By Allison Shelley
WebMD Health News
The most ambitious vaccine deployment in history promises to stop a pandemic that has already claimed 1.67 million lives. But what if a vaccine for COVID-19 had been available sooner, say as early as March?
It’s a question raised by Florian Krammer, PhD, a microbiologist at the Icahn School of Medicine at Mount Sinai in New York City. In a just-published commentary in the journal Cell, he reflects on the loss of life and says vaccines now will make a significant impact on ending the pandemic, but were needed much earlier.
Krammer’s lab recently found that SARS-CoV-2, the virus that causes COVID-19, was circulating in New York City as early as February, even though the first case wasn’t reported until March 1. Krammer has since turned his attention to another timeline and is evaluating how to speed up vaccine delivery.
In the Cell column, he writes, “While it is unlikely that vaccines would have stopped the virus from going global, a well-prepared infrastructure capable of producing vaccines 3-4 months into the outbreak (in March or April) would have saved many lives and would likely have normalized the situation in many geographic areas by now.”
The FDA this month issued an emergency use authorization for the Pfizer-BioNTech and Moderna vaccines in record time. Operation Warp Speed is living up to its moniker and so far is on track to deliver 300 million doses of vaccines to Americans in the coming months, but outgoing CDC director Robert Redfield still predicts it will be “the most difficult time in the public-health history of this nation.”
It is a grim prospect that seemed unthinkable last year when the Global Health Security Index ranked the United States number one in the world for its ability to respond to a major health emergency. With high-quality laboratories and scientific staff, a strategic national stockpile of equipment and emergency distribution and communication plans, the United States was poised to lead the international pandemic response, but struggled initially to leverage full capacities.
The race for a vaccine began in January when a Chinese scientist made the genetic sequence of SARS-CoV-2 openly available.
David Wang, PhD, knows the race well; he worked as part of the team that characterized the first severe acute respiratory syndrome (SARS) for the world in 2003 during that outbreak and helped lay the scientific groundwork for this one.
Wang was a post doc when CDC scientists were grappling with the mysterious pathogen imported from the Guangdong province in China that infected a patient, moving to health workers and other patients in hospitals who infected their close contacts, as the disease moved into the wider community.
Wang’s advisor at the time, Joseph DeRisi at the University of California San Francisco, joined a call with the CDC and had a hunch the genomic approach from his lab could help. The cornerstone of the strategy is a DNA microarray capable of simultaneously detecting hundreds of viruses.
It didn’t take long before his team had answers: it discovered a novel coronavirus (SARS-CoV) in patients infected with SARS. This virus was not closely related to any of the previously characterized coronaviruses — until now. SARS-CoV-2 is genetically related and more infectious. Although the first SARS virus was highly lethal,it faded out after intense public health measures.
So far, every spillover of a pathogen from wildlife to humans — from SARS in 2003 to the H1N1avian flu in 2009, MERS in 2012, the 2014 Ebola outbreak, Zika in 2016 to COVID-19 — has caught the scientific community off guard.
But what if instead of an eleventh-hour scramble to investigate an unidentified pathogen, there was a network of scientists on call to leap into action?
That’s the goal of a new network launched in August by Anthony Fauci, MD, director of the National Institute of Allergy and Infectious Diseases. Named the Centers for Research in Emerging Infectious Diseases (CREID), it has a team of scientists strategically placed around the world in major centers, with others entrenched on the fringes of human settlement where hunters and farmers may be exposed to new pathogens.
The network was funded with $82 million over 5 years.
It’s leveraging expertise to respond more quickly to outbreaks by “pivoting to work together,” said Jean Patterson, lead program officer for the CREID network.
Researchers can use a prototype pathogen approach to study how and where infectious diseases emerge from wildlife to make the leap into people. Reporting from 10 centers in the US and 28 other countries, scientists are developing diagnostic, therapeutic, and vaccine families that can be targeted and deployed faster the next time a “Pathogen X” unleashes into the world.
Krammer, who did not respond to interview requests, has speculated that new vaccines could be developed just 3 weeks after discovering a new virus, and could be used immediately in a phase 3 trial — vaulting past phase 1-2 trials. “Since a correlate of production was determined for a closely related virus, the correlate can be used to measure vaccine efficacy,” he writes.
Then, results from the clinical trial could be available close to 3 months later. And while clinical trials are underway, production could be ramped up globally and distribution chains activated in advance, so at that 3-month mark, vaccine rollout could start right away, he suggests.
New world records would be set. And in the event the virus that emerges is identical or nearly indistinguishable to one of the developed vaccines, existing stockpiles could already be used for phase 3 trials, which would buy even more time.
But how fast is too fast?
Wang, now a professor at the Washington University School of Medicine in St. Louis, says he’s not sure if doing a number of phase 1 and 2 trials on related viruses would be enough to replace initial studies for a vaccine for a new pathogen.
More investment into the understanding of immune response to a wide range of viruses will help inform future vaccine development, but the timeline proposed for the phase 3 trial would be an absolute best case scenario, he says. “And it is highly dependent on the rate of infection at the sites selected for the vaccine studies,” he says. In the Oxford AstraZeneca studies, there were concerns early on over whether there would be enough cases to gather evidence given the low rate of infection in the UK over the summer.
“For a virus that spreads less efficiently than SARSCoV-2, it may take significantly longer for enough events to occur in the vaccine population to evaluate efficacy,” says Wang.
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