Posted on by Dr. Francis Collins
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.
 Revealing COVID-19 transmission in Australia by SARS-CoV-2 genome sequencing and agent-based modeling. Rockett RJ, Arnott A, Lam C, et al. Nat Med. 2020 July 9. [Published online ahead of print]
Coronavirus (COVID-19) (NIH)
Vitali Sintchenko (University of Sydney, Australia)
Posted on by Dr. Francis Collins
This past weekend, I attended a scientific meeting in New York. As often seems to happen to me in a hotel, I tossed and turned and woke up feeling not very rested. The second night I did a bit better. Why is this? Using advanced neuroimaging techniques to study volunteers in a sleep lab, NIH-funded researchers have come up with a biological explanation for this phenomenon, known as “the first-night effect.”
As it turns out, the first night when a person goes to sleep in a new place, a portion of the left hemisphere of his or her brain remains unusually active, apparently to stay alert for any signs of danger. The new findings not only provide important insights into the function of the human brain, they also suggest methods to prevent the first-night effect and thereby help travelers like me in our ongoing quest to get a good night’s sleep.
Posted on by Dr. Francis Collins
Credit: Kraemer et al. eLife 2015;4:e08347
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.