The number represented by the line could be thought of as the velocity of cases in the U.S. It tells us how fast case counts are increasing or decreasing and does a good job of showing us the magnitude of each wave of cases.
The chart, however, fails to show the rate of acceleration of cases. This is the rate at which the number of new cases is speeding up or slowing down.
As an analogy, a car’s velocity tells you how fast the car is going. Its acceleration tells you how quickly that car is speeding up.
Using Covid-19 case data compiled by the Center for Systems Science and Engineering at Johns Hopkins University and Our World in Data, combined with data from the Centers for Disease Control and Prevention, STAT was able to calculate the rate of weekly case acceleration, pictured below.
AT A PRESS conference at the White House on June 22nd Anthony Fauci, the director of America’s National Institute of Allergy and Infectious Diseases, issued a warning. The delta variant of the SARS-CoV-2 virus, first identified in India in February, was spreading in America—and quickly. “The delta variant is currently the greatest threat in the US to our attempt to eliminate covid-19,” declared Dr Fauci. Boris Johnson, Britain’s prime minister, issued a similar warning a week earlier. To contain the rapid spread of the variant, European countries and Hong Kong have tightened controls on travellers from Britain.
According to GISAID, a data-sharing initiative for corona- and influenza-virus sequences, the delta variant has been identified in 78 countries (see chart). The mutation is thought to be perhaps two or three times more transmissible than the original virus first spotted in Wuhan in China in 2019. It is rapidly gaining dominance over others. According to GISAID’s latest four-week average, it represents more than 85% of sequenced viruses in Bangladesh, Britain, India, Indonesia and Russia. It may soon be the most prevalent strain in America, France, Germany, Italy, Mexico, South Africa, Spain and Sweden. (GISAID does not, in its summary data, distinguish between delta, B.1.617.2, and the “delta plus” mutation, AY.1, AY.2.)
The good news? Vaccines still sharply reduce the risk of being admitted to hospital with the Delta variant. The Scottish study found that the Pfizer/BioNTech vaccine provided 79% protection, two weeks on from the second dose, while the Oxford/AstraZeneca vaccine offered 60% protection. That lower rate may be due to the fact that it takes longer for immunity to develop with the Oxford/AstraZeneca vaccine, researchers said.
However, research released shortly after by Public Health England was even more promising. It found that the Pfizer/BioNTech vaccine provides 96% protection from hospitalization after two doses, while the Oxford/AstraZeneca is 92% effective at preventing hospitalization after both shots. The conclusion? It’s yet more evidence of the importance of making sure as many people as possible get vaccinated, and that they get both shots.
About 32% of the U.S. population is now fully vaccinated, but the vast majority are people older than 65 — a group that was prioritized in the initial phase of the vaccine rollout.
Although new infections are gradually declining nationwide, some regions have contended with a resurgence of the coronavirus in recent months — what some have called a “fourth wave” — propelled by the B.1.1.7 variant, first identified in the United Kingdom, which is estimated to be somewhere between 40% and 70% more contagious.
As many states ditch pandemic precautions, this more virulent strain still has ample room to spread among the younger population, which remains broadly susceptible to the disease.
Vaccine makers like Pfizer, Moderna and Johnson & Johnson coped with intense global demand for their original shots by manufacturing millions of doses while the vaccines were still in clinical trials. But that is not an option now, because the companies are still racing to fulfill orders for their existing Covid-19 vaccines — and some, including Johnson & Johnson and AstraZeneca, are struggling with major production setbacks. Pumping out second-generation shots would require factories to switch over manufacturing lines now used for the first wave of vaccines, and in some cases fire up new production processes.
The potential manufacturing gap is the latest challenge to President Joe Biden’s promise to bring the pandemic to a close. South Africa has already rejected AstraZeneca’s vaccine because an early trial showed it wasn’t effective against the B.1.351 strain that dominates there and has now reached the United States. Another variant spreading in America — P.1, first found in Brazil — has raised similar concerns about its ability to evade some of the vaccines now in use globally. Biden administration officials are working overtime to understand how the variants’ spread could alter vaccination strategies. But the lack of manufacturing capacity is limiting America’s options.
A Harvard immunologist said current vaccines appear to be effective enough to end the pandemic, despite growing concerns that more infectious COVID-19 variants would severely blunt the effectiveness of the preventative treatments and set the nation back in its fight against the disease.
At least four recent studies have identified coronaviruses closely related to the pandemic strain in bats and pangolins in Southeast Asia and Japan, a sign that these pathogens are more widespread than previously known and that there was ample opportunity for the virus to evolve.
Another new study suggests that a change in a single amino acid in a key component of the virus enabled or at least helped the virus become infectious in humans. Amino acids are organic compounds that form proteins.
Public-health officials say it is critical to identify the origin of the pandemic to take steps to avert future outbreaks, though it may take years to do so. These latest pieces of research add to evidence that the virus, called SARS-CoV-2, likely originated in bats and then evolved naturally to infect humans, possibly through an intermediary animal.
A similar trial in South Africa, where a new, more contagious variant is dominant, produced similar results. Researchers found the Johnson & Johnson vaccine to be slightly less effective at preventing all illness there – 64% overall – but was still 82% effective at preventing severe disease. The FDA report also indicates that the vaccine protects against other variants from Britain and Brazil too.
As Americans anxiously watch variants first identified in the United Kingdom and South Africa spread in the United States, scientists are finding a number of new variants that originated here. More concerning, many of these variants seem to be evolving in the same direction — potentially becoming contagious threats of their own.
In a study posted on Sunday, a team of researchers reported seven growing lineages of the novel coronavirus, spotted in states across the country. All of them have evolved a mutation in the same genetic letter.
“There’s clearly something going on with this mutation,” said Jeremy Kamil, a virologist at Louisiana State University Health Sciences Center Shreveportand a co-author of the new study.
British government scientists are increasingly finding the coronavirus variant first detected in Britain to be linked to a higher risk of death than other versions of the virus, a devastating trend that highlights the serious risks and considerable uncertainties of this new phase of the pandemic.
The scientists said last month that there was a “realistic possibility” that the variant was not only more contagious than others, but also more lethal. Now, they say in a new document that it is “likely” that the variant is linked to an increased risk of hospitalization and death.
Alongside antibodies, the immune system produces a battalion of T cells that can target viruses. Some of these, known as killer T cells (or CD8+ T cells), seek out and destroy cells that are infected with the virus. Others, called helper T cells (or CD4+ T cells) are important for various immune functions, including stimulating the production of antibodies and killer T cells.
T cells do not prevent infection, because they kick into action only after a virus has infiltrated the body. But they are important for clearing an infection that has already started. In the case of COVID-19, killer T cells could mean the difference between a mild infection and a severe one that requires hospital treatment, says Annika Karlsson, an immunologist at the Karolinska Institute in Stockholm. “If they are able to kill the virus-infected cells before they spread from the upper respiratory tract, it will influence how sick you feel,” she says. They could also reduce transmission by restricting the amount of virus circulating in an infected person, meaning that the person sheds fewer virus particles into the community.
T cells could also be more resistant than antibodies to threats posed by emerging variants. Studies by Sette and his colleagues have shown that people who have been infected with SARS-CoV-2 typically generate T cells that target at least 15–20 different fragments of coronavirus proteins1. But which protein snippets are used as targets can vary widely from person to person, meaning that a population will generate a large variety of T cells that could snare a virus. “That makes it very hard for the virus to mutate to escape cell recognition,” says Sette, “unlike the situation for antibodies.”