He identifies a cluster of non-medical drivers of deadly outbreaks—war, political instability, human migration, poverty, urbanization, anti-science and nationalist sentiment, and climate change—and maintains that advances in biomedicine must be accompanied by concerted action on these geopolitical matters.
War and Pestilence ride together as two of the Four Horsemen of the Apocalypse, and there is no shortage of historical precedent to demonstrate the aptness of the allegory. The great influenza pandemic that began in 1918 was propelled, in part, by troop movements and population shifts at the end of the First World War. Both the First and the Second World Wars produced typhus epidemics. Armed conflicts cause malnutrition, poor pest control, and sanitation problems; even the soil often becomes contaminated. Medical facilities are destroyed; doctors and nurses, diverted to combat duty, are unable to provide care, and vaccination and other mass-treatment programs usually falter.
It’s one of the tiniest machines on the planet — about a hundred times smaller than the average cell. It’s so small that no scientist can spot it through a typical light microscope. Only with an electron microscope can we see its spiky surface. It’s not alive, and it’s not what most of us would think of as “dead.” This teensy machine seems to survive in a kind of purgatory state, yet it has traveled across continents and oceans from host to host, and brought hundreds of nations to a standstill. Despite its diminutive size, the novel coronavirus, dubbed SARS-CoV-2, has seemingly taken the world by surprise with its virulence.
A hundred days after a Chinese government website announced the discovery of a “pneumonia of unknown cause”, it has become clearer that the dynamics behind the virus’s rapid expansion across the globe has relied heavily on such “cluster effects”.
Each of the countries most heavily hit by the pandemic has reported similar stories of social, cultural or religious gatherings where large numbers spent numerous hours in close company – holding hands, kissing, sharing drinks from the same glass – which then turbo-charged the spread of the pandemic.
“Most infections didn’t take place in supermarkets or restaurants,” Streeck said of his preliminary findings. In Heinsberg, his team of coronavirus detectives could find scant evidence of the virus being transmitted via the surfaces of door handles, smart phones or other objects.
Octavian Report “Rostrum” spoke with him about a major theme in Shakespeare’s work and life: disease. Specifically, pandemic plagues, which ravaged London repeatedly throughout Shakespeare’s career, shuttering the theaters, and which appear (obliquely and otherwise) in some of his greatest plays.
The latest episode of the Rostrum’s coronavirus series features James Shapiro, the Larry Miller professor of English and comparative literature at Columbia University, and a leading expert on Shakespeare. Shapiro has published widely on this subject, most recently Shakespeare in a Divided America. He is also an advisor to the Royal Shakespeare Company and to the Public Theater.
James S. Shapiro (born 1955) is Professor of English and Comparative Literature at Columbia University who specialises in Shakespeare and the Early Modern period. Shapiro has served on the faculty at Columbia University since 1985, teaching Shakespeare and other topics, and he has published widely on Shakespeare and Elizabethan culture.
NEJM talks with Dr. Julian Flores, who works in a Broward County, Florida, emergency room.
When he was interviewed, the count of Covid-19 cases stood at 412, less than 12 hours later, the new number was 505. He’s expecting the wave to hit hard there. Broward is home to Fort Lauderdale (think spring break) and Pompano Beach (think aging retirees). Couple those demographics with a lack of easy testing for the virus, and you’ve got a worrisome situation.
The race is on to find a vaccine against the new COVID-19 coronavirus. Professor Jonathan Heeney explains why a cautious approach is needed and how his team is using new technology developed for influenza and Ebola viruses to target the new infection.
It is hard now to conceive that two months ago, few people had heard of the new coronavirus. Now, the virus, which causes the disease COVID-19, has spread to every corner of the globe. The World Health Organization has officially declared the outbreak a pandemic.
With the threat of hundreds of thousands – possibly millions – of people being infected and healthcare systems becoming overwhelmed, the race is on to develop a vaccine that will protect individuals and slow the spread of the disease. But Professor Jonathan Heeney, Head of the Laboratory of Viral Zoonotics at the University of Cambridge, and one of the people working on a vaccine, says that coronaviruses present a particular challenge to vaccine developers.
Coronaviruses are named after their appearance: they are spherical objects, on the surface of which sit ‘spike’ proteins. The virus uses these spikes to attach to and invade cells in our body. Once inside, the virus uses the cell’s own machinery to help itself replicate and spread throughout the body, causing disease and allowing it to transmit onwards.
Traditionally, scientists would develop vaccines that programme the body to produce antibodies that recognise and block these spikes. But this strategy can misfire with coronaviruses due to a phenomenon known as ‘antibody-induced enhancement’ or ‘vaccine-induced enhancement’, says Heeney.
“If you make antibodies against the spike, they can end up binding to it and helping the virus invade important immune cells known as monocyte-macrophages. Rather than destroying the virus, these cells can then end up being reprogrammed by the viruses, exacerbating the immune response and making the disease much, much worse than it would otherwise be.”
Syndicated columnist Mark Shields and New York Times columnist David Brooks join Judy Woodruff to discuss the latest political news, including a surreal week in which much of American daily life shut down, bright spots of people helping each other in a time of need, President Trump’s handling of the crisis, the ongoing issue of political polarization and how government should respond.
“The finding in two randomised trials that advice to use ibuprofen results in more severe illness or complications helps confirm that the association seen in observational studies is indeed likely to be causal. Advice to use paracetamol (acetaminophen) is also less likely to result in complications.”
Scientists and senior doctors have backed claims by France’s health minister that people showing symptoms of covid-19 should use paracetamol (acetaminophen) rather than ibuprofen, a drug they said might exacerbate the condition.
Ian Jones, a professor of virology at the University of Reading, said that ibuprofen’s anti-inflammatory properties could “dampen down” the immune system, which could slow the recovery process. He added that it was likely, based on similarities between the new virus (SARS-CoV-2) and SARS I, that covid-19 reduces a key enzyme that part regulates the water and salt concentration in the blood and could contribute to the pneumonia seen in extreme cases. “Ibuprofen aggravates this, while paracetamol does not,” he said.