“We know the higher the viral load, the more contagious you are.”
Public health experts have warned the B.1.1.7 variant would become a problem in the United States since January. Now those predictions are coming true.
While it emerged in December in the United Kingdom, it’s now the cause of most new Covid-19 infections in the United States. As of Monday, there were 20,915 reported cases of the B.1.17 variant in the U.S.
Information around the variants feels a bit like the information we were getting at the beginning of the pandemic: We know some facts, we don’t know others, and what do know could change. There’s a lot of good faith research trying to figure out the characteristics of these new pathogens, and sometimes that information is confusing or even contradictory.
Here’s what science can and can not explain.
B.1.1.7 is more transmissible
We know that B.1.1.7 is between 40 and 90 percent more transmissible than the “wild” virus. It’s fairly common for viruses to mutate in ways that make their transmission more effective — after all, they want to survive. Most of the variants of concern that have popped up around the world have a similar mutation, though B.1.1.7 seems to be leading the pack in transmissibility.
Is B.1.1.7 more deadly?
This is where we encounter some mixed data.
Earlier in the year data did suggest that B.1.1.7 can lead to more severe infection. Two studies published in March gave us real cause for concern.
The first was from The University of Exeter and published in the peer-reviewed medical trade journal, BMJ. That study found that people older than 30 who contracted B.1.1.7 had a 64 percent higher risk of death 28 days after contracted the virus than those who contracted a non-B.1.1.7 version of the virus.
Five days later, a second study came out in Nature that seemed to confirm those findings. That study found that at the 28-day mark, people who contracted the B.1.1.7 variant had a 61 percent higher risk of death.
However, on Monday, two new studies suggested that B.1.1.7 does not increase disease severity — despite being more transmissible. Both were observational retrospective studies.
The first, published in The Lancet, used self-reported data from 37,000 people in the UK. Logging their symptoms on a COVID-19 symptom app, there was no difference in the severity or duration of illness between those who had B.1.1.7 and those who didn’t.
The second study, also published in The Lancet, focused on 341 patients admitted to hospitals in London. Of these patients, 198 had a B.11.7 infection and 143 had a non-B.1.1.7 infection. Analysis of this group suggests that while B.1.1.7 did increase viral load in patients, they were not more likely to have a severe or fatal case of COVID-19.
Why does viral load matter?
Some studies do suggest that a higher viral load, the amount of virus you’re exposed to, often results in more severe illness. For example, a study published in October in the journal Nature Communications found an association between higher viral loads of SARS-CoV-2 and “increased disease severity and mortality.”
But George Rutherford, Director of the Prevention and Public Health Group and professor of epidemiology and biostatistics at the University of California San Francisco, tells Inverse that higher viral loads don’t always mean more severe disease.
“We know the higher the viral load, the more contagious you are because you’re shedding more virus,” he says.
But in terms of getting sick, exposure to the virus is more like a tipping point. “Once you hit a certain threshold for developing an infection, more virus isn’t necessarily going to change the trajectory of your illness,” he says.
For example, the Lancet study that focused on the 341 patients found 36 percent of people with B.1.1.7 experienced severe illness. In the non-B.1.1.7 group, that number was 38 percent. Meanwhile, 16 percent of people with B.1.1.7 died within 28 days; 17 percent of the non-B.1.1.7 group died in the same time period.
The researchers also make an important note: because this was an observational retrospective study, it’s not a perfect compare-and-contrast. Different patients fit different profiles, making it more difficult to draw conclusions over what’s exactly going on. For example, the B.1.1.7 group tended to be younger and have fewer comorbidities than the non-B. 1.1.7 group.
What to make of this conflicting information— While it can be frustrating to not have definitive information about whether or not B.1.1.7 is deadlier than other strains, this is unfortunately just part of the process of figuring out how new pathogens work.
For now, we definitely know that B.1.1.7 is more transmissible and therefore is likely to result in higher viral loads — meaning people sick with B.1.1.7 are especially contagious. Ultimately, this means we need to stay vigilant about practices like social distancing, mask-wearing, ensuring good ventilation if we’re indoors, and getting vaccinated as soon as we’re eligible.
The Inverse analysis — There is good news.
While we don’t have perfect data for every vaccine, experts have good reason to believe that the current Covid-19 vaccines protect against severe illness and death from the B.1.1.7 variant. Even better, Moderna is currently testing an updated vaccine that specifically targets B.1.1.7.
While mixed information about variants is undeniably frustrating, and can be reminiscent of the chaotic early weeks of the pandemic, rest assured that we still know much more than we did then. We understand how the virus is transmitted, we have scientifically proven risk mitigation tools, and effective vaccines. We just have to make sure to use them.