How contagious is Delta? How long are you infectious? Is it more deadly? A quick guide to the latest science


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Lara Herrero, Griffith UniversityDelta was recognised as a SARS-CoV-2 variant of concern in May 2021 and has proved extremely difficult to control in unvaccinated populations.

Delta has managed to out-compete other variants, including Alpha. Variants are classified as “of concern” because they’re either more contagious than the original, cause more hospitalisations and deaths, or are better at evading vaccines and therapies. Or all of the above.

So how does Delta fare on these measures? And what have we learnt since Delta was first listed as a variant of concern?




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Is Delta defeating us? Here’s why the variant makes contact tracing so much harder


How contagious is Delta?

The R0 tells us how many other people, on average, one infected person will pass the virus on to.

Delta has an R0 of 5-8, meaning one infected person passes it onto five to eight others, on average.

This compares with an R0 of 1.5-3 for the original strain.

So Delta is twice to five times as contagious as the virus that circulated in 2020.



The Conversation, CC BY-ND

What happens when you’re exposed to Delta?

SARS-CoV-2 is the virus that causes COVID-19. SARS-CoV-2 is transmitted through droplets an infected person releases when they breathe, cough or sneeze.

In some circumstances, transmission also occurs when a person touches a contaminated object, then touches their face.

Four Turkish men walk across an open town space.
One person infected with Delta infects, on average, five to eight others.
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Once SARS-CoV-2 enters your body – usually through your nose or mouth – it starts to replicate.

The period from exposure to the virus being detectable by a PCR test is called the latent period. For Delta, one study suggests this is an average of four days (with a range of three to five days).

That’s two days faster than the original strain, which took roughly six days (with a range of five to eight days).



The Conversation, CC BY-ND

The virus then continues to replicate. Although often there are no symptoms yet, the person has become infectious.

People with COVID-19 appear to be most infectious two days before to three days after symptoms start, though it’s unclear whether this differs with Delta.

The time from virus exposure to symptoms is called the incubation period. But there is often a gap between when a person becomes infectious to others to when they show symptoms.

As the virus replicates, the viral load increases. For Delta, the viral load is up to roughly 1,200 times higher than the original strain.

With faster replication and higher viral loads it is easy to see why Delta is challenging contact tracers and spreading so rapidly.

What are the possible complications?

Like the original strain, the Delta variant can affect many of the body’s organs including the lungs, heart and kidneys.

Complications include blood clots, which at their most severe can result in strokes or heart attacks.

Around 10-30% of people with COVID-19 will experience prolonged symptoms, known as long COVID, which can last for months and cause significant impairment, including in people who were previously well.

Woman in a mask waits in hospital waiting room.
Even previously well people can get long COVID.
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Longer-lasting symptoms can include fatigue, shortness of breath, chest pain, heart palpitations, headaches, brain fog, muscle aches, sleep disturbance, depression and the loss of smell and taste.

Is it more deadly?

Evidence the Delta variant makes people sicker than the original virus is growing.

Preliminary studies from Canada and Singapore found people infected with Delta were more likely to require hospitalisation and were at greater risk of dying than those with the original virus.

In the Canadian study, Delta resulted in a 6.1% chance of hospitalisation and a 1.6% chance of ICU admission. This compared with other variants of concern which landed 5.4% of people in hospital and 1.2% in intensive care.

In the Singapore study, patients with Delta had a 49% chance of developing pneumonia and a 28% chance of needing extra oxygen. This compared with a 38% chance of developing pneumonia and 11% needing oxygen with the original strain.

Similarly, a published study from Scotland found Delta doubled the risk of hospitalisation compared to the Alpha variant.

Older man with cold symptoms lays down, wrapped in a blanket, cradling his head, holding a tissue to his nose.
Emerging evidence suggests Delta is more likely to cause severe disease than the original strain.
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How do the vaccines stack up against Delta?

So far, the data show a complete course of the Pfizer, AstraZeneca or Moderna vaccine reduces your chance of severe disease (requiring hospitalisation) by more than 85%.

While protection is lower for Delta than the original strain, studies show good coverage for all vaccines after two doses.

Can you still get COVID after being vaccinated?

Yes. Breakthrough infection occurs when a vaccinated person tests positive for SARS-Cov-2, regardless of whether they have symptoms.

Breakthrough infection appears more common with Delta than the original strains.

Most symptoms of breakthrough infection are mild and don’t last as long.

It’s also possible to get COVID twice, though this isn’t common.

How likely are you to die from COVID-19?

In Australia, over the life of the pandemic, 1.4% of people with COVID-19 have died from it, compared with 1.6% in the United States and 1.8% in the United Kingdom.

Data from the United States shows people who were vaccinated were ten times less likely than those who weren’t to die from the virus.

The Delta variant is currently proving to be a challenge to control on a global scale, but with full vaccination and maintaining our social distancing practices, we reduce the spread.




Read more:
Why is Delta such a worry? It’s more infectious, probably causes more severe disease, and challenges our vaccines


The Conversation


Lara Herrero, Research Leader in Virology and Infectious Disease, Griffith University

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Why more contagious variants are emerging now, more than a year into the COVID-19 pandemic



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David Welch, University of Auckland; Jemma Geoghegan, University of Otago; Joep de Ligt, ESR, and Nigel French, Massey University

New variants of SARS-CoV-2 have now evaded New Zealand’s border protections twice to spread into the community.

In the most recent outbreak, which placed Auckland into an alert level 3 lockdown, there are three active community cases of the more infectious B.1.1.7 lineage.

While we have seen the virus mutate over the entire course of the pandemic, it was not until mid-December 2020 that variants with measurably different behaviour emerged.

There are several reasons for this, including the continued exponential rise in cases globally. Every COVID-19 case gives the virus a chance to mutate, and if the number of infections continues to rise, more new variants are likely to emerge.

Pressure to mutate

The genetic code of SARS-CoV-2 is a string of RNA of about 30,000 bases, or letters. When the virus enters our cells, it hijacks them to make thousands of copies of itself, but the copying process is not perfect.

Mistakes, or mutations, happen on average once every couple of weeks in any chain of transmission. Most are changes in a single letter and don’t result in a notable difference, but some will change the physical form of the virus, with possible knock-on effects to how the new variant behaves.




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We know about these variants thanks to the sequencing efforts from different countries and their open sharing of this knowledge. The variants that have arisen recently — known as B.1.1.7 (first identified in the UK), B.1.351 (identified in South Africa) and P.1 (identified in Brazil) — all have a large number of mutations that have physically altered the virus.

Graph showing the rise in new variants of the virus that causes COVID-19
This graph shows the frequency of SARS-CoV-2 sequences deposited on the global database GISAID (visualised by Nextstrain). The three ribbons at the bottom right correspond to variants P.1 (red, also known as 501Y.V1), B.1.1.7 (orange, also known as 501Y.V2), and B.1.351 (yellowy-orange, also known as 501Y.V1).
Nextstrain, CC BY-SA

A number of these changes are on the outside of the virus, in the spike proteins it uses to infect cells. Such changes can also undermine our immune system’s ability to detect these new versions of the virus when it has only seen the old version.

The most obvious reason why new variants have been emerging recently is that the number of global cases increased massively in the last quarter of 2020. There were about 35 million cases recorded worldwide in the first nine months of 2020, but it took just two months to double that number. We are well on the way to doubling that number again soon.

Evading rising levels of immunity

A second reason is that the virus is responding to immunity that has started to build up in the population. Our immune system plays an important role in driving which mutations survive and are transmitted.

The immune system is constantly trying to identify and kill the virus, which can only infect new people if it escapes detection. While mutations occur randomly, ones that lead to a more transmissible variant or those that escape our immune system are preferentially selected and more likely to persist.

The mutations that characterise B.1.1.7, B.1.351 and P.1 have been shown to spread faster (especially B.1.1.7) and initial evidence points to a difference in the immune response (though not in B.1.1.7).

Another indication that immunity plays a big role is that the B.1.351 and P.1 variants came to prominence in areas with large first waves of COVID-19 where the population developed higher levels of immunity.

Lights as a tribute to victioms of COVID-19 in Brazil
Special lighting will honour victims of COVID-19 during the cancelled carnival period in Rio de Janeiro.
Wagner Meier/Getty Images

P.1 was identified in Brazil where up to 70% of the population were infected during the first wave. B.1.351 quickly became the dominant strain in the Eastern Cape region of South Africa which was similarly hard hit.

The new variants could infect a greater number of people than the original wild type of the virus, which might infect only people who had never been infected before.

This is one of the reasons why historically herd immunity for a new virus has not occurred through “natural disease progression” but only through vaccination.




Read more:
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The final part of the story is the fact that two of these variants (B.1.1.7 and P.1) differ by as many as 25 mutations from the closest known SARS-CoV-2 sequences. This is very unusual given that most viral sequences we see are within just a few mutations of others.

Such a rapid increase in diversity has been observed in chronic COVID-19 infections in immunocompromised hosts. Most people are ill for a week or two, but a few have to fight the disease for months. During that time, the virus continues to evolve, sometimes very quickly as a weakened immune system presents all sorts of challenges to the virus but fails to kill it off.

This kind of infection presents a “training ground” for the virus, as it continually adapts.

Will we see more new variants?

As long as the virus is around, it will continue to mutate. With vaccine protection and natural immunity in a growing number of people, there is greater pressure on virus variants that evade our immune defences.

The rate of new mutations varies greatly between viruses. The overall mutation rate of SARS-CoV-2 is about half that of the influenza virus and much slower than HIV. But the overall mutation rate doesn’t tell us everything. What really matters is the rate of mutations that physically alter the virus.

There is some early evidence this rate is about the same in SARS-CoV-2 as in influenza viruses. One reason for this is that SARS-CoV-2 has only recently jumped to people and is not yet “optimised” to spread in humans.

Essentially the original virus was only a few mutations away from better fitness, and there may be further easy changes that could make it even better adapted to humans. Once the virus is through this initial adaptation phase, there will be fewer opportunities for easy, fitness-improving changes and new variants may appear less frequently.

The variants that have been characterised so far are likely only a small subset of those in circulation. It is no coincidence they are known from countries with comprehensive sequencing programmes (notably the UK).

But the new variants are not the main driver of transmission globally. Most of the world is still susceptible to any variant of SARS-CoV-2, including the original version. The protective measures we have used successfully in Aotearoa to control the virus continue to work for any variant.

The best way to protect against all current variants and to prevent the emergence of further variants is to drive down the number of cases through ongoing control measures and vaccination.The Conversation

David Welch, Senior Lecturer, University of Auckland; Jemma Geoghegan, Senior Lecturer and Associate Scientist at ESR, University of Otago; Joep de Ligt, Science Lead Genomics & Bioinformatics, ESR, and Nigel French, Professor of Food Safety and Veterinary Public Health, Massey University

This article is republished from The Conversation under a Creative Commons license. Read the original article.

How contagious is the Wuhan coronavirus and can you spread it before symptoms start?


C Raina MacIntyre, UNSW

Cases of the Wuhan coronavirus have increased dramatically over the past week, prompting concerns about how contagious the virus is and how it spreads.

According to the World Health Organisation, 16-21% of people with the virus in China became severely ill and 2-3% of those infected have died.




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A key factor that influences transmission is whether the virus can spread in the absence of symptoms – either during the incubation period (the days before people become visibly ill) or in people who never get sick.

On Sunday, Chinese officials said transmission had occurred during the incubation period.

So what does the evidence tell us so far?

Can you transmit it before you get symptoms?

Influenza is the classic example of a virus that can spread when people have no symptoms at all.

In contrast, people with SARS (severe acute respiratory syndrome) only spread the virus when they had symptoms.

No published scientific data are available to support China’s claim transmission of the Wuhan coronavirus occurred during the incubation period.

However, one study published in the Lancet medical journal showed children may be shedding (or transmitting) the virus while asymptomatic. The researchers found one child in an infected family had no symptoms but a chest CT scan revealed he had pneumonia and his test for the virus came back positive.

This is different to transmission in the incubation period, as the child never got ill, but it suggests it’s possible for children and young people to be infectious without having any symptoms.

This is a concern because if someone gets sick, you want to be able to identify them and track their contacts. If someone transmits the virus but never gets sick, they may not be on the radar at all.

It also makes airport screening less useful because people who are infectious but don’t have symptoms would not be detected.

How infectious is it?

The Wuhan coronavirus epidemic began when people exposed to an unknown source at a seafood market in Wuhan began falling ill in early December.

Cases remained below 50 to 60 in total until around January 20, when numbers surged. There have now been more than 4,500 cases – mostly in China – and 106 deaths.




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Researchers and public health officials determine how contagious a virus is by calculating a reproduction number, or R0. The R0 is the average number of other people that one infected person will infect, in a completely non-immune population.

Different experts have estimated the R0 of the Wuhan coronavirus is anywhere from 1.4 to over five, however the World Health Organisation believes the RO is between 1.4 and 2.5.

Here’s how a virus with a R0 of two spreads:



The Conversation, CC BY-ND

If the R0 was higher than 2-3, we should have seen more cases globally by mid January, given Wuhan is a travel and trade hub of 11 million people.

How is it transmitted?

Of the person-to-person modes of transmission, we fear respiratory transmission the most, because infections spread most rapidly this way.

Two kinds of respiratory transmission are through large droplets, which is thought to be short-range, and airborne transmission on much smaller particles over longer distances. Airborne transmission is the most difficult to control.

SARS was considered to be transmitted by contact and over short distances by droplets but can also be transmitted through smaller aerosols over long distances. In Hong Kong, infection was transmitted from one floor of a building to the next.




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Initially, most cases of the Wuhan coronavirus were assumed to be from an animal source, localised to the seafood market in Wuhan.

We now know it can spread from person to person in some cases. The Chinese government announced it can be spread by touching and contact. We don’t know how much transmission is person to person, but we have some clues.

Coronaviruses are respiratory viruses, so they can be found in the nose, throat and lungs.

The amount of Wuhan coronavirus appears to be higher in the lungs than in the nose or throat. If the virus in the lungs is expelled, it could possibly be spread via fine, airborne particles, which are inhaled into the lungs of the recipient.

How did the virus spread so rapidly?

The continuing surge of cases in China since January 18 – despite the lockdowns, extended holidays, travel bans and banning of the wildlife trade – could be explained by several factors, or a combination of:

  1. increased travel for New Year, resulting in the spread of cases around China and globally. Travel is a major factor in the spread of infections

  2. asymptomatic transmissions through children and young people. Such transmissions would not be detected by contact tracing because health authorities can only identify contacts of people who are visibly ill

  3. increased detection, testing and reporting of cases. There has been increased capacity for this by doctors and nurses coming in from all over China to help with the response in Wuhan

  4. substantial person-to-person transmission

  5. continued environmental or animal exposure to a source of infection.




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However, with an incubation period as short as one to two days, if the Wuhan coronavirus was highly contagious, we would expect to already have seen widespread transmission or outbreaks in other countries.

Rather, the increase in transmission is likely due to a combination of the factors above, to different degrees. The situation is changing daily, and we need to analyse the transmission data as it becomes available.The Conversation

C Raina MacIntyre, Professor of Global Biosecurity, NHMRC Principal Research Fellow, Head, Biosecurity Program, Kirby Institute, UNSW

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Health Check: why do we yawn and why is it contagious?



File 20180509 34038 11hqktd.jpg?ixlib=rb 1.1
Yawning increases our alertness.
from shutterstock.com

Mark Schier, Swinburne University of Technology and Yossi Rathner, Swinburne University of Technology

Consider the scenario. You’re driving on a long, straight stretch of country highway at about 2pm on a sunny afternoon, and you’re desperately keen to reach your destination. You’re trying to stay alert and attentive, but sleep pressure is building up.

In response you yawn, sit up straighter in your seat, possibly fidget around a little and engage in other mannerisms that may increase your level of arousal.

Is this the purpose of yawning? Yawning is generally triggered by several things, including tiredness, fever, stress, drugs, social and other psychological cues. These are generally well documented and vary between individuals.

The question of why we yawn evokes a surprising amount of controversy for what is a relatively minor field of study. We don’t have evidence that can point us to the exact purpose of yawning.

But there are several theories about the purpose of yawning. These include increasing alertness, cooling the brain, and the evolutionary theory of alerting others in your group that you’re too tired to keep watch, and someone else should take over.

1. Helps us wake up

Yawning is known to increase with drowsiness. This has led to the arousal hypothesis of yawning. Associated with the yawning are increased movement and stretching behaviour. The increased fidgeting behaviour may help maintain vigilance as sleep pressure builds.




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Also, specific muscles in the ear (the tensor tympani muscles) are activated during yawning. This leads to a resetting of the range of movement and sensitivity of the eardrum and hearing, which increases our ability to monitor the world around us after we may have tuned out before the yawn.

Yawning is usually accompanied by stretching behaviour.
from shutterstock.com

Additionally, the opening and flushing of the eyes will probably lead to an increase in visual alertness.

2. Cools the brain

Another theory for why we yawn is the thermoregulatory hypothesis. This suggests that yawning cools the brain. Yawning causes a deep inhalation that draws cool air into the mouth, which then cools the blood going to the brain.

Proponents of this theory claim a rise in brain temperature is observed prior to yawning, with a decrease in temperature seen after the yawn.

But the research report that gave rise to this theory only shows excessive yawning may occur during an increase in brain and body temperature. It doesn’t suggest this has a cooling purpose.

Increased yawning rates are seen when fevers have been experimentally induced, which does suggest a correlation between body warming and yawning. But there is no clear evidence it leads to body cooling – just that body warming seems to be a trigger for yawning.

3. Sentry duty

Yawning-like behaviour has been observed in almost all vertebrates, suggesting that the reflex is ancient. The evolutionary based behavioural hypothesis draws on humans being social animals. When we are vulnerable to an attack from another species, a function of the group is to protect each other.

Part of our group contract has included sharing sentry duties, and there is evidence from other social animals of yawning or stretching signals when individuals are becoming lower in arousal or vigilance. This is important for changing activities to prevent the watch from slipping, or to indicate the need for another sentry.

Neuroscience explanations

The yawning reflex involves many structures in the brain.

One study that scanned the brains of those who were prone to contagious yawning found activation in the ventromedial prefrontal cortex of the brain. This brain region is associated with decision-making. Damage to this region is also associated with loss of empathy.




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Understanding others’ feelings: what is empathy and why do we need it?


Stimulation of a particular region of the hypothalamus, which contains neurons with oxytocin, causes yawning behaviour in rodents. Oxytocin is a hormone associated with social bonding and mental health.

Injecting oxytocin into various regions of the brain stem causes yawning, too.
These include the hippocampus (associated with learning and memory), ventral tegmental area (associated with the release of dopamine, the happy hormone) and the amygdala (associated with stress and emotions). Blocking the oxytocin receptors here prevents that effect.

Patients with Parkinson’s disease don’t yawn as frequently as others, which may be related to low dopamine levels. Dopamine replacement has been documented to increase yawning.

Your dog could be yawning on long car trips because it is stressed.
from shutterstock.com

Similarly, cortisol, the hormone that increases with stress, is known to trigger yawning, while removal of the adrenal gland (which releases cortisol) prevents yawing behaviour. This suggests that stress might play a role in triggering yawning, which could be why your dog may yawn so much on long car trips.

So, it seems yawning is somehow related to empathy, stress and dopamine release.

Why is it contagious?

Chances are you’ve yawned at least once while reading this article. Yawning is a contagious behaviour and seeing someone yawn often causes us to yawn as well.
But the only theory that’s been suggested here is that susceptibility to contagious yawning is correlated with someone’s level of empathy.

It is interesting to note, then, that there is decreased contagious yawning among people on the autism spectrum, and people who have high psychopathic tendency. And dogs, considered to be highly empathetic animals, can catch human yawns too.




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Contagious yawns show social ties in humans and bonobos


Overall, neuroscientists have developed a clear idea of a wide range of triggers for yawning, and we have a very detailed picture of the mechanism underlying yawning behaviour. But the functional purpose of yawning remains elusive.

The ConversationBack to our road trip, the yawning may be a physiological cue as the competition between vigilance and sleep pressure begins to favour drowsiness. But the overwhelming message is that sleep is winning and encouraging the driver to pull over for a break, and it shouldn’t be ignored.

Mark Schier, Senior Lecturer in Physiology, Swinburne University of Technology and Yossi Rathner, Lecturer in Human Physiology, Swinburne University of Technology

This article was originally published on The Conversation. Read the original article.