q148 mutation
  • Enzyme inducers (e.g., rifampin) increases its metabolism by inducing UDP-glucuronosyltransferase.
Elvitegravir: administered with cobicistat or ritonavirGI symptomsCurrently available only in a fixed-dose combination with tenofovir, emtricitabine, and cobicistat (which ↑ drug-drug interactions)
Bictegravir: coformulated with emtricitabine and TAF
  • Diarrhea
  • Headache
  • Weight gain
Intake with rifampin or dofetilide contraindicated
GI: gastrointestinal
OCT2: organic cation transporter-2
TAF: tenofovir alafenamide
UDP: uridine-5′-diphospho

Entry Inhibitors and Post-attachment Inhibitor

Entry inhibitors

  • CCR5 antagonist: maraviroc (MVC)
    • Mechanism of action: blocks CCR5 coreceptor, interfering with HIV entry
    • Side effects:
      • Hepatotoxicity
      • Rash or systemic allergic reactions
      • Cough, upper respiratory infections
      • Joint pains
    • Important features:
      • For predominantly CCR5-tropic virus (HIV-1)
      • Metabolism: renal and hepatic
      • In all regimens where maraviroc is combined with other antiretrovirals, dose adjustment is needed.
      • When combined with CYP3A inhibitors → maraviroc dose is lower; with CYP3A inducers → maraviroc dose is higher
      • Resistance develops when coreceptor switch occurs (shift in tropism).
  • Fusion inhibitor: enfuvirtide (INN)
    • Mechanism of action: binds gp41 of HIV, preventing fusion with CD4 T cell
    • Side effects: 
      • Complications at the injection site (pain, erythema, induration, and nodules)
      • Increased incidence of pneumonia 
    • Important features: 
      • For HIV-1 infection
      • Administered as subcutaneous injection
      • Does not inhibit CYP or affect CYP substrates
  • Attachment inhibitor: fostemsavir (FTR)
    • Mechanism of action: 
      • Fostemsavir: a prodrug that is converted to temsavir
      • Temsavir binds gp120, inhibiting virion attachment to the host T cell.
    • Side effects: 
      • Nausea
      • QT prolongation
      • Can increase liver enzymes in patients with hepatitis B/C
    • Important features:
      • For HIV-1 infection
      • Potent CYP3A inducer that decreases drug levels
HIV entry into a host cell

Schematic diagram of viral entry and steps inhibited by enfuvirtide and maraviroc:
The trimeric gp120 subunit of the viral envelope glycoprotein complex binds CD4 on the target cell surface, triggering a conformational change that promotes interactions with chemokine receptors (in this case CCR5). The trimeric transmembrane subunit gp41 is activated to mediate membrane fusion so that the viral contents can enter the cell. Maraviroc blocks the CCR5 coreceptor. Enfuvirtide binds gp41, preventing fusion.

Image: “HIV entry into a host cell” by Laboratory of Experimental Virology, Department of Medical Microbiology, Center for Infection and Immunity Amsterdam (CINIMA), Academic Medical Center, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands. License: CC BY 2.0

Post-attachment inhibitor

  • Drug: ibalizumab
  • Mechanism of action:
    • Monoclonal antibody
    • Binds CD4 molecule and blocks virion entry
  • Side effects:
    • Rash
    • GI symptoms
    • Dizziness
    • Increased creatinine
  • Important features:
    • For HIV-1 infection
    • For patients with multidrug resistance
    • Administered intravenously (after initial dose, given every 14 days)

Combined Antiretroviral Therapy (cART) Regimens

Antiretroviral guidelines for adults and adolescents (HHS, 2019)

  • Antiretroviral therapy (ART) recommended to:
    • Reduce morbidity and mortality
    • Reduce HIV transmission
  • ART must be initiated immediately after the diagnosis of HIV.
  • Recommended initial regimens:
    • Bictegravir + tenofovir alafenamide + emtricitabine 
    • Dolutegravir + tenofovir alafenamide/disoproxil fumarate + emtricitabine or lamivudine
    • Raltegravir + tenofovir alafenamide/disoproxil fumarate + emtricitabine or lamivudine 
  • Initial regimens that have to meet certain criteria:
    • Dolutegravir + abacavir + lamivudine: only for individuals who are HLA-B*5701 negative and without chronic hepatitis B 
    • Dolutegravir + lamivudine, except for:
      • Individuals with HIV RNA > 500,000 copies/mL
      • Individuals with hepatitis B virus (HBV) co-infection
      • Individuals in whom ART should be initiated before obtaining results of HIV genotypic resistance testing for reverse transcriptase or HBV testing

Antiretroviral management of pregnant women

  • Treatment-naïve pregnant women are recommended ART.
  •  Drug regimen consists of:
    • Dual NRTI backbone
    • 3rd drug (either integrase inhibitor or protease inhibitor)
  • Regimen:
    • NRTI backbone options:
      • Abacavir + lamivudine (Abacavir should not be used in patients positive for HLA-B*5701; not recommended if pretreatment HIV RNA is > 100,000 copies/mL)
      • Tenofovir disoproxil fumarate + emtricitabine
      • Tenofovir disoproxil fumarate + lamivudine
    • 3rd drug options:
      • Dolutegravir (small risk of neural-tube defects)
      • Raltegravir
      • Atazanavir + ritonavir (risk of maternal hyperbilirubinemia)
      • Darunavir + ritonavir

Antiretroviral management of newborns

  • Low risk of perinatal HIV transmission:
    • Considered in:
      • Mothers on ART during pregnancy, who are compliant
      • Confirmed HIV RNA level of < 50 copies/mL (viral suppression) near delivery
    • Neonatal medication: zidovudine for 4 weeks
  • High risk of perinatal HIV transmission:
    • Considered in:
      • Mothers without antepartum/intrapartum ART or only intrapartum ART
      • Mothers without viral suppression
      • Mothers with acute HIV during pregnancy or breastfeeding
    • Intrapartum: intravenous zidovudine if HIV RNA > 1,000 copies/mL
    • Birth up to 6 weeks (presumptive HIV therapy for neonates): 
      • Zidovudine + lamivudine + nevirapine 
      • Zidovudine + lamivudine + raltegravir
  • Presumed newborn exposure:
    • Considered in:
      • Mothers who have at least 1 positive HIV test at delivery or postpartum
      • Mothers whose newborns have a positive HIV-antibody test
    • Same as presumptive HIV therapy for neonates
  • Newborns with HIV (confirmed HIV virologic test): use 3-drug ART (using appropriate doses)


  1. Fletcher, C., Bartlett, J., Mitty, J. (2020) Overview of antiretroviral agents used to treat HIV. Retrieved 11 Jan 2021, from
  2. Flexner C.W. (2017). Antiretroviral agents and treatment of HIV infection. Brunton L.L., & Hilal-Dandan R, & Knollmann B.C.(Eds.), Goodman & Gilman’s: The Pharmacological Basis of Therapeutics, 13e. McGraw-Hill.
  3. Panel on Antiretroviral Guidelines for Adults and Adolescents. Guidelines for the Use of Antiretroviral Agents in Adults and Adolescents with HIV. Department of Health and Human Services. Retrieved 11 Jan 2021, from
  4. Panel on Antiretroviral Therapy and Medical Management of Children Living with HIV. Guidelines for the Use of Antiretroviral Agents in Pediatric HIV Infection. Retrieved 13 Jan 2021, from
  5. Panel on Treatment of Pregnant Women with HIV Infection and Prevention of Perinatal Transmission. Recommendations for the Use of Antiretroviral Drugs in Pregnant Women with HIV Infection and Interventions to Reduce Perinatal HIV Transmission in the United States. Retrieved 13 Jan 2021, from
  6. Safrin, Sharon (2021) “Antiviral Agents.” Basic & Clinical Pharmacology, 15e Eds. Bertram G. Katzung, and Todd W. Vanderah. McGraw-Hill.

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