select search filters
roundups & rapid reactions
before the headlines
Fiona fox's blog

expert reaction to questions about COVID-19 and viral load

There have been questions from journalists about viral load ad the COVID-19 outbreak.


Comments sent out on Thursday 26 March 2020


Dr Michael Skinner, Reader in Virology, Imperial College London, said:

“Some comments on virus dose, load and shedding.

“Viruses are not poisons, within the cell they are self-replicating. That means an infection can start with just a small number of articles (the ‘dose’). The actual minimum number varies between different viruses and we don’t yet know what that ‘minimum infectious dose’ is for COVID-19, but we might presume it’s around a hundred virus particles.

“When that dose reaches our respiratory tract, one or two cells will be infected and will be re-programmed to produce many new viruses within 12-24 hours (for COVID-19, we don’t yet know how many or over how long). The new viruses will infect many more nearby cells (which can include cells of our immune defence system too, possibly compromising it) and the whole process goes around again, and again, and again.

“At some time quite early in infection, our ‘innate immune system’ detects there’s a virus infection and mounts an innate immune response. This is not the virus-specific, ‘acquired immune response’ with which people are generally familiar (i.e. antibodies) but rather a broad, non-specific, anti-viral response (characterised by interferon and cytokines, small proteins that have the side effect of causing many of the symptoms: fever, headaches, muscle pain). This response serves two purposes: to slow down the replication and spread of the virus, keeping us alive until the ‘acquired immune response’ kicks in (which, for a virus we haven’t seen, is about 2 to 3 weeks) and to call-up and commission the ‘acquired immune response’ which will stop and finally clear the infection, as well as laying-down immune memory to allow a faster response if we are infected again in the future (this is the basis of the expected immunity in survivors and of vaccination).

“With COVID-19, these two arms of the immune system (innate and acquired) obviously work well for 80% of the population who recover from more or less mild influenza-like illness.

“In older people, or people with immunodeficiencies, the activation of the acquired immune system may be delayed. This means that the virus can carry on replicating and spreading in the body, causing chaos and damage as it does, but there’s another consequence. Another job of the acquired immune system is to stand-down the innate immune system; until that’s done the innate immune response will keep increasing as the virus replicates and spreads. Part of the innate immune response is to cause ‘inflammation’. That is useful in containing the virus early in an infection but can result in widespread damage of uninfected tissue (we call this a ‘bystander effect’) if it becomes too large and uncontrolled, a situation named ‘cytokine storm’ when it was first seen with SARS and avian influenza H5N1. It is difficult to manage clinically, requiring intensive care and treatment and carries with it high risk of death.

“The scenarios described above describe what happens following infection with ‘normal’ doses of virus, both in those who make a recovery, those who require intensive care and those (mainly elderly and/or immunosuppressed) who might succumb. Those with other comorbidities probably succumb due to additional stress of their already compromised essential systems by virus and/or cytokine storm.

“It is unlikely that higher doses that would be acquired by being exposed to multiple infected sources would make much difference to the course of disease or the outcome. It’s hard to see how the dose would vary by more than 10 fold. (Although differences have been seen in lab animal infections with some viruses, those animals are inbred (genetically similar to respond in the same way). It’s unlikely that we’d see the differences as statistically significant in out-bred humans.)

“We must be more concerned about situations where somebody receives a massive dose of the virus (we have no data on how large that might be but bodily fluids from those infected with other viruses can contain a million, and up to a hundred million viruses per ml), particularly through inhalation.

“Unfortunately, we don’t yet know enough about the distribution of the COVID-19 virus throughout the body of the infected patients in normal, and unusual situations.

“Under such circumstances the virus receives a massive jump start, leading to a massive innate immune response, which will struggle to control the virus to allow time for acquired immunity to kick-in while at the same time leading to considerable inflammation and a cytokine storm.

“For most of us, it’s hard to see how we could receive such a high dose; it’s going to be a rare event. In the COVID-19 clinic, the purpose of PPE is to prevent such large exposures leading to high dose infection. Situations we should be concerned about are potential high dose exposure of clinical staff conducting procedures on patients who are not known to be infected. I read about a Chinese description of an early stage COVID-19 infection of the lung, which only came about because lung cancer patients (not known to be infected) had lobectemies. There have been suggestions that such situations contributed to the deaths of medics in Wuhan, who were conducting normal procedures (including some that could generate aerosols of infected fluids) before the spread and risk had been appreciated.

“Obviously, testing of patients for infection should now be a priority for any such procedures. Some of the relevant elective procedures have been postponed or scaled back (for patient and staff safety) but we can’t do the same for non-elective procedures (especially in emergency and maternity departments).”


Prof Wendy Barclay, Action Medical Research Chair Virology, and Head of Department of Infectious Disease, Imperial College London, said:

“In general with respiratory viruses, the outcome of infection – whether you get severely ill or only get a mild cold – can sometimes be determined by how much virus actually got into your body and started the infection off.  It’s all about the size of the armies on each side of the battle, a very large virus army is difficult for our immune systems army to fight off.

“So standing further away from someone when they breathe or cough out virus likely means fewer virus particles reach you and then you get infected with a lower dose and get less ill.  Doctors who have to get very close to patients to take samples from them or to intubate them are at higher risk so need to wear masks.

“The fewer people in the room, the less likely it is than one person is coughing or breathing out infectious virus at any one time, so mixing with as few people as possible is the safest way.

“But there is no evidence for any suggestion that if everyone in a family is already sick they can they reinfect each other with more and more virus.  In fact for other viruses once you are infected it’s quite hard to get infected with the same virus on top.”


Prof Jonathan Ball, Professor of Molecular Virology, University of Nottingham, said:

“We know that the likelihood of virus transmission increases with duration and frequency of exposure of an uninfected individual with someone infected with the virus.  We also suspect that the amount of virus that an infected individual is producing – sometimes referred to as the viral load – and potentially shedding, will also impact on transmission; the higher the viral load the more infectious someone is likely to be.

“It is also possible that individuals with pneumonia who have a higher viral load might develop more serious disease, but disease development is complex and no doubt many factors will have an impact.”


Comments sent out on Tuesday 24 March 2020

Professor Willem van Schaik, Professor in Microbiology and Infection at the University of Birmingham, said:

“The minimal infective dose is defined as the lowest number of viral particles that cause an infection in 50% of individuals (or ‘the average person’). For many bacterial and viral pathogens we have a general idea of the minimal infective dose but because SARS-CoV-2 is a new pathogen we lack data. For SARS, the infective dose in mouse models was only a few hundred viral particles. It thus seems likely that we need to breathe in something like a few hundred or thousands of SARS-CoV-2 particles to develop symptoms. This would be a relatively low infective dose and could explain why the virus is spreading relatively efficiently.

“On the basis of previous work on SARS and MERS coronaviruses, we know that exposure to higher doses are associated with a worse outcome and this may be likely in the case of Covid-19 as well.  This means that health care workers that care for Covid-19 patients are at a particularly high risk as they are more likely to be exposed to a higher number of viral particles, particularly when there is a lack of personal protective equipment (PPE) as is reported in some UK hospitals (

“It seems unlikely that people can pick up small numbers of viruses from others (e.g. in a crowd) and that will tip the infection over the edge to become symptomatic as that must happen around the same time. In the current lockdown situation this seems even less likely as gatherings of more than two individuals are banned. Because the infectious dose is probably quite low, it is more likely that you will be infected by a single source rather than from multiple sources. Transmission can take place through small droplets in the air (like the ones that are produced after sneezing and which stay in the air for a few seconds). You can breathe in these droplets or they can land on surfaces. Unfortunately, SARS-CoV-2 survives reasonably well on most surfaces, so if somebody touches these and then touches their mouth or nose, there is a very real risk that they will be infected with the viruses. This is the main reason why hand washing is promoted as a precautionary measure.”


Dr Edward Parker, Research Fellow in Systems Biology at the London School of Hygiene and Tropical Medicine, said:

“After we are infected with a virus, it replicates in our body’s cells. The total amount of virus a person has inside them is referred to as their ‘viral load’. For COVID-19, early reports from China suggest that the viral load is higher in patients with more severe disease, which is also the case for Sars and influenza. 

“The amount of virus we are exposed to at the start of an infection is referred to as the ‘infectious dose’. For influenza, we know that that initial exposure to more virus – or a higher infectious dose – appears to increase the chance of infection and illness. Studies in mice have also shown that repeated exposure to low doses may be just as infectious as a single high dose.

“So all in all, it is crucial for us to limit all possible exposures to COVID-19, whether these are to highly symptomatic individuals coughing up large quantities of virus or to asymptomatic individuals shedding small quantities. And if we are feeling unwell, we need to observe strict self-isolation measures to limit our chance of infecting others.”


From Prof Richard Tedder, Visiting Professor in Medical Virology, Imperial College London:

What is “viral load”?

“This is a specific term used in medical virology which usually refers to the amount of measurable virus in a standard volume of material, usually blood or plasma. It is very commonly used to define how HIV responds in a patient to antiviral drugs; a patient taking such drugs would be pleased to know that their ‘viral load’ is reduced.”

What does viral load mean for Sars CoV 2 (aka Covid19 virus)?

“It is probably better to use the term ‘viral shedding’ which is actually in effect influenced by the amount of virus in the material being shed by an infected patient. In practice one could say that the virus load generated by the patient in whatever excreta they shed defines ‘shedding’ and its risk.

“From looking broadly at the overall data on the material which comes from a nose swab the amount of virus varies over a 1 million fold range. This is probably influenced by the stage of the disease, the efficiency with which the infection has colonised the patient at the time of sampling, and the amount of nasal sample on the swab. The amount of virus which comes from an infected person is influenced by two factors: the ‘load’ in the excreta and the volume of the excreta.

Why does the amount of virus shed matter?

1. “The inoculum, i.e. the infecting dose of virus is more likely to lead to infection in the “recipient” the higher the amount of the virus there is in the excreta.

2. The virus will survive and remain infectious outside the body, as viruses do; BUT infectivity will fall away with time. How quickly this fall occurs is measured as the time taken for virus infectivity to reduce by half. This is termed ‘half life’ or T1/2 and for this virus is measured in hours. In fact this is best thought of as ‘rate of decay’.

3. The rate of decay is fastest on copper with a T1/2 around 1 hour, in air as an aerosol T1/2 is also around 1 hour, cardboard is 3 and 1/2 hours, plastic and steel T1/2 is around 6 hours.

“For example, if one million viruses were placed on various surfaces it would require 20 half lives to become undetectable and non-infectious, so 20 hours if in an aerosol, 20 hours on copper, 60-70 hours on cardboard and finally 120-130 hours on plastic and steel.

“Of course, when one deals with infectivity rather than detectability, extinguishing infectivity is far quicker.  Studies with cultured virus starting at relatively high levels have shown loss of infectivity within around 12-15 hours on copper, under 10 hours on cardboard, around 50 hours on steel and 70 hours on plastic. The data for infectivity in aerosols were not comparable and were of a different time course.”


All our previous output on this subject can be seen at this weblink:


Declared interests

None received.

in this section

filter RoundUps by year

search by tag