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Understanding coronavirus
\"Since the identification of the first cases of the coronavirus in December 2019 in Wuhan, China, there has been a significant amount of confusion regarding the origin and spread of the so-called 'coronavirus', officially named SARS-CoV-2, and the cause of the disease COVID-19. Conflicting messages from the media and officials across different countries and organizations, the abundance of disparate sources of information, unfounded conspiracy theories on the origins of the newly emerging virus and the inconsistent public health measures across different countries, have all served to increase the level of anxiety in the population. Where did the virus come from? How is it transmitted? How does it cause disease? Is it like flu? What is a pandemic? What can we do to stop its spread? Written by a leading expert, this concise and accessible introduction provides answers to the most common questions surrounding coronavirus for a general audience\"-- Provided by publisher.
Book
Phase I/II study of COVID-19 RNA vaccine BNT162b1 in adults
In March 2020, the World Health Organization (WHO) declared coronavirus disease 2019 (COVID-19), which is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)
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, a pandemic. With rapidly accumulating numbers of cases and deaths reported globally
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, a vaccine is urgently needed. Here we report the available safety, tolerability and immunogenicity data from an ongoing placebo-controlled, observer-blinded dose-escalation study (ClinicalTrials.gov identifier NCT04368728) among 45 healthy adults (18–55 years of age), who were randomized to receive 2 doses—separated by 21 days—of 10 μg, 30 μg or 100 μg of BNT162b1. BNT162b1 is a lipid-nanoparticle-formulated, nucleoside-modified mRNA vaccine that encodes the trimerized receptor-binding domain (RBD) of the spike glycoprotein of SARS-CoV-2. Local reactions and systemic events were dose-dependent, generally mild to moderate, and transient. A second vaccination with 100 μg was not administered because of the increased reactogenicity and a lack of meaningfully increased immunogenicity after a single dose compared with the 30-μg dose. RBD-binding IgG concentrations and SARS-CoV-2 neutralizing titres in sera increased with dose level and after a second dose. Geometric mean neutralizing titres reached 1.9–4.6-fold that of a panel of COVID-19 convalescent human sera, which were obtained at least 14 days after a positive SARS-CoV-2 PCR. These results support further evaluation of this mRNA vaccine candidate.
In a dose-escalation study of the COVID-19 RNA vaccine BNT162b1 in 45 healthy adults, RBD-binding IgG concentrations and SARS-CoV-2 neutralizing titres in sera increased with dose level and after a second vaccine dose.
Journal Article
The COVID-19 virus
Factual yet simple text about the rise of COVID-19, how it spreads, and steps we can take to avoid spreading disease to others. Colorful diagrams show how viruses enter a host and replicate in cells, and explain how lower-respiratory illnesses affect people.
Book
Seasonal coronavirus protective immunity is short-lasting
A key unsolved question in the current coronavirus disease 2019 (COVID-19) pandemic is the duration of acquired immunity. Insights from infections with the four seasonal human coronaviruses might reveal common characteristics applicable to all human coronaviruses. We monitored healthy individuals for more than 35 years and determined that reinfection with the same seasonal coronavirus occurred frequently at 12 months after infection.
The durability of immunity to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is unknown. Lessons from seasonal coronavirus infections in humans show that reinfections can occur within 12 months of initial infection, coupled with changes in levels of virus-specific antibodies.
Journal Article
Oral Simnotrelvir for Adult Patients with Mild-to-Moderate Covid-19
Simnotrelvir has in vitro activity against SARS-CoV-2. In this phase 2–3 trial in China, simnotrelvir given within 72 hours after symptom onset led to symptom resolution approximately 36 hours faster than placebo.
Journal Article
The COVID-19 catastrophe : what's gone wrong and how to stop it happening again
The global response to the Covid-19 pandemic is the greatest science policy failure in a generation. We knew this was coming. Warnings about the threat of a new pandemic have been made repeatedly since the 1980s and it was clear in January that a dangerous new virus was causing a devastating human tragedy in China. And yet the world ignored the warnings. Why? In this short and hard-hitting book, Richard Horton, editor of the medical journal The Lancet, scrutinizes the actions that governments around the world took - and failed to take - as the virus spread from its origins in Wuhan to the global pandemic that it is today. He shows that many Western governments and their scientific advisors made assumptions about the virus and its lethality that turned out to be mistaken. Valuable time was lost while the virus spread unchecked, leaving health systems unprepared for the avalanche of infections that followed. Drawing on his own scientific and medical expertise, Horton outlines the measures that need to be put in place, at both national and international levels, to prevent this kind of catastrophe from happening again. We're supposed to be living in an era where human beings have become the dominant influence on the environment, but Covid-19 has revealed the fragility of our societies and the speed with which our systems can come crashing down. We need to learn the lessons of this pandemic and we need to learn them fast because the next pandemic may arrive sooner than we think.
Book
Structural basis of receptor recognition by SARS-CoV-2
A novel severe acute respiratory syndrome (SARS)-like coronavirus (SARS-CoV-2) recently emerged and is rapidly spreading in humans, causing COVID-19
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,
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. A key to tackling this pandemic is to understand the receptor recognition mechanism of the virus, which regulates its infectivity, pathogenesis and host range. SARS-CoV-2 and SARS-CoV recognize the same receptor—angiotensin-converting enzyme 2 (ACE2)—in humans
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,
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. Here we determined the crystal structure of the receptor-binding domain (RBD) of the spike protein of SARS-CoV-2 (engineered to facilitate crystallization) in complex with ACE2. In comparison with the SARS-CoV RBD, an ACE2-binding ridge in SARS-CoV-2 RBD has a more compact conformation; moreover, several residue changes in the SARS-CoV-2 RBD stabilize two virus-binding hotspots at the RBD–ACE2 interface. These structural features of SARS-CoV-2 RBD increase its ACE2-binding affinity. Additionally, we show that RaTG13, a bat coronavirus that is closely related to SARS-CoV-2, also uses human ACE2 as its receptor. The differences among SARS-CoV-2, SARS-CoV and RaTG13 in ACE2 recognition shed light on the potential animal-to-human transmission of SARS-CoV-2. This study provides guidance for intervention strategies that target receptor recognition by SARS-CoV-2.
The crystal structure of the receptor-binding domain of the SARS-CoV-2 spike in complex with human ACE2, compared with the receptor-binding domain of SARS-CoV, sheds light on the structural features that increase its binding affinity to ACE2.
Journal Article
Digital contact tracing for pandemic response : ethics and governance guidance
\"Technologies of digital contact tracing have been used in several countries to help in the surveillance and containment of COVID-19. These technologies have promise, but they also raise important ethical, legal, and governance challenges that require comprehensive analysis in order to support decision-making. Johns Hopkins University recognized the importance of helping to guide this process and organized an expert group with members from inside and outside the university. This expert group urges a stepwise approach that prioritizes the alignment of technology with public health needs, building choice into design architecture and capturing real-world results and impacts to allow for adjustments as required\"-- Provided by publisher.
Book
Coronavirus hemagglutinin-esterase and spike proteins coevolve for functional balance and optimal virion avidity
Human coronaviruses OC43 and HKU1 are respiratory pathogens of zoonotic origin that have gained worldwide distribution. OC43 apparently emerged from a bovine coronavirus (BCoV) spillover. All three viruses attach to 9-O-acetylated sialoglycans via spike protein S with hemagglutinin-esterase (HE) acting as a receptordestroying enzyme. In BCoV, an HE lectin domain promotes esterase activity toward clustered substrates. OC43 and HKU1, however, lost HE lectin function as an adaptation to humans. Replaying OC43 evolution, we knocked out BCoV HE lectin function and performed forced evolution-population dynamics analysis. Loss of HE receptor binding selected for second-site mutations in S, decreasing S binding affinity by orders of magnitude. Irreversible HE mutations led to cooperativity in virus swarms with low-affinity S minority variants sustaining propagation of highaffinity majority phenotypes. Salvageable HE mutations induced successive second-site substitutions in both S and HE. Apparently, S and HE are functionally interdependent and coevolve to optimize the balance between attachment and release. This mechanism of glycan-based receptor usage, entailing a concerted, finetuned activity of two envelope protein species, is unique among CoVs, but reminiscent of that of influenza A viruses. Apparently, general principles fundamental to virion–sialoglycan interactions prompted convergent evolution of two important groups of human and animal pathogens.
Journal Article