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Will Warm Weather Slow Spread of Novel Coronavirus?

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Summer gear and a face mask
Credit: Modified from iStock/energyy

With the start of summer coming soon, many are hopeful that the warmer weather will slow the spread of SARS-CoV-2, the novel coronavirus that causes COVID-19. There have been hints from lab experiments that increased temperature and humidity may reduce the viability of SARS-CoV-2. Meanwhile, other coronaviruses that cause less severe diseases, such as the common cold, do spread more slowly among people during the summer.

We’ll obviously have to wait a few months to get the data. But for now, many researchers have their doubts that the COVID-19 pandemic will enter a needed summertime lull. Among them are some experts on infectious disease transmission and climate modeling, who ran a series of sophisticated computer simulations of how the virus will likely spread over the coming months [1]. This research team found that humans’ current lack of immunity to SARS-CoV-2—not the weather—will likely be a primary factor driving the continued, rapid spread of the novel coronavirus this summer and into the fall.

These sobering predictions, published recently in the journal Science, come from studies led by Rachel Baker and Bryan Grenfell at Princeton Environmental Institute, Princeton, NJ. The Grenfell lab has long studied the dynamics of infectious illnesses, including seasonal influenza and respiratory syncytial virus (RSV). Last year, they published one of the first studies to look at how our warming climate might influence those dynamics in the coming years [2].

Those earlier studies focused on well-known human infectious diseases. Less clear is how seasonal variations in the weather might modulate the spread of a new virus that the vast majority of people and their immune systems have yet to encounter.

In the new study, the researchers developed a mathematical model to simulate how seasonal changes in temperature might influence the trajectory of COVID-19 in cities around the world. Of course, because the virus emerged on the scene only recently, we don’t know very much about how it will respond to warming conditions. So, the researchers ran three different scenarios based on what’s known about the role of climate in the spread of other viruses, including two coronaviruses, called OC43 and HKU1, that are known to cause common colds in people.

In all three scenarios, their models showed that climate only would become an important seasonal factor in controlling COVID-19 once a large proportion of people within a given community are immune or resistant to infection. In fact, the team found that, even if one assumes that SARS-CoV-2 is as sensitive to climate as other seasonal viruses, summer heat still would not be enough of a mitigator right now to slow its initial, rapid spread through the human population. That’s also clear from the rapid spread of COVID-19 that’s currently occurring in Brazil, Ecuador, and some other tropical nations.

Over the longer term, as more people develop immunity, the researchers suggest that COVID-19 may likely fall into a seasonal pattern similar to those seen with diseases caused by other coronaviruses. Long before then, NIH is working intensively with partners from all sectors to make sure that safe, effective treatments and vaccines will be available to help prevent the tragic, heavy loss of life that we’re seeing now.

Of course, climate is just one key factor to consider in evaluating the course of this disease. And, there is a glimmer of hope in one of the group’s models. The researchers incorporated the effects of control measures, such as physical distancing, with climate. It appears from this model that such measures, in combination with warm temperatures, actually might combine well to help slow the spread of this devastating virus. It’s a reminder that physical distancing will remain our best weapon into the summer to slow or prevent the spread of COVID-19. So, keep wearing those masks and staying 6 feet or more apart!

References:

[1] Susceptible supply limits the role of climate in the early SARS-CoV-2 pandemic. Baker RE, Yang W, Vecchi GA, Metcalf CJE, Grenfell BT. Science. 2020 May 18. [Online ahead of print.]

[2] Epidemic dynamics of respiratory syncytial virus in current and future climates. Baker RE, Mahmud AS, Wagner CE, Yang W, Pitzer VE, Viboud C, Vecchi GA, Metcalf CJE, Grenfell BT.Nat Commun. 2019 Dec 4;10(1):5512.

Links:

Coronavirus (COVID-19) (NIH)

Bryan Grenfell (Princeton University, Princeton, NJ)

Rachel Baker (Princeton University, Princeton, NJ)


Coping with the Collision of Public Health Crises: COVID-19 and Substance Use Disorders

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For the past half-dozen years, I’ve had the privilege of attending the Rx Drug and Heroin Abuse Summit. And I was counting on learning more about this national crisis this April in Nashville, where I was scheduled to take part in a session with Dr. Nora Volkow, Director of NIH’s National Institute on Drug Abuse. But because of the physical distancing needed to help flatten the deadly curve of the coronavirus-19 (COVID-19) pandemic, it proved to be impossible for anyone to attend in person. Still, the summit did go on for almost three days—virtually!

Dr. Volkow and I took part by sharing a video of a recent conversation we had via videoconference. Since we couldn’t take live questions, we solicited some in advance. Here’s a condensed transcript highlighting portions of our dialogue that focused on the impact of the COVID-19 pandemic on individuals struggling with substance abuse disorders, along with all those who are trying to help them.

VOLKOW: Hello, Francis. Nice to see you, virtually!

COLLINS: Nice to see you too. I’m in my home office here, where I’ve been pretty much for the last three weeks. I’ve been stepping outdoors to occasionally get a breath of fresh air, but trying to live up to all those recommendations about social distancing—or at least physical distancing. I’m trying to keep my social connections going, even if they’re electronic.

I think we’re all feeling this is a time of some stress for us at NIH. We are trying to do everything we can to address this COVID crisis and speed up the process of developing vaccines and therapeutics and all kinds of other things. How are you doing? What’s it like being sequestered back in your home space when you are somebody with so much energy?

VOLKOW: Francis, it’s not easy. I actually am very, very restless. We probably are all experiencing that anxiety of uncertainty, looking at the news and how devastating it is. But I think what makes it easier is if we can do something. Working with everything that we have to try to help others, I think, provides some relief.

COLLINS: Yes, we’re going to talk about that right now. In fact, let’s talk about the way in which this crisis, the global pandemic called COVID-19, is colliding with another public health crisis, which is that of substance use disorder. You recently wrote about this collision in an article in the Annals of Internal Medicine. What does this mean? What are some of the unique challenges that COVID-19 brings to people suffering from addiction?

VOLKOW: I’m glad you are bringing up this point because it’s one of the issues of greatest concern for all of us who are working in the field of substance use disorders. We had not yet been able to contain the epidemic of opioid fatalities, and then we were hit by this tsunami of COVID.

We immediately can recognize the unique challenges of COVID-19 for people having an addiction. Some of these are structural; the healthcare system is not prepared to take care of them. They relate also to stigma and social issues. The concept of social distancing makes such people even more vulnerable because it interferes with many of the support systems that can help them to reach recovery. And, on top of that, drugs themselves negatively influence human physiology, making one more vulnerable to getting infected and more vulnerable to worse outcomes. So that’s why there is tremendous concern about these two epidemics colliding with one another.

COLLINS: How has this influenced treatment delivery for people with substance use disorders, who are counting on that to be able to keep themselves from slipping backward?

VOLKOW: Well, that has been very challenging. We’re hearing from multiple sources that it’s become harder for patients to be able to access treatment. And that relates, for example, to access of medications for opioid use disorders, which are the main strategy—and the most effective one—that we have to prevent people from dying from overdoses.

Some clinics are decreasing the number of patients that they can take care of. The healthcare system is also much less able to initiate persons on buprenorphine. And because of social isolation, if you overdose, the likelihood that someone can rescue you with naloxone is much lower. We don’t yet have statistics on about how that’s influencing fatalities, but we are very concerned.

COLLINS: Nora, you are one of the lead persons for NIH’s Helping to End Addiction Long-term (HEAL) initiative. How has the COVID-19 pandemic affected all the grand research plans that we had put in place as part of our big vision of how NIH could help with the substance use disorder crisis?

VOLKOW: Well, $900 million had recently been deployed on research. That is incredibly meritorious, and some of that research had already started. Unfortunately, it has had to stop almost completely. Why? Because the research that’s relying on the healthcare system, for example, is no longer able to focus on research when they have other clinical needs to meet.

Also, research to bring medication-assisted treatments to prison inmates has stopped. Prisons are not allowing the researchers to go on site because they are closing the doors to outsiders, since they are places at high risk for the spread of COVID-19. Furthermore, some institutional review boards (IRBs) are actually closing, making it impossible to recruit patients for the clinical trials. So, most studies have come to a halt. The issue now is how can we become creative and use virtual technologies to advance some of the goals that we aim to achieve with the HEAL initiative.

COLLINS: Of course, this applies to many other areas of NIH-supported research. Most clinical trials, unless they’re for life-threating conditions, are pretty much in a state of hibernation. We can’t justify having people get out there in ways that might put them at risk of COVID-19. So, yes, it’s a tough time for clinical research all over. And that’s certainly what’s happened with the opioid use disorder problems. Still, I think our teams are really devoted to making sure they make the best of this time, doing things that they can do in terms of planning and setting up data systems.

Meanwhile, bring us up to date on what’s happened as far as the state of the opioid crisis. Are there trends there that we ought to look at for a minute?

VOLKOW: Yes, it’s important to actually keep our eyes on the epidemic, because it’s changing so very rapidly. It’s gone from prescription opioids to heroin to synthetic opioids like fentanyl. And what we have observed ramping up over the past two or three years is an increase in fatalities from the use of psychostimulant drugs.

For example, the number of deaths from methamphetamine has increased five-fold over a period of six years. Similarly, deaths from cocaine are going up. The reality is that people are now dying not just from opioids, but from mixtures of drugs and stimulant drugs, most notably methamphetamine.

COLLINS: So, what can we learn from what we’ve been doing about opioid addiction, and try to apply that to this emerging methamphetamine crisis?

VOLKOW: Unfortunately, we do not have effective medications to treat methamphetamine addiction like we do for opioid use disorders. We also do not have an overdose reversal like we have with naloxone. So, in that respect, it is more challenging.

COLLINS: People sometimes think we’re only focused on trying to treat the problems that we have now. What about prevention? One of the questions we received in our HEAL mailbox was: How can small town communities create an environment where addiction does not take root in the next generation of young people? I’m sure you want to talk about the rewarding power of social interactions, even though right now we’re being somewhat deprived of those, at least face-to-face.

VOLKOW: I’m glad you’re bringing up that question, Francis. Because when you asked at the start of our conversation about how I am doing, I sort of said, “Well, it’s not easy.” But the positive component was that sense that we have a shared mission: we can help others. And the lack of a sense of mission, the lack of a purpose in life, has been identified as one of the factors that make people more vulnerable to take drugs.

Feeling irrelevant, feeling that no one cares for you, is probably one of the most devastating feelings a human being can have. Epidemiological studies show that social isolation and neglect increase dramatically the risk of taking drugs, and, if you are trying to stop taking drugs, it increases that risk of relapse. And so that’s an issue right now of great concern. The challenge is “How do we provide social support for people at risk of substance abuse during the COVID-19 pandemic?”

Also, independent of COVID-19, I think that we as a nation have to face the concept that we have made America vulnerable to drugs because we have eroded that social sense of community. If we are to prevent future generations from getting addicted to drugs, we should build meaningful interactions between people. We should give each individual an opportunity to be part of a society that appreciates them. We do need each other in very, very fundamental ways. We need others for our well-being. If we don’t have that then we become very vulnerable.

COLLINS: Well, here’s one last question from the mailbox. Somebody notes that the “L” in HEAL stands for “long-term.” That is, Helping End Addiction Long-term. The questioner asks: “What’s our vision of a long-term goal and how do we imagine getting there?”

Mine very simply is that we would have an environment that would support people in productive ways, so that the distractions of things that turn out to be destructive are not so tempting, and that the possibility of having meaning in everyone’s life becomes greater.

Ironically, because of COVID-19, we are in the midst of a circumstance where economic distress is pressing on people and social distancing is being required. Seems like we’re going the wrong way. But if you look back in history, often these times of national crisis have been times when people did have the chance to survey what really matters around them, and perhaps to regain a sense of meaning and significance. That’s my maybe slightly over-optimistic view of the current era that we’re in.

Nora, what do you think?

VOLKOW: Francis, I will agree with you. I think that we need to create a society that provides social support and allows people to participate in a meaningful way. If we want to achieve integration of people into society, one of the things that we need to do urgently is remove the stigma of addiction because when you stigmatise someone, you are socially isolating them.

No one likes to be mistreated or discriminated against. So, if you are a person who is addicted and you are afraid of discrimination, you will not seek help. You will continue to isolate. So I think as we’re dealing with the opioid crisis, as we’re dealing with COVID-19, we cannot tolerate discrimination. We cannot tolerate stigma. And we need to be very creative to identify it and to create models that will actually eliminate it.

COLLINS: That’s a wonderful view of where we need to get to. All of these developments give me hope for our capacity to deal with this crisis by working together.

I want to say to all of you who’re listening to this in your own virtual spaces, how much I admire the work that you all are doing, in a selfless way, to try to help our nation deal with what has clearly been a terrible tragedy in far too many lives. I wish you all the best in continuing those creative and energetic efforts, even in the midst of the COVID-19 pandemic. NIH wants to be your ally. We want to be your source of information. We want to be your source of evidence for what works. We want to be your friends.

So, thank you for listening, and thank you, Nora Volkow, for joining me in this discussion today with all of the talent and leadership that you represent. I wish the best health to all of you. Stay safe and keep the progress going!

Links:

Video: Fireside Chat Between NIH, NIDA Heads Addresses COVID-19, the HEAL Initiative, and the Opioids Crisis (National Institute on Drug Abuse/NIH)

COVID-19 Resources (NIDA)

COVID-19: Potential Implications for Individuals with Substance Use Disorders, Nora’s Blog (NIDA)

NIDA Director outlines potential risks to people who smoke and use drugs during COVID-19 pandemic (NIDA)

Collision of the COVID-19 and Addiction Epidemics. Volkow ND. Ann Intern Med. 2 April 2020. [Epub ahead of print]

Helping to End Addiction Long-term (HEAL) Initiative (NIH)

Rx Drug Abuse & Heroin Summit, A 2020 Virtual Experience


Genomic Study Points to Natural Origin of COVID-19

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COVID-19 Update

No matter where you go online these days, there’s bound to be discussion of coronavirus disease 2019 (COVID-19). Some folks are even making outrageous claims that the new coronavirus causing the pandemic was engineered in a lab and deliberately released to make people sick. A new study debunks such claims by providing scientific evidence that this novel coronavirus arose naturally.

The reassuring findings are the result of genomic analyses conducted by an international research team, partly supported by NIH. In their study in the journal Nature Medicine, Kristian Andersen, Scripps Research Institute, La Jolla, CA; Robert Garry, Tulane University School of Medicine, New Orleans; and their colleagues used sophisticated bioinformatic tools to compare publicly available genomic data from several coronaviruses, including the new one that causes COVID-19.

The researchers began by homing in on the parts of the coronavirus genomes that encode the spike proteins that give this family of viruses their distinctive crown-like appearance. (By the way, “corona” is Latin for “crown.”) All coronaviruses rely on spike proteins to infect other cells. But, over time, each coronavirus has fashioned these proteins a little differently, and the evolutionary clues about these modifications are spelled out in their genomes.

The genomic data of the new coronavirus responsible for COVID-19 show that its spike protein contains some unique adaptations. One of these adaptations provides special ability of this coronavirus to bind to a specific protein on human cells called angiotensin converting enzyme (ACE2). A related coronavirus that causes severe acute respiratory syndrome (SARS) in humans also seeks out ACE2.

Existing computer models predicted that the new coronavirus would not bind to ACE2 as well as the SARS virus. However, to their surprise, the researchers found that the spike protein of the new coronavirus actually bound far better than computer predictions, likely because of natural selection on ACE2 that enabled the virus to take advantage of a previously unidentified alternate binding site. Researchers said this provides strong evidence that that new virus was not the product of purposeful manipulation in a lab. In fact, any bioengineer trying to design a coronavirus that threatened human health probably would never have chosen this particular conformation for a spike protein.

The researchers went on to analyze genomic data related to the overall molecular structure, or backbone, of the new coronavirus. Their analysis showed that the backbone of the new coronavirus’s genome most closely resembles that of a bat coronavirus discovered after the COVID-19 pandemic began. However, the region that binds ACE2 resembles a novel virus found in pangolins, a strange-looking animal sometimes called a scaly anteater. This provides additional evidence that the coronavirus that causes COVID-19 almost certainly originated in nature. If the new coronavirus had been manufactured in a lab, scientists most likely would have used the backbones of coronaviruses already known to cause serious diseases in humans.

So, what is the natural origin of the novel coronavirus responsible for the COVID-19 pandemic? The researchers don’t yet have a precise answer. But they do offer two possible scenarios.

In the first scenario, as the new coronavirus evolved in its natural hosts, possibly bats or pangolins, its spike proteins mutated to bind to molecules similar in structure to the human ACE2 protein, thereby enabling it to infect human cells. This scenario seems to fit other recent outbreaks of coronavirus-caused disease in humans, such as SARS, which arose from cat-like civets; and Middle East respiratory syndrome (MERS), which arose from camels.

The second scenario is that the new coronavirus crossed from animals into humans before it became capable of causing human disease. Then, as a result of gradual evolutionary changes over years or perhaps decades, the virus eventually gained the ability to spread from human-to-human and cause serious, often life-threatening disease.

Either way, this study leaves little room to refute a natural origin for COVID-19. And that’s a good thing because it helps us keep focused on what really matters: observing good hygiene, practicing social distancing, and supporting the efforts of all the dedicated health-care professionals and researchers who are working so hard to address this major public health challenge.

Finally, next time you come across something about COVID-19 online that disturbs or puzzles you, I suggest going to FEMA’s new Coronavirus Rumor Control web site. It may not have all the answers to your questions, but it’s definitely a step in the right direction in helping to distinguish rumors from facts.

Reference:
[1] The proximal origin of SARS-CoV-2. Andersen KG, Rambaut A, Lipkin WI, Holmes EC, Garry RF. Nat Med, 17 March 2020. [Epub ahead of publication]

Links:

Coronavirus (COVID-19) (NIH)

COVID-19, MERS & SARS (National Institute of Allergy and Infectious Diseases/NIH)

Andersen Lab (Scripps Research Institute, La Jolla, CA)

Robert Garry (Tulane University School of Medicine, New Orleans)

Coronavirus Rumor Control (FEMA)

NIH Support: National Institute of Allergy and Infectious Diseases; National Human Genome Research Institute


To Beat COVID-19, Social Distancing is a Must

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Teleworking with family at home
gettyimages/SDI Productions

Even in less challenging times, many of us try to avoid close contact with someone who is sneezing, coughing, or running a fever to avoid getting sick ourselves. Our attention to such issues has now been dramatically heightened by the emergence of a novel coronavirus causing a pandemic of an illness known as COVID-19.

Many have wondered if we couldn’t simply protect ourselves by avoiding people with symptoms of respiratory illness. Unfortunately, the answer is no. A new study shows that simply avoiding symptomatic people will not go far enough to curb the COVID-19 pandemic. That’s because researchers have discovered that many individuals can carry the novel coronavirus without showing any of the typical symptoms of COVID-19: fever, dry cough, and shortness of breath. But these asymptomatic or only mildly ill individuals can still shed virus and infect others.

This conclusion adds further weight to the recent guidance from U.S. public health experts: what we need most right now to slow the stealthy spread of this new coronavirus is a full implementation of social distancing. What exactly does social distancing mean? Well, for starters, it is recommended that people stay at home as much as possible, going out only for critical needs like groceries and medicines, or to exercise and enjoy the outdoors in wide open spaces. Other recommendations include avoiding gatherings of more than 10 people, no handshakes, regular handwashing, and, when encountering someone outside of your immediate household, trying to remain at least 6 feet apart.

These may sound like extreme measures. But the new study by NIH-funded researchers, published in the journal Science, documents why social distancing may be our best hope to slow the spread of COVID-19 [1]. Here are a few highlights of the paper, which looks back to January 2020 and mathematically models the spread of the coronavirus within China:

• For every confirmed case of COVID-19, there are likely another five to 10 people with undetected infections.
• Although they are thought to be only about half as infectious as individuals with confirmed COVID-19, individuals with undetected infections were so prevalent in China that they apparently were the infection source for 86 percent of confirmed cases.
• After China established travel restrictions and social distancing, the spread of COVID-19 slowed considerably.

The findings come from a small international research team that included NIH grantee Jeffrey Shaman, Columbia University Mailman School of Public Health, New York. The team developed a computer model that enabled researchers to simulate the time and place of infections in a grid of 375 Chinese cities. The researchers did so by combining existing data on the spread of COVID-19 in China with mobility information collected by a location-based service during the country’s popular 40-day Spring Festival, when travel is widespread.

As these new findings clearly demonstrate, each of us must take social distancing seriously in our daily lives. Social distancing helped blunt the pandemic in China, and it will work in other nations, including the United States. While many Americans will likely spend weeks working and studying from home and practicing other social distancing measures, the stakes remain high. If this pandemic isn’t contained, this novel coronavirus could well circulate around the globe for years to come, at great peril to us and our loved ones.

As we commit ourselves to spending more time at home, progress continues to be made in using the power of biomedical research to combat this novel coronavirus. A notable step this week was the launch of an early-stage human clinical trial of an investigational vaccine, called mRNA-1273, to protect against COVID-19 [2]. The vaccine candidate was developed by researchers at NIH’s National Institute of Allergy and Infectious Diseases (NIAID) and their collaborators at the biotechnology company Moderna, Inc., Cambridge, MA.

This Phase 1 NIAID-supported trial will look at the safety of the vaccine—which cannot cause infection because it is made of RNA, not the whole coronavirus—in 45 healthy adults. The first volunteer was injected this past Monday at Kaiser Permanente Washington Health Research Institute, Seattle. If all goes well and larger follow-up clinical studies establish the vaccine’s safety and efficacy, it will then be necessary to scale up production to make millions of doses. While initiating this trial in record time is reason for hope, it is important to be realistic about all of the steps that still remain. If the vaccine candidate proves safe and effective, it will likely take at least 12–18 months before it would be widely available.

In the meantime, social distancing remains one of the best weapons we have to slow the silent spread of this virus and flatten the curve of the COVID-19 pandemic. This will give our health-care professionals, hospitals, and other institutions more valuable time to prepare, protect themselves, and aid the many people whose lives may be on the line from this coronavirus.

Importantly, saving lives from COVID-19 requires all of us—young, old and in-between—to take part. Healthy young people, whose risk of dying from coronavirus is not zero but quite low, might argue that they shouldn’t be constrained by social distancing. However, the research highlighted here demonstrates that such individuals are often the unwitting vector for a dangerous virus that can do great harm—and even take the lives of older and more vulnerable people. Think about your grandparents. Then skip the big gathering. We are all in this together

References:

[1] Substantial undocumented infection facilitates the rapid dissemination of novel coronavirus (SARS-CoV2). Li R, Pei S, Chen B, Song Y, Zhang T, Yang W, Shaman J. Science. 16 March 2020. [Preprint ahead of publication]

[2] NIH clinical trial of investigational vaccine for COVID-19 begins. NIH News Release, March 16, 2020.

Links:

Coronavirus (COVID-19) (NIH)

COVID-19, MERS & SARS (National Institute of Allergy and Infectious Diseases/NIH)

Coronavirus (COVID-19) (Centers for Disease Control and Prevention, Atlanta)

NIH Support: National Institute of Allergy and Infectious Diseases; National Institute of General Medical Sciences


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