“The appetite for molecular monitoring has really increased, because people are now seeing what the cost of its absence looks like,” says Mason. That cost is especially high in New York City, where the coronavirus has so far killed more than 12,000 people, including dozens of transit workers.
Outside of MetaSUB, other microbiome researchers are also applying their microbial forensic methods to track how SARS-CoV-2 spreads between people. One of them is Jack Gilbert, who is perhaps best known for spearheading the ambitious Earth Microbiome Project. In pre-pandemic times, he had developed techniques for tracing people’s movements based on their unique microbial signatures. In a 2019 study, Gilbert and his colleagues were able to identify which college students had visited which dorm rooms, based on the trail of germs they left behind. While at the University of Chicago, he led the largest-ever analysis of a hospital’s microbiome, creating detailed maps of microbial exchanges between patients, staff, and surfaces. Now at the University of California San Diego, Gilbert has launched a similar study with a local hospital aimed at understanding how much virus Covid-19 patients are shedding—into the air and onto bedrails, door handles, floors, and the health care workers who take care of them.
Laboratory experiments at the National Institutes of Health have shown that SARS-CoV-2 can survive in aerosols suspended in the air for up to three hours and on some surfaces for days. Other researchers in China and Singapore have been gathering data from inside hospitals, analyzing how environmental conditions, like temperature and humidity, might affect the virus’s ability to stick around. Gilbert wants to add another factor to that equation: the patient’s own microbiome. “Our hypothesis is that unique bacteria present in the respiratory tract of a patient might alter the persistence of the virus in the built environment,” says Gilbert.
The idea has some precedent. Inside the human body, bacterial cells outnumber human cells 10 to one. When a virus invades a human body, it has to interact with the microbial community already in residence. For a long time, doctors have observed that viral respiratory infections can trigger co-infections by pneumonia-causing bacteria in the lungs. This was generally presumed to be a result of the virus knocking back the human immune system, allowing an opportunistic bacteria to start attacking its host. But more recent research has shown that some respiratory viruses, including influenza, can bind directly to several species of bacteria, which makes both the bacteria and the virus better at grabbing on to human cells. In a study published last year, microbiologists at the University of Texas Southwestern Medical Center discovered that binding to bacteria can give some respiratory viruses another advantage—it allows them to stay alive longer in the cold, harsh desert of an otherwise antiseptic hospital room. The virus family they studied, the picornaviruses, which include the virus that causes the common cold, appeared to use the bacteria as a life raft, with the molecular bonds between them stabilizing the virus’s protein shell against heat, light, and even bleach.
Gilbert suspects the same could be true for SARS-CoV-2. “It could be that if you happen to have the wrong bug at the time you get infected, that makes you a super-spreader,” says Gilbert. “Super-spreaders,” people who can infect not one or two but potentially dozens of others, can have an outsize impact on how fast new outbreaks take off. But the mechanisms behind super-spreading remain poorly understood. Gilbert hopes to be able to offer some clues sometime next month, when his team finishes analyzing the thousand or so samples they’ve collected so far. The data could help doctors rapidly identify which people are more likely to be super-spreaders, so those people can take additional precautions.
Other research projects will take much longer to begin providing insight. Gilbert’s UCSD colleague and Earth Microbiome Project cofounder, Rob Knight, recently launched a series of longitudinal studies with Southern California hospitals exploring whether the other bugs that live in people’s lungs are associated with different Covid-19 outcomes. The goal is to eventually develop biomarkers that can predict a person’s susceptibility to more severe forms of the disease. While age and preexisting conditions are the biggest risk factors for Covid-19, the mysterious illness has also inexplicably killed many young, previously healthy people. Studies are already ongoing to see if people’s genetics play a role. Why not the microbiome?