Reminding others that “masks save lives” isn’t just sound advice. It’s a scientific fact that wearing one in public can help to slow the spread of SARS-CoV-2, the virus responsible for the coronavirus disease 2019 (COVID-19) pandemic.
I’m very careful to wear a mask outside my home whenever I’m out and about. I do it not necessarily to protect myself, but to protect others. If by chance I’ve been exposed to the virus and am currently incubating it, I wouldn’t want to spread it to other people. And any of us could be an unknowing superspreader. We owe it to everyone we encounter, especially those who are more vulnerable, to protect them. As my NIH colleague Tony Fauci recently demonstrated, it’s possible to wear your mask even while you’re outside exercising.
But there are still skeptics around. So, just how much does a facial covering protect those around you? Quite a bit, according to researchers who created a sophisticated mathematical model to take a more detailed look . Their model shows that even if a community universally adopted a crude cloth covering that’s far less than 100 percent protective against the virus, this measure alone could significantly help to reduce deaths.
These findings, funded partly by NIH, were published recently in Nature Communications. They come from Colin Worby, Broad Institute of MIT and Harvard, Cambridge, MA, and Hsiao-Han Chang, National Tsing Hua University, Taiwan.
The researchers noted several months ago that recommendations on wearing a mask varied across the United States and around the world. To help guide policymakers, the researchers simulated outbreaks in a closed, randomly interacting population in which the supply and effectiveness of crude cloth or disposable, medical-grade masks varied.
Under different outbreak scenarios and mask usages, the researchers calculated the total numbers of expected SARS-CoV-2 infections and deaths from COVID-19. Not surprisingly, they found that the total number of deaths and infections declined as the availability and effectiveness of face masks increased.
The researchers’ model primarily considered the distribution of medical-grade, surgical masks. But because such masks are currently available in limited supply, they must be prioritized for use by health care workers and others at high risk. The researchers go on to note that the World Health Organization and others now recommend wearing homemade face coverings in public, especially in places where the virus is spreading. While it’s true the ability of these face coverings to contain the virus is more limited than medical-grade masks, they can help and will lead to many fewer deaths.
Another recent paper also suggests that while wearing a mask is primarily intended to prevent the wearer from infecting others, it may also help lower the dose, or inoculum, of SARS-CoV-2 that the wearer might receive from others, resulting in milder or asymptomatic infections . If correct, that’s another great reason to wear a mask.
Already, more than 175,000 people in the United States have died from COVID-19. The latest estimates  from the Institute for Health Metrics and Evaluation (IHME) at the University of Washington’s School of Medicine, Seattle, predict that the COVID-19 death toll in the U.S. may reach nearly 300,000 by December 1.
But that doesn’t have to happen. As this new study shows, face coverings—even those that are far from perfect—really can and do save lives. In fact, IHME data also show that consistent mask-wearing—starting today—could save close to 70,000 lives in the months to come. Saving those lives is up to all of us. Don’t leave home without your mask.
Contact tracing, a term that’s been in the news lately, is a crucial tool for controlling the spread of SARS-CoV-2, the novel coronavirus that causes COVID-19. It depends on quick, efficient identification of an infected individual, followed by identification of all who’ve recently been in close contact with that person so the contacts can self-quarantine to break the chain of transmission.
Properly carried out, contact tracing can be extremely effective. It can also be extremely challenging when battling a stealth virus like SARS-CoV-2, especially when the virus is spreading rapidly.
But there are some innovative ways to enhance contact tracing. In a new study, published in the journal Nature Medicine, researchers in Australia demonstrate one of them: assembling genomic data about the virus to assist contact tracing efforts. This so-called genomic surveillance builds on the idea that when the virus is passed from person to person over a few months, it can acquire random variations in the sequence of its genetic material. These unique variations serve as distinctive genomic “fingerprints.”
When COVID-19 starts circulating in a community, researchers can fingerprint the genomes of SARS-CoV-2 obtained from newly infected people. This timely information helps to tell whether that particular virus has been spreading locally for a while or has just arrived from another part of the world. It can also show where the viral subtype has been spreading through a community or, best of all, when it has stopped circulating.
The recent study was led by Vitali Sintchenko at the University of Sydney. His team worked in parallel with contact tracers at the Ministry of Health in New South Wales (NSW), Australia’s most populous state, to contain the initial SARS-CoV-2 outbreak from late January through March 2020.
The team performed genomic surveillance, using sequencing data obtained within about five days, to understand local transmission patterns. They also wanted to compare what they learned from genomic surveillance to predictions made by a sophisticated computer model of how the virus might spread amongst Australia’s approximately 24 million citizens.
Of the 1,617 known cases in Sydney over the three-month study period, researchers sequenced viral genomes from 209 (13 percent) of them. By comparing those sequences to others circulating overseas, they found a lot of sequence diversity, indicating that the novel coronavirus had been introduced to Sydney many times from many places all over the world.
They then used the sequencing data to better understand how the virus was spreading through the local community. Their analysis found that the 209 cases under study included 27 distinct genomic fingerprints. Based on the close similarity of their genomic fingerprints, a significant share of the COVID-19 cases appeared to have stemmed from the direct spread of the virus among people in specific places or facilities.
What was most striking was that the genomic evidence helped to provide information that contact tracers otherwise would have lacked. For instance, the genomic data allowed the researchers to identify previously unsuspected links between certain cases of COVID-19. It also helped to confirm other links that were otherwise unclear.
All told, researchers used the genomic evidence to cluster almost 40 percent of COVID-19 cases (81 of 209) for which the community-based data alone couldn’t identify a known contact source for the infection. That included 26 cases in which an individual who’d recently arrived in Australia from overseas spread the infection to others who hadn’t traveled. The genomic information also helped to identify likely sources in the community for another 15 locally acquired cases that weren’t known based on community data.
The researchers compared their genome surveillance data to SARS-CoV-2’s expected spread as modeled in a computer simulation based on travel to and from Australia over the time period in question. Because the study involved just 13 percent of all known COVID-19 cases in Sydney between late January through March, it’s not surprising that the genomic data presents an incomplete picture, detecting only a portion of the possible chains of transmission expected in the simulation model.
Nevertheless, the findings demonstrate the value of genomic data for tracking the virus and pinpointing exactly where in the community it is spreading. This can help to fill in important gaps in the community-based data that contact tracers often use. Even more exciting, by combining traditional contact tracing, genomic surveillance, and mathematical modeling with other emerging tools at our disposal, it may be possible to get a clearer picture of the movement of SARS-CoV-2 and put more targeted public health measures in place to slow and eventually stop its deadly spread.
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 . 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 .
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!
For decades, the mosquito-transmitted Zika virus was mainly seen in equatorial regions of Africa and Asia, where it caused a mild, flu-like illness and rash in some people. About 10 years ago, the picture began to expand with the appearance of Zika outbreaks in the Pacific islands. Then, last spring, Zika popped up in South America, where it has so far infected more than 1 million Brazilians and been tentatively linked to a steep increase in the number of babies born with microcephaly, a very serious condition characterized by a small head and brain . And Zika’s disturbing march may not stop there.
In a new study in the journal The Lancet, infectious disease modelers calculate that Zika virus has the potential to spread across warmer and wetter parts of the Western Hemisphere as local mosquitoes pick up the virus from infected travelers and then spread the virus to other people . The study suggests that Zika virus could eventually reach regions of the United States in which 60 percent of our population lives. This highlights the need for NIH and its partners in the public and private sectors to intensify research on Zika virus and to look for new ways to treat the disease and prevent its spread.