News Release

First published peer reviews of the WHO solidarity trials

Plus forthcoming peer reviews of SARS-CoV-2-related research from rapid reviews: COVID-19

Peer-Reviewed Publication

The MIT Press

CAMBRIDGE, MA - November 10, 2020Rapid Reviews: COVID-19 (RR:C19) is an open-access overlay journal published by the MIT Press that accelerates peer review of COVID-19-related research preprints. This week, the journal published the first peer reviews of the WHO SOLIDARITY trials that suggest four re-purposed antiviral drugs--Remdesivir, Hydroxychloroquine, Lopinavir, and Interferon-β1a--have no effect on important clinical outcomes in hospitalized COVID-19 patients. All four reviewers rate the research as RELIABLE.

In addition, the editors are currently soliciting reviews of the following COVID-19 preprints. These preprints have been selected for review because they have the potential to enhance our understanding of SARS-CoV-2 or have been flagged as potentially misleading. Preprints with two finished reviews should be published within 10-14 days. Additional information or early access to these peer-reviews is available upon request.

Highlights from Rapid Reviews editorial team:

  • "Sterilizing immunity against SARS-CoV-2 infection in mice by a single-shot and modified Imidazoquinoline TLR7/8 Agonist-Adjuvanted Recombinant spike protein vaccine" by Sonia Jangra, et al.

    This preprint claims that a novel amphiphilic imidazoquinolinone (IMDQ-PEG-CHOL) TLR7/8 adjuvant targets adjuvant activity to draining lymph nodes, promoting a more robust immune adaptive immune response without promoting off-target systemic inflammation. Functionally, the authors show use of this adjuvant enhances influenza and SARS-CoV-2 vaccine efficiency and elicits a balanced neutralizing antibody response.

    Why we're excited about it: More potent and targeted adjuvants are important for enhancing vaccine efficacy, decreasing unwanted side effects, and potentially decreasing the amount of antigen needed to elicit a protective immune response. Very little has been reported relative to reports focusing on antigen engineering. The research is both scientifically compelling and translationally relevant.

  • "The papain-like protease of coronaviruses cleaves ULK1 to disrupt host autophagy" by Yasir Mohamud, et al.

    Post infection of a betacoronavirus, levels of ULK1, an autophagy regulating serine-threonine kinase, drop significantly due to the papain-like protease of SARS-CoV-2. ULK1 transcription is upregulated upon viral infection, which aids in viral replication early in infection, but is cleaved by the protease late infection, preventing autophagy.

    Why we're excited about it: Understanding the mechanisms of autophagy increases the chances of designing new antivirals and understanding the mechanism of action for current treatments.

  • "Durable SARS-CoV-2 B cell immunity after mild or severe disease" by Clinton O. Ogega, et al.

    Analysis of S protein receptor binding domain (S-RBD)-specific memory B cells in patients with mild disease and those hospitalized shows that 13 out of 14 participants have these memory B cells, including 4 of the 5 patients with the lowest plasma level of neutralizing antibodies. This evidence suggests that infected individuals develop an S-RBD-specific memory B cell that could help elicit a robust immune response upon reinfection.

    Why we're excited about it: Multiple studies have shown loss of SARS-CoV-2 neutralizing antibodies over time post-infection, presenting risk of reinfection. However, in 13 out of 14 patients, S-RBD-specific memory B cells were detected, meaning memory B cells could elicit an accelerated and robust response to reinfection after recovery from mild or severe COVID-19.

Physical Sciences/Engineering

Biological/Chemical Sciences

Public Health

Medical Sciences


RR:C19 is published by the MIT Press and the editorial offices are located at UC Berkeley, headed by editor-in-chief Stefano M. Bertozzi, Professor of Health Policy and Management and Dean Emeritus of the School of Public Health at University of California Berkeley. The journal is funded by a grant from the Patrick J. McGovern Foundation and hosted on PubPub, an open-source publishing platform from the Knowledge Futures Group.

To learn more about this project and its editorial board, or to sign up for future news and alerts, visit

Media Contacts

Jessica Pellien
Associate Director of Publicity
Fortier Public Relations

Kate Silverman Wilson
Community and Resource Development Associate
The MIT Press

About the MIT Press
Established in 1962, the MIT Press is one of the largest and most distinguished university presses in the world and a leading publisher of books and journals at the intersection of science, technology, art, social science, and design. MIT Press books and journals are known for their intellectual daring, scholarly standards, interdisciplinary focus, and distinctive design.

About the UC Berkeley School of Public Health
For 75 years and counting, the UC Berkeley SPH has been dedicated to making a transformative impact on the health of populations through its values of health as a right, strength through diversity, think forward, and impact first. To eliminate inequity and injustice that affects the health and dignity of all people, SPH is committed to radical public health collaborations that challenge conventional thinking, leverage technology, and build bridges between research, public policy, education, and action.

About the Patrick J. McGovern Foundation
The Patrick J. McGovern Foundation is dedicated to improving lives globally with technology, data and AI. The Foundation is the legacy of IDG founder Patrick J. McGovern, who believed in the potential for technology to democratize information, improve the human condition and advance social good.

About the Knowledge Futures Group
The Knowledge Futures Group, a nonprofit originally founded as a partnership between the MIT Press and MIT Media Lab, builds and sustains technology for the production, curation, and preservation of knowledge in service of the public good.

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