COVID school closures may 'slightly stunt' U.S. economic growth: Fed paper

 U.S. school closures due to the COVID-19 pandemic may end up stunting U.S. economic growth over the long term by reducing the number of college-educated workers and increasing the number of high-school dropouts, according to a paper published Monday by the San Francisco Federal Reserve Bank.

The educational sector is a huge engine here of jobs for the U.S. economy, with a workforce of about 8 million Americans before the pandemic. Schools in large swaths of the United States are currently operating online, or only partially in-person. The new Biden administration has been pushing to return students to the classroom, noting the toll that school closures have taken on education and family life.

The San Francisco Fed paper sheds new light on the economic toll.

Its authors drew on a study published last year estimating that school closures could result in fewer children earning a bachelor’s degree, and as much as a 1 percentage point increase in the share of children not finishing high school.

With college-educated workers far out-earning those with less education, the projected decline in overall educational attainment could trim annual U.S. output by an average of a quarter of a percentage point over the next 70 years, the paper found.

The hit to GDP would peak in 2045, at just shy of $150 billion in that single year, the researchers estimated.

The closures may also contribute to income inequality because lower-income families likely have fewer resources to make up for lost learning than higher-income households, they wrote.

“Disruptions to children’s learning today can have a persistent and large impact on the production capacity of the economy and harm future growth,” wrote economists John Fernald, Huiyu Li, and Mitchell Ochse. “The long-run effects of learning disruptions on the economy will depend crucially on how fast the economy recovers, which will impact how much lost education during the pandemic can be remediated.”

https://www.reuters.com/article/us-usa-economy-education/covid-school-closures-may-slightly-stunt-u-s-economic-growth-fed-paper-idUSKBN2AG2BG

KemPharm to add jobs if FDA OKs new ADHD treatment

 Drug maker KemPharm Inc. is on the verge of a company breakthrough. 

The Food and Drug Administration in March may approve the Celebration-based company’s attention deficit hyperactivity disorder drug KP415. The treatment stands out from other ADHD treatments on the market because of how quickly it kicks in and how long it lasts, and it may be a financial boost for the pre-revenue company. 

KemPharm (Nasdaq: KMPH) is partnered with Gurnet Point Capital and portfolio company, Menlo Park, California-based Corium Inc., which will commercialize the drug once approved. That, and other ongoing drug developments, will necessitate future hiring to KemPharm’s staff of 23 workers, co-founder and CEO Travis Mickle told Orlando Business Journal. 

The growth of innovative companies like KemPharm is important because it can create high-wage jobs. Those companies also create innovative solutions for businesses and consumers, help develop a community and make it easier for other new companies to form in the future.

The pharmaceutical and life sciences industry is projected to experience growth in the number of merger and acquisition deals in 2021, according to a report from London-based accounting giant PricewaterhouseCoopers. The industry is expected to generate between $250 billion-$275 billion in deals, up from $184 billion in 2020. The industry’s need for scale and innovation will fuel this growth, Sky Milch, PWC’s U.S. deal leader for the pharmaceuticals and life sciences, said in the report. 

“Larger transformational pharma and medical device deals, combined with a flurry of biotech deals, will be the driver.”

Here, Mickle shares more about how the approval of KP415 would transform the company, how the new drug differs from others and more. 

How does KP415 differ from other ADHD treatments on the market? We designed it to be similar to the product that I developed early in my career at a company known as New River Pharmaceuticals and that product is a multibillion-dollar treatment for ADHD known as Vyvanse. KP415 is kind of the other side of that coin. Vyvanse is an amphetamine-based treatment, similar to Adderall and Adderall XR. KP415 is actually a Ritalin-based or methylphenidate-based treatment. People pretty much split how they take these, like 40/60 or 60/40, depending on age and whatever works, but they both work for most patients. What we wanted to do was bring some of the patient benefits that we had heard so much about with Vyvanse to those folks that use the methylphenidate or Ritalin class of drugs more often. 

What does that mean for the user? Our clinical data shows that it starts at about a half an hour after it's administered, and it lasts for 13 hours. Say Johnny or Sally wake up at seven o'clock. By 7:30, well before they leave the house for the day, or in today's world before they go to a quiet place in the house for the day, you know the drug starts to work. They start to feel the effect and are able to focus. It’d be great if they remember their backpack and their shoes. By eight o'clock, at the end of the day, through activities and homework and dinner, it's still working. You still have that effect, but it starts to wear off so they can get to bed, and that truly is the benefit that folks haven't seen with these products.

Do you expect to grow your staff this year? I think that's more than likely going to happen. I think we have so much going on in different aspects, whether it's drug development, working with our established partners that are commercializing our products with us, whatever it is. You need resources to do so, and we focused our attention on getting the business to this point. Now we have to actually go back in and build in the necessary infrastructure. There's so much going on I expect that's going to be a natural effect. It’s nothing that today I can tell you definitively how many people that looks like.

KemPharm recently has eliminated $93.1 million in debt and regained its listing on the Nasdaq. What does that enable the company to do that it couldn’t before? We have an attractive pipeline of products. We have a unique technology, and all of those have been kind of put on the sideline a little bit. Now we're bringing them back up. Everything behind the business is fixed. Many pharma companies don't survive the amount of debt that we had without a revenue source. It was truly remarkable. 

Two of KemPharm’s current drug candidates would treat ADHD and stimulant use disorder. Why does the firm focus in these areas? Prodrugs for me were always an attractive area to be in because it’s fairly straightforward scientifically, and you can add a lot of benefit… ADHD has been my focus my entire career. My children have it. I have it. I understand what it's like to live with it, and to be a parent in a home around it.

https://www.bizjournals.com/orlando/news/2021/02/05/psych-drug-maker-kempharm-to-add-jobs-if-fda-oks-n.html

COVID-19 linked to potentially dangerous eye abnormalities

 Researchers using MRI have found significant abnormalities in the eyes of some people with severe COVID-19, according to a study published in the journal Radiology. The study results support the need for eye screening in these patients to provide appropriate treatment and management of potentially severe ophthalmological manifestations of COVID-19.

The COVID-19 pandemic has affected more than 100 million people since it began early in 2020. While the virus primarily attacks the lungs, it has been linked with eye abnormalities like conjunctivitis, also known as pink eye, and retinopathy, a disease of the retina that can result in a loss of vision. Eye abnormalities visible on MRI exams have been reported but there is limited research on the nature and frequency of these abnormalities.

To find out more, the French Society of Neuroradiology (SFNR) initiated a study of 129 patients with severe COVID-19 who underwent brain MRI.

Of the 129 patients, nine (7%) had abnormal MRI findings of the globe, or eyeball. The MRI scans showed one or more nodules in the back part, or posterior pole, of the eyeball. Eight of the nine patients had spent time in the intensive care unit (ICU) for COVID-19.

"We showed that a few patients with severe COVID-19 from the French COVID-19 cohort had one or several nodules of the posterior pole of the globe," said study lead author Augustin Lecler, M.D., Ph.D., associate professor at the University of Paris and neuroradiologist from the Department of Neuroradiology at the Foundation Adolphe de Rothschild Hospital in Paris. "This is the first time these findings have been described using MRI."

All nine patients had nodules in the macular region, the area in the back of the eye responsible for our central vision. Eight had nodules in both eyes.

The results suggest that screening should be considered in all patients with severe COVID-19 to detect these nodules. In clinical practice, this screening could include dedicated exploration of the eyes with high-resolution MRI, the researchers said. Additional recommended exams include fundoscopy, which uses a magnifying lens and a light to check the back of the inside of the eye, and optical coherence tomography, a noninvasive test that provides a 3D picture of the structure of the eye.

Dr. Lecler noted that severe eye problems might largely go unnoticed in the clinic, as COVID-19 patients hospitalized in the ICU are often being treated for much more severe, life-threatening conditions.

"Our study advocates for screening of all patients hospitalized in the ICU for severe COVID-19," Dr. Lecler said. "We believe those patients should receive specific eye-protective treatments."

The mechanism behind nodule formation remains unknown, the researchers said, although it could be related to inflammation triggered by the virus. Inadequate drainage of the veins of the eyes, a problem found in patients who spend time in the ICU in the prone position or intubated, may also be a factor. Seven of the nine patients with eye abnormalities in the study had been placed in a prone position in the ICU for an extended time.

The researchers are performing follow-up clinical and MRI examinations in the survivors to monitor the nodules and see if they carry any clinical consequences such as vision loss or visual field impairment.

They are also performing MRI examinations in new patients with severe COVID-19 from the second and third waves of the pandemic, using more comprehensive ophthalmological tests to correlate with the MRI results.

The effects on patients with moderate COVID-19 are currently under investigation.

"We have launched a prospective study with dedicated high-resolution MR images for exploring the eye and orbit in patients with light to moderate COVID," Dr. Lecler said. "Therefore, we will be able to know whether our findings were specific to severe COVID patients or not."

The findings support previous research that showed COVID-19 exacts a greater toll in people with existing health problems. Of the nine patients with eye nodules, two had diabetes, six were obese and two had hypertension.

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"Ocular MRI Findings in Patients with Severe COVID-19: A Retrospective Multicenter Observational Study." Collaborating with Dr. Lecler were François Cotton, M.D., Ph.D., François Lersy, M.D., Stéphane Kremer, M.D., Ph.D., and Françoise Héran, M.D., on behalf of the SFNR's COVID study group.

https://www.eurekalert.org/pub_releases/2021-02/rson-clt021021.php

Targeting Nsp1 protein could be a pathway for COVID-19 therapy

 A study that identifies how a coronavirus protein called Nsp1 blocks the activity of genes that promote viral replication provides hope for new COVID-19 treatments.

Since the start of the pandemic, scientists have worked endlessly to understand SARS-CoV-2, the coronavirus that causes COVID-19. Even with the arrival of vaccines, the virus is still spreading and there is a need to develop alternative therapies. Scientists hope to achieve this by studying how SARS-CoV-2 infects cells and propagates itself while avoiding the body's natural immune system.

Now researchers at UT Southwestern have added another piece to this puzzle with their study published in Science Advances.

"When a virus infects a cell, the way the host cell reacts is to alter cellular pathways (or networks) in certain ways to counteract the viral infection. Viruses can target many of these pathways to favor their own replication," says Beatriz Fontoura, Ph.D., professor of cell biology at UTSW and corresponding author of the paper.

Viruses replicate by suppressing the host cell's genes in favor of their own. One way they do this is by blocking the export of messenger RNA (mRNA) from the nucleus of the cell to another compartment called the cytoplasm. Some of these RNAs code for proteins that can only be made by the cell in the cytoplasm. So, by blocking their export from the nucleus, viruses prevent some proteins from being made (e.g., antiviral proteins) and simultaneously free up the cell's machinery for their own replication.

"We've been studying the NS1 protein of the influenza virus and we have shown that one of its functions is to block mRNA nuclear export. Due to some similarities between NS1 from flu and Nsp1 from coronaviruses in their roles in suppressing antiviral response in the host cell, we decided to test whether these two proteins shared a similar function," says Ke Zhang, Ph.D., a postdoctoral researcher in Fontoura's lab and first author of the paper.

The researchers landed on the protein Nsp1. Coronavirus Nsp1 has been described as a multifunctional protein capable of altering viral replication and suppressing the production of other proteins, some of which are involved in immune response. Fontoura's group sought to find out how Nsp1 does this and if it uses a mechanism similar to that of the influenza virus protein NS1.

Indeed, the group found that like NS1 from influenza, SARS-CoV-2 Nsp1 inhibits host cell mRNA nuclear export by binding to the export factor NXF1. This new role of Nsp1 complements the protein's other function, blocking host cell mRNA translation into protein. By obstructing two steps that lead to the production of proteins, Nsp1 suppresses a cell's ability to respond to the viral infection, allowing SARS-CoV-2 to replicate. So what would happen, researchers wondered, if Nsp1 could be stopped from performing one of these functions?

In a proof-of-principle experiment, the researchers infected cells with SARS-CoV-2 and added an excess of NXF1 to see if this would block virus replication. Strikingly, that's exactly what they found. When the cells had access to more NXF1 than the SARS-CoV-2 virus could suppress, the cells were able to stop the virus from multiplying.

The study offers insight into the mechanism behind how coronaviruses, and SARS-CoV-2 in particular, are able to promote their replication inside host cells. Understanding this mechanism provides a building block for potential therapeutics.

"If you find a way to block the interaction between Nsp1 and NXF1 or increase the amount of NXF1 in the cell, you'll get mRNAs out of the nucleus and may get a protective effect, as suggested by our experiments," says Fontoura.

COVID-19 treatments focus on management of symptoms while the body fights off the infection with its natural defenses. A key area of interest in viral therapies is to target the infected cells to stop the virus from replicating. Focusing on Nsp1 or its interaction with NXF1 represents a possible way to do this.

"We still need to know more, like the structure of Nsp1 bound to NXF1, which would shed light on how this blocks mRNA export and how we can revert it," says Zhang. "The research is promising, but in order to develop therapies down the line, we first need to better understand the mechanism."

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This research was supported by funds from the National Institutes of Health (R01-AI154635 and U54 CA260560 Project 2), a Career Enhancement Program Award SPORE; a Mary Kay Foundation International Postdoctoral Scholar Fellowship; the Canadian Institutes of Health Research; the Center for Research on Influenza Pathogenesis; DARPA grant HR0011-19-2-0020; a Lung Cancer SPORE; the Cancer Prevention and Research Institute of Texas; and philanthropic donations from the JPB Foundation, the Open Philanthropy Project, and anonymous donors.

https://www.eurekalert.org/pub_releases/2021-02/usmc-tnp021521.php

How the immune system paves the way for SARS-CoV-2

 Most people infected with SARS-CoV-2 are able to recover from the disease at home - even if they might experience very stressful disease progressions. Some have no symptoms at all. But about ten percent of those affected become so severely ill that they have to be treated in a hospital. The assumption that a weak immune system is behind a severe progression is short-sighted. Especially with critical progressions, the immune system works under intense pressure, but does not manage to control the virus.

A Berlin research group has now observed how SARS-CoV-2 uses an immune system defense mechanism to increasingly hijack the body's mucous membrane cells and multiply there. Their study has just appeared in the journal EMBO Molecular Medicine. "This may give us part of the explanation as to why the immune system has difficulty regulating or even defeating the infection in some people," says Dr. Julian Heuberger, scientist at the Division of Hepatology and Gastroenterology in Charité - Universitätsmedizin Berlin's Medical Department. He is the first author of the study and a member of an Emmy Noether Research Group led by PD Dr. Michael Sigal at Charité and the Berlin Institute for Medical Systems Biology (BIMSB), part of the Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC). For the study, the research group cooperated with researchers from the Max Planck Institute for Infection Biology (MPIIB), Freie Universität Berlin and Hong Kong University.

SARS-CoV-2 uses defense mechanism as a port of entry

Actually, the human body has a very effective defense mechanism against invaders, based on the interaction of various immune cells. T cells play an important role in this: When they encounter viruses in the organism, they destroy the affected cells. They also secrete the signaling molecule interferon-gamma (IFN-γ). On the one hand, IFN-γ fights infectious agents. On the other hand, it calls other immune cells to the scene.

Heuberger and his colleagues have now shown how SARS-CoV-2 can turn this protective mechanism mediated by IFN-γ into its opposite. For in addition to immune cells, the body's mucous membrane cells also respond to IFN-γ by forming more ACE2 receptors. SARS-CoV-2 needs these ACE2 receptors as a port of entry into the cells. Infected cells, in turn, make more ACE2. In this way, both the IFN-γ response of epithelial cells and the virus itself intensify the SARS-CoV-2 infection.

Cell differentiation observed in colon organoids

Patients infected with SARS-CoV-2 sometimes show gastrointestinal symptoms. In order to observe the immune cascade in the intestinal cells, Heuberger cultivated organoids of the human colon. An organoid is a kind of mini-organ in a petri dish, barely the size of a pinhead. The colon organoids are based on cells that come from intestinal biopsies. They grow in three-dimensionally arranged units and replicate the physiology of mucous membrane cells in the human intestinal tract. "These colon organoids are a very helpful tool," Heuberger emphasizes. "We can use them to explore the complex interplay of different signaling pathways that control cell differentiation from stem cells to specialized epithelial cells."

The scientists first treated the cultured intestinal cells with IFN-γ to simulate the body's immune response. Then they infected the organoids with SARS-CoV-2. Using gene expression analysis and a laser scanning microscope - a special optical microscope that scans a sample point by point - they were able to measure increased ACE2 expression in the organoids. In addition, quantitative polymerase chain reaction (PCR) detected increased virus production.

In other words, more IFN-γ means more ACE2. More ACE2 means more viruses can enter the cells. The more viruses that enter the cells, the more viruses produced. Thus, the immune response and the surface cell response to infection pave the way for SARS-CoV-2.

Balancing an excessive IFN-γ response with medication

"We hypothesize that a strong immune response may increase the susceptibility of mucous membrane cells to SARS-CoV-2," says the head of the study, Dr. Michael Sigal. He directs the Gastrointestinal Barrier, Regeneration and Carcinogenesis Lab at Charité and the MDC and is a gastroenterologist at Charité. "If the IFN-γ concentration is higher from the outset or the infection triggers a very excessive production of IFN-y, the viruses probably have an easier time entering the cells." However, the conditions under which this actually happens must still be investigated in clinical trials.

The results of the study carry the idea of a treatment approach for severe COVID-19 courses, Heuberger feels: "One possible strategy could be to balance the IFN-γ response with drugs." However, this would first require a very detailed analysis of the mechanisms underlying the IFN-γ response.

https://www.eurekalert.org/pub_releases/2021-02/mdcf-hti021521.php

Cellectis Stock Jumps Following Natural Killer Cell Deal with Cytovia

 Shares of gene-editing pioneer company Cellectis Therapeutics were up nearly 10% in premarket trading after the company forged a deal with Cambridge, Mass.-based Cytovia Therapeutics to develop immunotherapies based on gene-edited allogeneic CAR T-cells.

France-based Cellectis has been honing the development and implementation of TAL nucleases (TALEN), which are based on a class of proteins derived from transcription activator-like effectors. Cellectis will pair its gene-editing TALEN technology with Cytovia’s induced pluripotent stem cell (iPSC) platform for CAR (Chimeric Antigen Receptors) NK (natural Killer) cell therapy technology.

Cellectis is granting Cytovia a worldwide license to its TALEN gene-editing technology, enabling Cytovia to modify NK cells addressing multiple gene targets for therapeutic use in several cancer indications.

Cellectis will develop custom TALEN, which Cytovia will use to edit iPSCs. Cytovia will be responsible for the differentiation and expansion of the gene-edited iPSC master cell bank into NK cells and will conduct the pre-clinical evaluation, clinical development, and commercialization of the mutually-agreed-upon selected therapeutic candidates. The companies did not disclose the initial targets of the collaboration but said they hope to enter the clinic in 2022.

Daniel Teper, chairman and chief executive officer of Cytovia, said he was excited about working with Cellectis and its team of experienced gene-editing specialists who will be able to further accelerate Cytovia’s NK cell program.

“Cellectis has a deep understanding and proven expertise in gene-edited cell therapies, and their gene-editing technology, TALEN®, will yield NK and CAR-NK treatments with improved potency, persistence, and safety for a variety of cancers, including solid tumors. We look forward to leveraging Cellectis’ insights and experience to help move Cytovia’s CAR-NKs into clinical trials by 2022,” Teper said in a statement.

André Choulika, CEO of Cellectis, also expressed his excitement about the collaboration.

“We are looking forward to this collaboration and the opportunity to further expand the potency of our proprietary TALEN gene-editing technology to iPSCs and CAR-NKs. Down the road, this collaboration should allow for NK cell therapies to be made available to cancer patients, which is very much in line with Cellectis’ mission to provide life-saving product candidates to address unmet patient needs in this field.”

Financial terms of the collaboration include up to $760 million of development, regulatory and sales milestones from Cytovia to Cellectis for the first 5 TALEN gene-edited iPSC-derived NK products. Cellectis will also receive single-digit royalty payments on the net sales of all partnered products commercialized by Cytovia. Cellectis will receive an equity stake of $15 million in Cytovia stock or an upfront cash payment of $15 million if certain conditions are not met by Dec. 31 of this year.

For Cytovia, the partnership with Cellectis follows a licensing agreement with the National Cancer Institute announced in January to use its gene-edited iPSC-derived NK cell technology to develop GPC3 CAR NK cell therapeutics. Cytovia also signed a Cooperative Research and Development Agreement with the National Cancer Institute. Under the CRADA, Cytovia will collaborate with the NCI to develop and evaluate gene-edited iPSC-derived GPC3 CAR NK cells. Cytovia expects to file an initial new drug application for its GPC3 CAR NK cells in the first half of 2022.

https://www.biospace.com/article/cellectis-and-cytovia-partner-to-develop-natural-killer-cells/

How the U.S. can respond to coronavirus variants, and prepare for future evolution

 Coronavirus variants are here. Now what?

A new report from infectious disease experts provides policy recommendations for how the United States can blunt the impact of the variants that have already emerged, as well as build a genomic surveillance system so the country can better identify, track, and assess other variants that might emerge as the SARS-CoV-2 coronavirus continues to evolve.

The suggestions include maintaining the policies that have been shown to drive down viral transmission, prioritizing contact tracing and case investigation of infections found to be caused by one of the variants of concern, and building a scaled-up and more coordinated national genomic sequencing strategy. The Covid-19 package that Congress is assembling now will likely include an influx of funding for genomic surveillance, so the researchers are trying to envision what such a national system should look like. 

Already, three variants have emerged that, in different ways, present challenges for the U.S. The B.1.1.7 variant, which was first seen in the United Kingdom, is more transmissible than earlier forms of the virus, and, research increasingly indicates, more lethal. Then there are P.1 and B.1.351, which were first seen in Brazil and South Africa, respectively. They appear to be better at reinfecting people who’ve recovered from an initial bout of Covid-19. Some vaccines have also been found to be less effective against B.1.351, and given that it shares some of its mutations with P.1., experts fear the same could be true with the latter.

STAT spoke with Caitlin Rivers, an infectious disease epidemiologist at the Johns Hopkins Center for Health Security and a co-author of the report, about its recommendations. Excerpts from the conversation are below, lightly edited for clarity. 

Your first recommendation to deal with the current variants is to maintain policies that slow transmission. But governors or mayors are looking at the pretty steep decline in cases right now and being like, great, we can ease some stuff. Some have ended mask mandates, and some are allowing more activities like indoor dining, or easing capacity limits at businesses. Why is this not the time for that in your eyes?

Two reasons. One, although we have come down a lot from the peak of the surge in early January, we’re still well ahead of the two previous surges. So things are better, but they’re not good. So for that reason alone, I would recommend continuing to keep restrictions in place until we get case counts down until a much more reasonable level.

And the second reason is the variants. Right now they are circulating at a pretty low level in the United States — it varies from place to place — but low on average. But we’ve seen in places where the B.1.1.7 variants gets a toehold, it causes resurgences. And the lower we can be at the starting point if B.1.1.7 does start to become established, the better position we’ll be in in the longer term. We’re setting ourselves up now to have a better future. 

What are some of the limits of the U.S. genomic surveillance system? Where are the bottlenecks?

We have great capacity in this country to do this work. We have a lot of sequencing capacity, we have a lot of science capacity for the characterization. What we’re really missing is the coordination — how to bring it all together and make sure that all of this effort and information is coming together into a system that helps to support our response. 

Scale is also a bottleneck. There are a lot of the building blocks that we need for a successful genomic surveillance system. CDC is doing this work, private sequencing companies are doing this work, academic labs are involved in characterization, but it hasn’t been at the scale that’s required to support the magnitude of the response that we need. And it’s not coordinated enough to make the most out of those existing elements.

How quickly can the genomic surveillance system in the country be strengthened? Is it something that would take a long time or could some things be done more quickly?

We could be doing a lot more with what we have, because there is a lot of sequencing capacity in the United States. There is a lot left on the table that we could be making better use of.

The other motivation is that there are substantial funds for this in the American rescue package, and so it’s looking ahead to see how could we use those funds and how could they go to building a functional system.

Based on the available data, which are limited, how do you view what’s happening with the variants in the U.S. right now?

The B.1.1.7 variant is definitely at higher prevalence than the other two. We have seen that in the U.K., it precipitated a severe resurgence that prompted a lockdown. That is the concern here — that it would become established and would reverse some of the progress we’re seeing. 

The other two are circulating, as far as we can tell, at much lower levels, although we’re not looking all that hard. The bigger concern with those is immune escape [when the virus mutates in such a way that immune protection from an earlier infection or a vaccine isn’t as robust]. So particularly, as we look forward, having a good system in place that is able to watch out for those and other variants and adapt our countermeasures accordingly is going to be really important.

Another point: There’s a lot of talk right now about genomic surveillance, but what I don’t hear as much conversation about is characterization. Just because you’ve identified a new variant doesn’t mean you know what to make of it. Envisioning how you turn those sequencing results into something meaningful for public health is really important.

So you’re saying if you identify a new variant that you think has some sort of impact on transmission or immunity, for example, how do you go from identifying you have a new variant to figuring out what, if anything, it means? Is that what characterization means?

Yes, that’s exactly it. 

Can you explain what you’re envisioning what the next few months might look like with the variants and cases? 

The variants are a bit of a curveball. I could see a scenario where B.1.1.7 could slow down our progress and maybe precipitate resurgences in some communities — maybe not nationwide, because some communities have fairly substantial levels of population immunity, but some places could go back up again. But as we pass through the summer and into next winter, this is where we want this surveillance system to come into place. If there are variants that are showing immune escape, what we don’t want is to become unprepared and suffer another wave because this hypothetical variant is no longer a good match for the vaccines.

https://www.statnews.com/2021/02/16/qa-how-the-u-s-can-respond-to-coronavirus-variants-and-prepare-for-future-evolution/