COVID-19: What is the R number?

R is a way of measuring an infectious disease's capacity to spread.

Leon Neal/Getty Images

In just a few short weeks, we've all made the collective journey from pandemic ignoramuses to budding armchair virologists with a decent grasp of once-arcane terms like personal protective equipment, social distancing and "flatten the curve".


But there's one phrase that might still leave a few justifiably scratching their heads: the R number. The coronavirus has one, and governments around the world are keen to see it shrink as much as possible. But what is it?

R refers to the "effective reproduction number" and, basically put, it's a way of measuring an infectious disease's capacity to spread. The R number signifies the average number of people that one infected person will pass the virus to.

The R number isn't fixed, but can be affected by a range of factors, including not just how infectious a disease is but how it develops over time, how a population behaves, and any immunity already possessed thanks to infection or vaccination. Location is also important: a densely populated city is likely to have a higher R than a sparsely peopled rural area.

Because Sars-CoV-2 – to give the novel coronavirus its full honorific – is a new pathogen, scientists at the start of the outbreak were scrambling to calculate its R0, or "R nought": the virus's transmission among a population that has no immunity. Studies on early cases in China indicated it was between 2 and 2.5; more recent estimates have placed it as high as 6.6.

To put these figure in context, says Wired science editor Matt Reynolds, they're worse than seasonal flu, which has an R0 of 1.3, but miles better than measles, whose R0 is between 12 and 18. The kicker, though, is that for each of those diseases we have a vaccine, and so the effective reproduction number – the R – is way below 1.

Why do we need an R of less than 1?

This threshold – an R of 1 – will become increasingly crucial over the next few months. As the UK government explained in the video that accompanied its press briefing on 30 April, an R figure that is even slightly over 1 can lead quickly to a large number of cases thanks to exponential growth.

Here's how that works. Say a disease has an R of 1.5. This may seem like a manageable figure, but a glance at the figures quickly proves that isn't the case. An R of 1.5 would see 100 people infect 150, who would in turn infect 225, who would infect 338. In three rounds of infection, the number of people with the virus would have more than quadrupled to 438. As worldwide cases now exceed 3.5 million, this helps explain why the novel coronavirus was able to rip so quickly among a global population with no previous immunity.

Image: BBC


Conversely, an R of less than 1 means that the virus will eventually peter out – the lower the R, the more quickly this will happen. An R of 0.5 means that 100 people would infect only 50, who would infect 25, who would infect 13. As the number of cases drops and ill people either die or recover, the virus will be brought under control – as long as the R can be kept low.

The ongoing battle to reduce R

So an R of 1 and above tends towards exponential growth. An R of below 1 tends towards the end of the outbreak. All we need to do is keep the R below 1. Simple, right?

Not so fast. As stated above, the R value is ever-changing. Thanks to lockdown measures, many governments have been able to push R to below 1. In the UK, chief scientific officer Patrick Vallence said that the nation's R number is currently thought to be between 0.6 and 0.9, though it varies regionally and in London could be as low as 0.5 to 0.7.

This was only achieved, however, thanks to a heroic, unprecedented series of adjustments which have brought our lives and our economies to a juddering halt – and all of this to produce an R of 0.6 to 0.9. This doesn't give us a huge amount of leeway.

Lockdown helped drop Germany's R down to about 0.7 in early April, but researchers at the Robert Koch Institute in Berlin said it had recently increased back to 0.9, before sinking again to 0.75. Even within lockdown, if people start losing patience with restrictions or need to go out to work, R could quickly rise again.

Another difficulty that scientists and policymakers are facing is that it's still not entirely clear how much of a role each measure plays. Is shutting schools doing the heavy lifting, or restricting access to shops? How much of a boost could wearing masks provide?

As governments tentatively ease lockdown restrictions around the world, they will be monitoring R very carefully for signs of a sudden jump. If R sneaks above 1 even a fraction, it could trigger a damaging second wave of the virus.

Once R is consistently low and the number of cases is manageable, governments can implement more precise measures to restrict R, such as contact-tracing and location-tracking apps – approaches that paid dividends when introduced early on in nations such as South Korea and Singapore.

Measuring R

There are a number of ways to calculate R, as Wired notes. One is by monitoring hospitalisation and death figures to get a sense of how many people have the virus – but the problem with this is that, since the virus's incubation period is so long, it only gives an accurate picture of a few weeks ago. To check transmission rates in a more accurate way, scientists at Imperial College London in the UK have started testing randomised 25,000 groups of the population to see how many are ill.

It's important to note that R isn't the only key measure in assessing the impact of this pathogen, says the BBC. Another crucial yardstick is the number of cases of COVID-19, the disease caused by Sars-CoV-2. If we have a large number of cases and an R of 1 or just below, that still equates to a large number of infections – so ideally we need to restrict both R and bring down the number of cases at the same time.

An additional key measure to look out for is the number of ICU beds available in any given country, since this will have a big effect on mortality rate.

Ultimately, the best weapon in the fight to reduce R is a vaccine. But exactly when this will be available – or indeed if it will ever happen at all – is currently unclear.

Reprinted with permission of the World Economic Forum. Read the original article.

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Reactive oxygen species (ROS) accumulate in the gut of sleep-deprived fruit flies, one (left), seven (center) and ten (right) days without sleep.

Image source: Vaccaro et al, 2020/Harvard Medical School
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We don't have to tell you what it feels like when you don't get enough sleep. A night or two of that can be miserable; long-term sleeplessness is out-and-out debilitating. Though we know from personal experience that we need sleep — our cognitive, metabolic, cardiovascular, and immune functioning depend on it — a lack of it does more than just make you feel like you want to die. It can actually kill you, according to study of rats published in 1989. But why?

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The study, from researchers at Harvard Medical School (HMS), is published in the journal Cell.

An unexpected culprit

The new research examines the mechanisms at play in sleep-deprived fruit flies and in mice — long-term sleep-deprivation experiments with humans are considered ethically iffy.

What the scientists found is that death from sleep deprivation is always preceded by a buildup of Reactive Oxygen Species (ROS) in the gut. These are not, as their name implies, living organisms. ROS are reactive molecules that are part of the immune system's response to invading microbes, and recent research suggests they're paradoxically key players in normal cell signal transduction and cell cycling as well. However, having an excess of ROS leads to oxidative stress, which is linked to "macromolecular damage and is implicated in various disease states such as atherosclerosis, diabetes, cancer, neurodegeneration, and aging." To prevent this, cellular defenses typically maintain a balance between ROS production and removal.

"We took an unbiased approach and searched throughout the body for indicators of damage from sleep deprivation," says senior study author Dragana Rogulja, admitting, "We were surprised to find it was the gut that plays a key role in causing death." The accumulation occurred in both sleep-deprived fruit flies and mice.

"Even more surprising," Rogulja recalls, "we found that premature death could be prevented. Each morning, we would all gather around to look at the flies, with disbelief to be honest. What we saw is that every time we could neutralize ROS in the gut, we could rescue the flies." Fruit flies given any of 11 antioxidant compounds — including melatonin, lipoic acid and NAD — that neutralize ROS buildups remained active and lived a normal length of time in spite of sleep deprivation. (The researchers note that these antioxidants did not extend the lifespans of non-sleep deprived control subjects.)

fly with thought bubble that says "What? I'm awake!"

Image source: Tomasz Klejdysz/Shutterstock/Big Think

The experiments

The study's tests were managed by co-first authors Alexandra Vaccaro and Yosef Kaplan Dor, both research fellows at HMS.

You may wonder how you compel a fruit fly to sleep, or for that matter, how you keep one awake. The researchers ascertained that fruit flies doze off in response to being shaken, and thus were the control subjects induced to snooze in their individual, warmed tubes. Each subject occupied its own 29 °C (84F) tube.

For their sleepless cohort, fruit flies were genetically manipulated to express a heat-sensitive protein in specific neurons. These neurons are known to suppress sleep, and did so — the fruit flies' activity levels, or lack thereof, were tracked using infrared beams.

Starting at Day 10 of sleep deprivation, fruit flies began dying, with all of them dead by Day 20. Control flies lived up to 40 days.

The scientists sought out markers that would indicate cell damage in their sleepless subjects. They saw no difference in brain tissue and elsewhere between the well-rested and sleep-deprived fruit flies, with the exception of one fruit fly.

However, in the guts of sleep-deprived fruit flies was a massive accumulation of ROS, which peaked around Day 10. Says Vaccaro, "We found that sleep-deprived flies were dying at the same pace, every time, and when we looked at markers of cell damage and death, the one tissue that really stood out was the gut." She adds, "I remember when we did the first experiment, you could immediately tell under the microscope that there was a striking difference. That almost never happens in lab research."

The experiments were repeated with mice who were gently kept awake for five days. Again, ROS built up over time in their small and large intestines but nowhere else.

As noted above, the administering of antioxidants alleviated the effect of the ROS buildup. In addition, flies that were modified to overproduce gut antioxidant enzymes were found to be immune to the damaging effects of sleep deprivation.

The research leaves some important questions unanswered. Says Kaplan Dor, "We still don't know why sleep loss causes ROS accumulation in the gut, and why this is lethal." He hypothesizes, "Sleep deprivation could directly affect the gut, but the trigger may also originate in the brain. Similarly, death could be due to damage in the gut or because high levels of ROS have systemic effects, or some combination of these."

The HMS researchers are now investigating the chemical pathways by which sleep-deprivation triggers the ROS buildup, and the means by which the ROS wreak cell havoc.

"We need to understand the biology of how sleep deprivation damages the body so that we can find ways to prevent this harm," says Rogulja.

Referring to the value of this study to humans, she notes,"So many of us are chronically sleep deprived. Even if we know staying up late every night is bad, we still do it. We believe we've identified a central issue that, when eliminated, allows for survival without sleep, at least in fruit flies."

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