A Boston hotel that was linked to a coronavirus outbreak after it hosted a local biotech company's conference earlier this year likely led to about 20,000 cases. The Daily Telegraph reports that according to the authors of a study, the outbreak linked to the Marriott Long Wharf Hotel was previously only thought to have caused 99 cases, but after studying nearly all the confirmed early cases of the illness in the area by looking at changes in the genetic makeup of coronaviruses, the researchers were able to assess the broader impact of the “super-spreading event”.
Scientists in the aftermath of the outbreak conducted what is believed to be the largest genomic analysis of any US outbreak so far, to provide an exceptionally detailed look at how coronavirus cases exploded in the pandemicʼs first wave. A team based in Boston analysed the 27 February conference, organised in a hotel in the city by drug company Biogen. They took the virus home with them to the Boston suburbs, Indiana and North Carolina, to Slovakia, Australia and Singapore.
Over the following two weeks, the virus that circulated among conference attendees was implicated in at least 35 new cases. In April, the same distinctive viral sub-strain swirled through two Boston homeless shelters, where it infected 122 residents.
An analysis of the genome explained the work of 54 researchers in the field. The 20,000 figure was not included in the report, but the authors are quoted as saying that their calculations were based on viruses isolated from 772 patients in Essex, Middlesex, Norfolk, and Suffolk counties. Their report will now be peer-reviewed for publication in a scientific journal. At the time of the conference, only 15 cases had been confirmed in the US, and the organisers of the event had no reason not to proceed, they felt.
“We didnʼt know better,” said Jacob Lemieux, a physician and infectious disease expert at Massachusetts General Hospital and lead author of the study. “The difference now is there is increasing scientific evidence to show what can happen from a single event like that. We do know better. So, we need to learn the lesson.” Scientists were able to precisely track the virus originating at the conference thanks to a mistake made during the coronavirusʼ replication process – simple switch of two letters in the virusʼs 30,000-character genetic code.
After the conference, each time the infection spread, the mutation spread with it. Every one of the 28 people linked to the conference whose genome was sequenced carried the conferenceʼs characteristic mutation. The mutation was dubbed “C2416T” for its location at the 2,416th spot on the genome and the two nucleic acids, cytosine (C) and uracil (T), that got switched.
Sequencing also revealed how the coronavirus evolved even as the Biogen conference was going on. About a quarter of attendees were sickened by a virus whose genome contained both the C2416T mutation and a second mutation, G26233T. In one case, the scientists found both versions of the virus replicating in a single set of lungs.
This shows that the G26233T variant is a descendant of the germ that originally arrived at the meeting, said Lemieux. As of mid-July, the variant had been found in about one-third of the cases sequenced in Massachusetts and three per cent of all genomes studied thus far in the US. The variant has shown up as far afield as Alaska, Luxembourg and Senegal.
Bronwyn MacInnis, associate director of viral genomics at the Broad Institute of MIT and Harvard University, and a co-author of the study, said the genome analysis was the "crown jewel" of understanding COVID-19's spread. She argued that every coronavirus sample collected in the US should be sent to a genetics lab for sequencing, with the results then shared with health officials and contact tracers, deepening their understanding of their local outbreaks.
“If youʼre spending whatever money large organizations seem to be putting into large-scale testing, throwing away that very same extracted (RNA) that could tell you about how cases are connected within your organisation or within communities is just throwing away the crown jewels of what you really want to know,” she said.
Scientists and the National Academies say that the US currently lacks the resources to carry out surveillance in a comprehensive way. McInnis gave the example of a school, where students became infected. If genetic analysis showed they shared a common strain, the virus was most likely transmitted at school, suggesting the facility should close or at least conduct a thorough review of infection-control procedures.
But if the infections were genetically unrelated, itʼs likely the students contracted the illness elsewhere – in which case the students should stay home, but the school could remain open. “Itʼs not testing that can answer that question,” she said. “Itʼs having genomic data to tell you whether they appear to be connected.”
Abstract
SARS-CoV-2 has caused a severe, ongoing outbreak of COVID-19 in Massachusetts with 111,070 confirmed cases and 8,433 deaths as of August 1, 2020. To investigate the introduction, spread, and epidemiology of COVID-19 in the Boston area, we sequenced and analyzed 772 complete SARS-CoV-2 genomes from the region, including nearly all confirmed cases within the first week of the epidemic and hundreds of cases from major outbreaks at a conference, a nursing facility, and among homeless shelter guests and staff. The data reveal over 80 introductions into the Boston area, predominantly from elsewhere in the United States and Europe. We studied two superspreading events covered by the data, events that led to very different outcomes because of the timing and populations involved. One produced rapid spread in a vulnerable population but little onward transmission, while the other was a major contributor to sustained community transmission, including outbreaks in homeless populations, and was exported to several other domestic and international sites. The same two events differed significantly in the number of new mutations seen, raising the possibility that SARS-CoV-2 superspreading might encompass disparate transmission dynamics. Our results highlight the failure of measures to prevent importation into MA early in the outbreak, underscore the role of superspreading in amplifying an outbreak in a major urban area, and lay a foundation for contact tracing informed by genetic data.
Authors
Jacob Lemieux, Katherine J Siddle, Bennett M Shaw, Christine Loreth, Stephen Schaffner, Adreanne Gladden-Young, Gordon Adams, Timelia Fink, Chris H Tomkins-Tinch, Lydia A Krasilnikova, Katherine C Deruff, Melissa Rudy, Matthew R Bauer, Kim A Lagergorg, Erica Normandin, Sinead B Chapman, Steven K Reilly, Melis N Anahtar, Aaron E Lin, Amber Carter, Cameron Myhrvold, Molly Kemball, Suschma Chaluvadi, Caroline Cusick, Katelyn Flowers, Anna Neumann, Felecia Cerrato, Maha Farhat, Damien Slater, Jason B Harris, John Branda, David Hooper, Jessie M Gaeta, Travis M Shaw, Travis P Baggett, James O'Connell, Andreas Gnirke, Tami D Lieberman, Anthony Philippakis, Meagan Burns, Catherine Brown, Jeremy Luban, Edward T Ryan, Sarah E Turbett, Regina C LaRocque, William P Hanage, Glen Gallagher, Lawrence C Madoff, Sandra Smole, Virginia M Pierce, Eric S Rosenberg, Pardis Sabeti, Daniel J Park, Bronwyn L MacInnis
[link url="https://www.telegraph.co.uk/news/2020/08/25/boston-conference-linked-20000-coronavirus-cases/?WT.mc_id=e_DM1280028&WT.tsrc=email&etype=Edi_FAM_New_ES&utmsource=email&utm_medium=Edi_FAM_New_ES20200826&utm_campaign=DM1280028"]Full report in The Daily Telegraph[/link]
[link url="https://www.medrxiv.org/content/10.1101/2020.08.23.20178236v1"]medRxiv abstract[/link]