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Monoclonal Antibody Therapy For High-Risk COVID 19 Patients With Mild To Moderate Disease

Abdul Aleem; Amy K. Slenker.

Please note: This is a technical read.

Introduction Since being declared a global pandemic by the World Health Organization WHO), Coronavirus disease 2019 (COVID-19), the illness caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has had a devastating effect on global health and the world economy. The virus primarily affects the respiratory system and is spread from person to person via respiratory particles from coughing and sneezing. The majority of transmission occurs from close contact with presymptomatic, asymptomatic, or symptomatic carriers. The early course of the pandemic was characterized by the rapid spread of the virus that created an urgency to mitigate this new viral illness with experimental therapies and drug repurposing. Since then, due to an intense global research effort, significant progress has been made that has resulted in the development of novel therapeutics and vaccines at an unprecedented speed, leading to favorable patient outcomes. Currently, a variety of therapeutic options that include antiviral medications, monoclonal antibodies, and immunomodulatory agents are available in the management of COVID-19. However, the therapeutic potential and clinical use of these drugs are limited and specifically based on the stage of the illness.

The pathogenesis of COVID-19 illness occurs in two distinct phases, an early stage characterized by profound SARS-CoV-2 viral replication followed by a late phase characterized by a hyperinflammatory state induced by the release of cytokines such as tumor necrosis factor-α (TNF α), granulocyte-macrophage colony-stimulating factor (GM-CSF), Interleukin (IL) 1, IL-6, interferon (IFN)-γ, and activation of the coagulation system resulting in a prothrombotic state. Antiviral therapy and antibody-based treatments are likely to be more effective if used during the early phase of the illness, and immunomodulating therapies either alone or in combination with antiviral and antibody-based therapies may be more effective when used in the later stage to combat the cytokine-mediated hyperinflammatory state that causes severe illness.[1]

Individuals of all ages are at risk for infection and severe disease. However, individuals aged ≥65 years and with underlying medical comorbidities (obesity, cardiovascular disease, chronic kidney disease, diabetes, chronic lung disease, smoking, cancer, solid organ or hematopoietic stem cell transplant recipients) are at increased risk of developing severe COVID-19 infection. The percentage of COVID-19 patients requiring hospitalization was six times higher in those with preexisting medical conditions than those without medical conditions (45.4% vs. 7.6%) based on an analysis by Stokes et al. of confirmed cases reported to the US Centers for Disease Control and Prevention (CDC) during January 22 to May 30, 2020.[2]

A promising approach to address the COVID-19 associated mortality and prevent the increased utilization of healthcare resources is by terminating the progression of viral replication, thereby preventing the progression to the hyperinflammatory stage of COVID-19, which causes severe illness in high-risk nonhospitalized patients. Initially, the focus of treatment was directed mainly towards hospitalized patients with COVID-19 illness. However, the clinical focus throughout the pandemic has expanded toward combatting the illness early on by reducing the viral load in patients with early disease, thus attempting to halt the disease progression.

Monoclonal antibodies targeting the spike protein of the SARS-CoV-2 have yielded positive in vitro results.[3][4] They are considered a promising approach in managing nonhospitalized patients with mild to moderate COVID-19 who are at high risk of developing severe illness. This review discusses the mechanism of action of monoclonal antibodies against SARS-CoV-2 and current clinical indications of monoclonal antibody therapy for nonhospitalized patients with mild to moderate COVID-19 illness who are at high risk of developing severe illness. According to the US National Institutes for Health (NIH), management of nonhospitalized patients with COVID-19 includes:[5] Supportive/symptomatic care, reducing the risk of transmission, and advising patients when to seek in-person medical evaluation

  • Advising patients with dyspnea to seek in-person medical evaluation

  • Anti-SARS-CoV-2 monoclonal antibodies are recommended for mild to moderate severity outpatients that are at high risk of progressing to severe disease

  • For patients discharged from the emergency department on supplemental oxygen, they recommend dexamethasone 6 mg once daily for the duration of oxygen supplementation, not to exceed ten days

  • For patients not on oxygen therapy, they recommend against the use of dexamethasone

  • They found insufficient evidence for or against the use of remdesivir in patients discharged from the emergency department on supplemental oxygen

Monoclonal Antibodies in COVID-19 Monoclonal antibodies (mAbs) are immune system proteins developed from a single cell lineage that demonstrate a high affinity for their target cell. Monoclonal antibodies were first developed by Köhler and Milstein in 1975 using hybridoma technology.[6] Since then, significant progress has been made in the molecular engineering world that has enabled the establishment of monoclonal antibodies as targeted therapies in various neoplastic conditions, autoimmune, post-transplant immunosuppression, and infectious diseases.[7] When used as antiviral therapies, neutralizing antibodies play an integral part in achieving passive antiviral immunity and are also instrumental in preventing or regulating many viral illnesses. Over the years, passive immunization against many viral diseases was achieved by administering polyclonal sera obtained from convalescent human donors or animals. However, polyclonal antibody preparations are increasingly being replaced by monoclonal antibodies by virtue of them, demonstrating a favorable safety profile and target specificity when used in different viral diseases.[8] Palivizumab was the first antiviral monoclonal antibody approved by the US Food and Drug Administration (FDA) for prophylaxis of respiratory syncytial virus (RSV) in high-risk infants.[9] Over the years, significant developments in antibody engineering, improved understanding of the biology of viruses, and the direct and indirect effect of monoclonal antibodies on viral infections has resulted in the development of many novel monoclonal antibodies. Like other antiviral drugs, monoclonal antibodies, when used as antiviral agents, are also susceptible to developing resistance as a result of alterations in the viral genome which can alter the pathogenic potential of the virus resulting in the emergence of viral escape mutants, which may render the virus-resistant to a specific monoclonal antibody. To counter this viral escape phenomenon, a combination of monoclonal antibodies, commonly referred to as antibody cocktails, have been proposed with the rationale that combining two specific monoclonal antibodies that complement each other can prevent neutralization escape by targeting multiple viral epitopes. There are an estimated 70 monoclonal antibodies currently in development or clinical trials to treat COVID-19. The FDA has granted four agents an emergency use authorization (EUA) for clinical use as combination antibody cocktails and one agent as monotherapy.

Mechanism of Action of Monoclonal Antibodies Against SARS-CoV-2 Pathophysiology of COVD-19 is described by the entry of SARS-CoV-2, the causative virus, into the hosts' cells by binding the SARS-CoV-2 spike or S protein (S1) to the angiotensin-converting enzyme 2 (ACE2) receptors expressed abundantly on the respiratory epithelium, such as type II alveolar epithelial cells. This process is mediated by the receptor-binding domain (RBD) on the spike protein followed by priming of the spike protein (S2) by the host transmembrane serine protease 2 (TMPRSS2) that facilitates cell entry and subsequent viral replication.[10] Monoclonal antibodies prevent the viral attachment by binding to a non-overlapping epitope on the surface spike protein RBD of SARS-CoV-2 with high affinity, thereby blocking the binding of the virus to the human ACE2 receptor.

Effect of Different Monoclonal Antibodies Against SARS-CoV-2 with Clinical Trial Summaries

  • CAS/IMDEV (formerly called REGN-COV2; casirivimab and imdevimab) is an antibody cocktail containing two noncompeting IgG1 antibodies (casirivimab and imdevimab), which target SARS-CoV-2 spike RBD and have been shown to neutralize the viral load in vivo, preventing virus-induced pathological sequelae when administered prophylactically or therapeutically in non-human primates.[3] The rationale behind combining two antibodies in a cocktail approach is to minimize mutational viral escape. Interim analysis results from a double-blind trial involving 275 non-hospitalized patients with COVID-19 who were randomized to receive placebo, 2.4 g of CAS/IMDEV (casirivimab 1,200 mg and imdevimab 1,200 mg) or 8 g of CAS/IMDEV (casirivimab 2,400 mg and imdevimab 2,400 mg) showed that the CAS/IMDEV antibody cocktail reduced viral load with a more significant effect in patients whose immune response had not yet been stimulated or who had a high viral load at baseline. This interim analysis also established the safety profile of this cocktail antibody, similar to that of the placebo group.[11] Preliminary data from a Phase 3 trial of CAS/IMDEV revealed a 70% reduction in hospitalization or death in non-hospitalized patients with COVID-19. In vitro data is available regarding the effect of CAS/IMDEV on SARS-CoV-2 variants of concern (VoC) that reveal retained activity.[12]

  • Bamlanivimab (LY-CoV555 or LY3819253) is a potent neutralizing monoclonal antibody derived from convalescent plasma obtained from a patient with COVID-19. REGN-COV2 also targets the RBD of the spike protein of SARS-CoV-2 or S protein and has been shown to potently neutralize SARS-CoV-2 and reduce viral replication in non-human primates.[13][14] Results from the phase 2 trial (BLAZE-1) involving outpatients with a recent diagnosis of mild to moderate COVID-19 who were randomized to receive 1 of 3 doses (700 mg, 2800 mg, or 7000 mg) of bamlanivimab or placebo reported that patients who received bamlanivimab monotherapy did not have a significant decline in viral load compared to placebo. However, in this cohort, bamlanivimab reduced the risk of COVID-19 hospitalization or emergency department (ED) visits on day 29 by 70%. This interim analysis also established the safety profile of bamlanivimab, which was similar to that of the placebo group at all three doses.[15] A preprint study reported that bamlanivimab still binds to the Y501-RBD of SARS-CoV-2 (B.1.1.7, 20I/501Y.V1) in vitro, as efficiently as the previous N501-RBD of the original strain.[15] A separate preprint study by the same authors reported that the B.1.351/501Y.V2 variant and P.1/501Y.V3 variant, which share three similar mutations (K417N, E484K, and N501Y), completely lost binding to bamlanivimab in vitro, causing complete loss of efficacy of bamlanivimab.[16] Bamlanivimab received EUA by FDA in November 2020 for clinical use in non-hospitalized patients with mild to moderate COVID-19 who are at increased risk for developing severe disease and/or hospitalization; however, the company that manufactures this product requested that the FDA revoke the EUA for bamlanivimab alone on April 16th, 2021 in light of the emergence of earlier SARS-CoV-2 variants which demonstrated resistance to bamlanivimab monotherapy.[14] However, the EUA for bamlanivimab has since been reinstated when used in combination with etesevimab, another monoclonal antibody.

  • Bamlanivimab and Etesevimab (LY-CoV555 or LY3819253 and LY-CoV016 or LY3832479; BAM/ETE) are potent anti-spike combinations neutralizing monoclonal antibody treatments used to treat outpatients with a recent diagnosis of mild to moderate COVID-19 who have high-risk comorbidities for severe COVID-19 infection. In vitro experiments revealed that etesevimab binds to a different epitope than bamlanivimab and neutralizes resistant variants with mutations in the epitope bound by bamlanivimab.[4] In Phase 2 of the BLAZE-1 trial, bamlanivimab and etesevimab were associated with a significantly reduced SARS-CoV-2 viral load than placebo.[13][17] Interim data from the Phase 3 BLAZE-1 trial indicates that therapy reduced the risk of hospitalization by 70%, with no deaths in persons receiving BAM/ETE. The BAM/ETE combination first received an EUA in February 2021 for treatment of mild to moderate COVID-19 in appropriate patients. In light of in vitro studies showing that these monoclonal antibodies were ineffective against the Beta (B.1.351); and Gamma (P.1) variants, the EUA was revoked in June 2021; with the Delta (B.1.617.2) variant now the predominant variant, the EUA was subsequently reinstated in August 2021.[12]

  • Sotrovimab (VIR-7831) is a potent anti-spike neutralizing monoclonal antibody that demonstrated in vitro activity against the following variants: Alpha (B.1.1.7), Beta, Gamma, and Delta. Results from a preplanned interim analysis (not yet peer-reviewed) of the multicenter, double-blind placebo-controlled Phase 3, COMET-ICE trial by Gupta et al. that evaluated the clinical efficacy and safety of sotrovimab demonstrated that one dose of sotrovimab (500 mg) reduced the risk of hospitalization or death by 85% in high-risk non-hospitalized patients with mild to moderate COVID-19 compared with those receiving placebo.

FDA Issued Emergency Use Authorization (EUA) of Different Monoclonal Antibodies in the Management of COVID-19

  • CAS/IMDEV was granted emergency use authorization from FDA in November 2020 for clinical use in non-hospitalized patients (aged ≥12 years and weighing ≥40 kg) with laboratory-confirmed SARS-CoV-2 infection and mild to moderate COVID-19 who are at high risk for progressing to severe disease and/or hospitalization. This combination has since been granted EUA from the FDA for post-exposure prophylaxis (PEP) for appropriate candidates.

  • BAM/ETE has emergency use authorization from FDA for clinical use in non-hospitalized patients with mild to moderate COVID-19 who are at increased risk for developing severe disease and/or hospitalization, as well as for PEP for appropriate candidates.

  • Sotrovimab monotherapy was granted emergency use authorization for clinical use in non-hospitalized patients (aged ≥12 years and weighing ≥40 kg) with laboratory-confirmed SARS-CoV-2 infection and mild to moderate COVID-19 who are at high risk for progressing to severe disease and/or hospitalization. Unlike CAS/IMDEV and BAM/ETE, the US government is not providing funding for the administration of sotrovimab.

Issues of Concern Although monoclonal antibodies are generally well-tolerated, administration of monoclonal antibodies, in general, is associated with the risk of immune-mediated reactions that include anaphylaxis, serum sickness, and antibody generation. Besides these reactions, the adverse effects of monoclonal antibodies are also related to their specific targets. The adverse effects of antiviral monoclonal antibodies used in COVID-19 are unknown, mainly due to the limited availability of published literature. Safety data from clinical trials evaluating monoclonal antibodies reported are summarized below.

  • The most frequently reported adverse effects with the use of combination therapy of bamlanivimab and etesevimab were nausea and diarrhea. Other adverse events such as infusion-related immediate hypersensitivity reactions manifesting as pruritus, flushing, rash, and facial swelling were also noted with the combination therapy of bamlanivimab and etesevimab.[17]

  • A low incidence of serious adverse events and infusion-related or hypersensitivity reactions were observed with CAS/IMDEV.[11]

  • The most frequently reported adverse effects with the use of sotrovimab include infusion-related hypersensitivity reactions, rash, and diarrhea.

Clinical Significance As per the Fact Sheet for Healthcare Providers provided by the US FDA on November 2020 and February 2021 granting emergency use authorization (EUA) for the use of casirivimab and imdevimab, bamlanivimab and etesevimab, and sotrovimab, adult and pediatric patients with mild to moderate COVID-19 illness are considered to be high risk if they meet at least one of the following criteria:

  • ≥ 65 years of age

  • Have underlying chronic kidney disease (CKD)

  • Have underlying diabetes mellitus (DM)

  • Have underlying immunosuppressive disease

  • Are currently on immunosuppressive therapy

  • Have a body mass index (BMI) ≥ 35 kg/m^2

  • ≥ 55 years of age and have cardiovascular disease or hypertension or COPD/other chronic respiratory diseases

  • Aged between 12 to 17 years and have a BMI ≥ 85 percentile for that age and gender-based on CDC growth charts, OR

  • Have sickle cell disease, or

  • Have congenital or acquired heart disease, or

  • Have neurodevelopmental disorders, or

  • Have dependence on a medical-related technology device (e.g., tracheostomy, gastrostomy on positive pressure ventilation unrelated to COVID-19, or

  • Have underlying asthma, reactive airway, or chronic respiratory disease that requires daily medication for control.

Authorized Dosages of Different Monoclonal Antibodies Against SARS-CoV-2 Casirivimab and Imdevimab

  • The authorized dosage under the FDA issued EUA is 1200 mg of casirivimab and 1200 mg of imdevimab administered together as a subcutaneous injection OR as a single IV infusion for 60 minutes in adults and pediatric patients (12 years of age and older weighing at least 40 kgs) who have a positive SARS-CoV-2 test and who had symptoms for ten days or less.

Bamlanivimab and Etesevimab

  • The authorized dosage under the FDA issued EUA is 700 mg of bamlanivimab and 1400 mg of etesevimab administered together as a single IV infusion for 60 minutes in adults and pediatric patients (12 years of age and older weighing at least 40 kgs) who have a positive SARS-CoV-2 test and who had symptoms for ten days or less.


  • The authorized dosage under the FDA issued EUA is 500 mg of sotrovimab by IV infusion over 30 minutes in adults and pediatric patients (12 years of age and older weighing at least 40 kgs) who have a positive SARS-CoV-2 test and who had symptoms for ten days or less and are at high risk for progression to severe COVID-19 disease.

Other Issues Based on the fact sheets by FDA EUA of casirivimab plus imdevimab, bamlanivimab plus etesevimab, and sotrovimab, these monoclonal antibodies:

  • Are not authorized for use in patients or hospitalized with COVID-19, or who require oxygen therapy due to COVID-19, or who require increasing baseline oxygen therapy due to COVID-19 in those who were previously on chronic oxygen therapy at baseline due to a non-COVID-19 related comorbidity

  • Must not be administered to patients with known hypersensitivity to any ingredient of casirivimab, imdevimab, bamlanivimab, etesevimab, or sotrovimab.

The FDA also cautions against the use of casirivimab and imdevimab or bamlanivimab and etesevimab in hospitalized patients with COVID-19 requiring high flow oxygen or mechanical ventilation as it may be associated with worse clinical outcomes. Patients treated with monoclonal antibody therapies should continue self-isolation measures and follow infection control measures such as wearing masks, practicing social distancing, cleaning and disinfecting surfaces, and washing hands frequently according to CDC guidelines.


  1. Gandhi RT, Lynch JB, Del Rio C. Mild or Moderate Covid-19. N Engl J Med. 2020 Oct 29;383(18):1757-1766.]

2. Stokes EK, Zambrano LD, Anderson KN, Marder EP, Raz KM, El Burai Felix S, Tie Y, Fullerton KE. Coronavirus Disease 2019 Case Surveillance - United States, January 22-May 30, 2020. MMWR Morb Mortal Wkly Rep. 2020 Jun 19;69(24):759-765.

3. Baum A, Ajithdoss D, Copin R, Zhou A, Lanza K, Negron N, Ni M, Wei Y, Mohammadi K, Musser B, Atwal GS, Oyejide A, Goez-Gazi Y, Dutton J, Clemmons E, Staples HM, Bartley C, Klaffke B, Alfson K, Gazi M, Gonzalez O, Dick E, Carrion R, Pessaint L, Porto M, Cook A, Brown R, Ali V, Greenhouse J, Taylor T, Andersen H, Lewis MG, Stahl N, Murphy AJ, Yancopoulos GD, Kyratsous CA. REGN-COV2 antibodies prevent and treat SARS-CoV-2 infection in rhesus macaques and hamsters. Science. 2020 Nov 27;370(6520):1110-1115.

4. Shi R, Shan C, Duan X, Chen Z, Liu P, Song J, Song T, Bi X, Han C, Wu L, Gao G, Hu X, Zhang Y, Tong Z, Huang W, Liu WJ, Wu G, Zhang B, Wang L, Qi J, Feng H, Wang FS, Wang Q, Gao GF, Yuan Z, Yan J. A human neutralizing antibody targets the receptor-binding site of SARS-CoV-2. Nature. 2020 Aug;584(7819):120-124.

5. Coronavirus Disease 2019 (COVID-19) Treatment Guidelines [Internet]. National Institutes of Health (US); Bethesda (MD): Apr 21, 2021.

6. Köhler G, Milstein C. Continuous cultures of fused cells secreting antibody of predefined specificity. 1975. J Immunol. 2005 Mar 01;174(5):2453-5.

7. Hansel TT, Kropshofer H, Singer T, Mitchell JA, George AJ. The safety and side effects of monoclonal antibodies. Nat Rev Drug Discov. 2010 Apr;9(4):325-38.

8. Both L, Banyard AC, van Dolleweerd C, Wright E, Ma JK, Fooks AR. Monoclonal antibodies for prophylactic and therapeutic use against viral infections. Pediatr Pol. 2013 Sep-Oct;88(5):T15-T23.

9. Boivin G, Caouette G, Frenette L, Carbonneau J, Ouakki M, De Serres G. Human respiratory syncytial virus and other viral infections in infants receiving palivizumab. J Clin Virol. 2008 May;42(1):52-7.

10. Hoffmann M, Kleine-Weber H, Schroeder S, Krüger N, Herrler T, Erichsen S, Schiergens TS, Herrler G, Wu NH, Nitsche A, Müller MA, Drosten C, Pöhlmann S. SARS-CoV-2 Cell Entry Depends on ACE2 and TMPRSS2 and Is Blocked by a Clinically Proven Protease Inhibitor. Cell. 2020 Apr 16;181(2):271-280.e8.

  1. Weinreich DM, Sivapalasingam S, Norton T, Ali S, Gao H, Bhore R, Musser BJ, Soo Y, Rofail D, Im J, Perry C, Pan C, Hosain R, Mahmood A, Davis JD, Turner KC, Hooper AT, Hamilton JD, Baum A, Kyratsous CA, Kim Y, Cook A, Kampman W, Kohli A, Sachdeva Y, Graber X, Kowal B, DiCioccio T, Stahl N, Lipsich L, Braunstein N, Herman G, Yancopoulos GD., Trial Investigators. REGN-COV2, a Neutralizing Antibody Cocktail, in Outpatients with Covid-19. N Engl J Med. 2021 Jan 21;384(3):238-251.

12. Wang P, Nair MS, Liu L, Iketani S, Luo Y, Guo Y, Wang M, Yu J, Zhang B, Kwong PD, Graham BS, Mascola JR, Chang JY, Yin MT, Sobieszczyk M, Kyratsous CA, Shapiro L, Sheng Z, Huang Y, Ho DD. Antibody Resistance of SARS-CoV-2 Variants B.1.351 and B.1.1.7. bioRxiv. 2021 Feb

13. Jones BE, Brown-Augsburger PL, Corbett KS, Westendorf K, Davies J, Cujec TP, Wiethoff CM, Blackbourne JL, Heinz BA, Foster D, Higgs RE, Balasubramaniam D, Wang L, Bidshahri R, Kraft L, Hwang Y, Žentelis S, Jepson KR, Goya R, Smith MA, Collins DW, Hinshaw SJ, Tycho SA, Pellacani D, Xiang P, Muthuraman K, Sobhanifar S, Piper MH, Triana FJ, Hendle J, Pustilnik A, Adams AC, Berens SJ, Baric RS, Martinez DR, Cross RW, Geisbert TW, Borisevich V, Abiona O, Belli HM, de Vries M, Mohamed A, Dittmann M, Samanovic M, Mulligan MJ, Goldsmith JA, Hsieh CL, Johnson NV, Wrapp D, McLellan JS, Barnhart BC, Graham BS, Mascola JR, Hansen CL, Falconer E. LY-CoV555, a rapidly isolated potent neutralizing antibody, provides protection in a non-human primate model of SARS-CoV-2 infection. bioRxiv. 2020 Oct 09; [PubMed]

14. Chen P, Nirula A, Heller B, Gottlieb RL, Boscia J, Morris J, Huhn G, Cardona J, Mocherla B, Stosor V, Shawa I, Adams AC, Van Naarden J, Custer KL, Shen L, Durante M, Oakley G, Schade AE, Sabo J, Patel DR, Klekotka P, Skovronsky DM., BLAZE-1 Investigators. SARS-CoV-2 Neutralizing Antibody LY-CoV555 in Outpatients with Covid-19. N Engl J Med. 2021 Jan 21;384(3):229-237.

15. Liu H, Zhang Q, Wei P, Chen Z, Aviszus K, Yang J, Downing W, Peterson S, Jiang C, Liang B, Reynoso L, Downey GP, Frankel SK, Kappler J, Marrack P, Zhang G. The basis of a more contagious 501Y.V1 variant of SARS-COV-2. bioRxiv. 2021 Feb 02;

16. Liu H, Wei P, Zhang Q, Chen Z, Aviszus K, Downing W, Peterson S, Reynoso L, Downey GP, Frankel SK, Kappler J, Marrack P, Zhang G. 501Y.V2 and 501Y.V3 variants of SARS-CoV-2 lose binding to Bamlanivimab in vitro. bioRxiv. 2021 Feb 16;

17. Gottlieb RL, Nirula A, Chen P, Boscia J, Heller B, Morris J, Huhn G, Cardona J, Mocherla B, Stosor V, Shawa I, Kumar P, Adams AC, Van Naarden J, Custer KL, Durante M, Oakley G, Schade AE, Holzer TR, Ebert PJ, Higgs RE, Kallewaard NL, Sabo J, Patel DR, Klekotka P, Shen L, Skovronsky DM. Effect of Bamlanivimab as Monotherapy or in Combination With Etesevimab on Viral Load in Patients With Mild to Moderate COVID-19: A Randomized Clinical Trial. JAMA. 2021 Feb 16;325(7):632-644.

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