Herd Immunity

Herd immunity has been talked about a lot in recent days, particularly here in the UK. I’ve been asked by a few people to explain what herd immunity is, and how it protects vulnerable members of a population. I won’t comment on the strategies being employed by any particular country or politician with regard to herd immunity to COVID-19. But I am going to try and explain what it is and how it works, so here goes.

Antibodies are Y-shaped proteins involved in fighting off disease

When you are exposed to a pathogen (a micro-organism that causes disease), your immune system responds to fight it. Important weapons in the immune system’s arsenal are chemicals called antibodies. I won’t go into how they work – if folks are interested, I’ll do a separate post. Antibodies are specific – each antibody will only fight the particular pathogen it was designed for. When you are first exposed to a pathogen, it takes several days for your immune system to start making antibodies.

After you recover, white blood cells called memory B-cells remain in your bloodstream. They do exactly what the name implies – they ‘remember’ how to make antibodies to that pathogen. This means that if you are exposed to that particular pathogen again, your immune system will start making antibodies straight away, and will defeat the infection before you develop any symptoms. This is called immunity.

Immunity can be developed in two ways – naturally, through catching and recovering from an infection; and artificially, through vaccination. I’m going to talk about vaccination in another post, because a few people have asked about it in regard to COVID-19, so I won’t go into the details here. Basically, vaccination is away of provoking your immune system into making antibodies, and memory B-cells, without you having to get the illness; it usually uses a dead or weakened form of the pathogen.

So, how does herd immunity work? The diagram below will help explain:

The diagram shows the number of people in a population that are immune from a disease. On the left, we can see that the majority of the population are immune to the disease. The probability of those who are not immune coming into contact with the infection is low, and so is the probability that they will infect each other.

Now look at the population on the right, where there is a high proportion of individuals who are not immune. If just one of those individuals contracts the disease, the probability of them coming into contact with someone else who is not immune is high, and the disease will be able to spread through the non-immune members of the population.

How is herd immunity developed? In the case of common and mild infections, it occurs naturally. For example, there is significant natural herd immunity to some strains of flu that only cause mild illness. For more serious infections, herd immunity is developed artificially through mass vaccination programs.

In any population, there will be people who cannot be vaccinated or do not have immunity to a disease. Some vaccines can’t be given to people with compromised immune systems, such as those undergoing chemotherapy. Others may be allergic to one of the vaccine’s ingredients; for example, the flu vaccine can’t be given to people who are allergic to chicken eggs. There will also be people who have had the vaccine but do not have immunity. It takes time to build up immunity following a vaccine, so those who have only had the vaccine recently may not yet be immune. In addition, those who have been vaccinated but whose immune system is compromised may be vulnerable to the disease.

Let’s look again at the population on the left of the diagram. From the previous paragraph, you have no doubt realised that if this represents a population where mass vaccination is in place, the majority of people who have no immunity are also those who are most vulnerable to serious illness and life-threatening complications. Herd immunity protects them by minimising the risk of them coming into contact with the disease. On the right, however, there is no such protection.

Take the example of measles. Measles is a serious viral infection that can result in life-changing or even fatal complications. There is, however, a safe and effective vaccine, and where mass vaccination programs are in place, herd immunity protects the vulnerable. If uptake of the vaccine is poor, then this protection is no longer there and vulnerable individuals are at a high risk of catching the disease.

Serhiy Butenko died from complications of measles, despite being vaccinated, because his immune system was compromised.

You’ve probably never heard of Serhiy Butenko, but his case illustrates this perfectly. Ukraine has a serious measles problem due to poor uptake of the vaccine; in 2018, there were approximately 54,000 cases. Serhiy Butenko was an 18-year-old medical student in Ukraine who had been vaccinated against measles as a child. In early 2018, he was recovering from a bad bout of mononucleosis (glandular fever) that had severely depleted his immune system. He was exposed to measles, and because his immune system was suppressed, he became ill despite having been vaccinated. He developed pneumonia, which is a common complication of measles, and in February 2018 he died after several days in intensive care. Serhiy is a good example of someone who would be protected by herd immunity.

So what about COVID-19? At the moment, there is no vaccine, so the only way to develop herd immunity is for the majority of the population to catch it and recover. Which is fine if you are one of the vast majority who would only experience mild illness, but not ideal if you are one of those who is at high risk of more serious illness. I said I wouldn’t comment on the strategy of any specific government with regard to herd immunity, but speaking as one of those at-risk individuals (I have asthma), I am not entirely convinced by this thinking. Still, I will wait to pass judgement until the scientific evidence supporting this strategy has been released, and I can evaluate it for myself.

How do scientists study new viruses? Epidemiology

If there is anything to be thankful for about the COVID-19 outbreak, it’s that it is happening at a time when scientists have more tools than ever available to study new diseases. Doctors and scientists studying the virus have already made discoveries that even as recently as 15 – 20 years ago would probably have taken several years. Chloe, who is 9, has asked me to explain how scientists study new viruses. Four of the most important methods are epidemiology, genome sequencing, microscopy and crystallography, and in this post I will explain about epidemiology.

Victorian cartoon showing the conditions in big cities that allowed cholera to spread.

Epidemiology is the science of how a disease spreads. It may not sound that interesting but it’s one of the oldest methods of studying disease. The science of epidemiology started in 1854, and was the result of an outbreak of cholera. Cholera is an infection of the intestines that is caused by bacteria. It causes severe diarhea and vomiting, and left untreated it frequently results in death. Cholera bacteria are spread when faeces (as in poo) from infected people get into a water supply, and other people drink the water.

John Snow, the doctor who investigated how cholera spreads.

In the 1850s, cholera was a major problem in big cities because of overcrowding and poor living conditions. Poor people were crowded together in slums and did not have clean water or proper sewage systems – ideal conditions for cholera to spread. In 1854 there was a large outbreak of cholera in London, and it was centred on Broad Street in Soho, and the surrounding areas. A doctor named John Snow used a map to mark where cases were located, and noticed that they were all occurring in houses that used the same water pump, located in Broad Street. John Snow realised that cholera was being spread by water from the pump, and had the handle removed.

Dr John Snow’s map of the 1854 cholera outbreak. Houses were there was cholera are shown in black, and the Broad Street pump is circled in red.
The Broad Street pump, with the handle removed. It’s actually a replica.

Snow’s investigations did not stop there. He started looking at cholera cases for the whole of London, and realised that the majority were occuring in areas supplied by two water companies, both taking their water from the River Thames and supplying it to households without any attempt to clean it. Parts of London that were supplied by companies that got their water from clean sources, and filtered it before supplying it to households, had far fewer cases of cholera.

In 1858, engineer Joseph Bazalgette began work on a system of sewers and pumping stations to prevent sewage from running through the streets or being dumped in cesspools underneath houses. As a result, cholera was completely eliminated from London’s water system. The spread of other diseases such as thyphus and thyphoid decreased dramatically.

So, how will will scientists be using epidemiology to study COVID-19? In the first few days and weeks after the virus appeared, scientists in China used epidemiology to investigate whether the victims had anything in common. Just as John Snow was able to link the 1854 cholera outbreak to the Broad Street pump, Chinese epidemiologists were able to link COVID-19 to a livestock market in Wuhan. This led them to realise that the virus had originated in animals sold at the market, which is really important information for other scientists studying it.

Map showing cases of COVID-19 in China and surrounding countries on January 23rd 2020

Once the virus started spreading more widely, epidemiologists will be looking at where the virus appears and how quickly it spreads. Epidemiologists working for organisations like the World Health Organisation (WHO) are constantly monitoring the spread of the virus. This provides important information about how the virus is spreading. It also allows scientists to evaluate how well measures to prevent or slow down the spread are working; they can then use this information to advise governments on what they should do to try and slow down the spread of the virus in their own country.

I hope this has been useful. If you want to see the latest map from the WHO, you can find it by following this link:


How do viruses change?

In this post I will try to answer three questions that are related to each other. How do new viruses evolve, how do viruses spread from animals to humans, and can viruses change when they start to spread.

In my last post, I talked about how viruses contain a strand of DNA or RNA which holds all the information needed to make new copies of the virus. When a virus reproduces, part of the process is making a new copy of either the RNA or the DNA.

DNA, which stores information.

If you’ve ever had to copy something out, you’ll know that from time-to-time, you make a mistake. The same thing can happen when new copies of the virus’ DNA or RNA are made. These mistakes are called replication errors. The altered DNA or RNA can still be used to make new viruses, but they will be different – this is called a mutation.

Replication errors do not produce completely new viruses. Instead, they produce new versions of the original virus – these are called strains. Viruses which store their information as RNA have more replication errors than those with DNA. There are two reasons for this. RNA is designed to store information for shorter periods of time, so it is less stable than DNA. Also, remember, the virus is using the organelles of a cell to copy itself. The organelles in a cell are designed to copy DNA, not RNA. They have all sorts of safety mechanisms to prevent replication errors when copying DNA, but these won’t work for RNA. The common cold is caused by RNA viruses, this is why there are so many different strains of it.

Flu is also caused by an RNA virus. As well as replication errors, flu viruses can do something called re-assortment. Basically, if two different strains of flu infect the same person or animal, they can mix their RNA together and then recombining it, giving a new strain which is very different to the old ones. The most recent example of this was swine flu in 2009.

So, what about coronavirus COVID-19? It’s an RNA virus, so whenever it reproduces there may be replication errors. Most replication errors actually cause changes that make viruses weaker, and these strains die out very quickly. Very occasionally a replication error will give a new strain that survives.

So, is COVID-19 a completely new virus? The answer is no, and this relates to the second question, which is about how viruses spread from animals into humans. If you’ve read my post about how viruses work, you’ll know that they invade cells and take them over in order to make new viruses. The first step in this is to stick onto the surface of a cell.

Spikes on the virus must match exactly with receptors on a cell.

The envelope of a virus is covered in proteins, called spikes, which it uses to attach itself to a cell. These proteins will attach to proteins on the cell surface called receptors. For this to happen, the shape of the spike has to match up with the receptor – like a key fitting into a lock, or two jigsaw puzzle pieces fitting together. If the key, or the puzzle piece, is even slightly the wrong shape, it won’t fit.

There are a lot of viruses that affect animals but which humans can’t catch – this is because the spikes are the wrong shape to attach to human cells. Every so often though, a mutation will occur which alters the shape of the spikes, so that they can attach to human cells. Humans can now catch the new strain of the virus.

COVID-19 spread from animals when a mutation changed the shape of the spikes so they now match receptors on human cells.

So, how did this happen with COVID-19? Viruses are more likely to cross from animals into humans if there is a lot of contact between them. Wuhan, in China, where the virus was first seen, has a large market where live animals are sold. The city is also very overcrowded, so it’s easy for viruses to spread. Scientists think that the virus spread to humans from animals being sold in the market. They aren’t sure which animal, but coronaviruses are common in bats, and in an animal called a pangolin – both of those were on sale in Wuhan.

The final question is, do viruses change when they start to spread? The answer is, yes. The more a virus spreads, the more it reproduces, so the more opportunity for replication errors. With a virus like flu, there is also more chance of the same person or animal being infected by two different strains, leading to re-assortment. So, how will COVID-19 change as it spreads? The answer is that any changes are likely to be very small, because they will be due to replication errors – coronaviruses can’t undergo re-assortment like flu viruses do. Changes are likely to be very minor and will not alter how the virus affects humans. Scientists working on a vaccine will also be making sure that it will still work if there are changes to the virus.

I hope you have found that useful! In my next post, I will be looking at how scientists study new viruses and find out how they work.

What is a virus?

This is the first in a series of posts where I hope to answer some questions I’ve been asked about coronavirus by children. The first question I will try and answer is: what is a virus?

To understand viruses, we first need to understand a few things about cells. Your body is made up of millions of cells, which are the smallest form of life.

Human cells from inside the cheek,
seen under a microscope.

Cells are tiny – they are about 100 millionths of a metre in diameter. You can see them under a light microscope – if you are in Year 7 or 8 you have probably done this at school.

There are lots of different types of cells, and some look very different to the picture on the right. But there are certain structures, called organelles, that nearly all cells have, and these are shown in the diagram below.

The cell membrane is around the outside of the cell and controls what goes in and out of the cell. The inside of the cell is called the cytoplasm. Mitochondria are the cell’s power source – they take glucose (from our food) and react it with oxygen (from the lungs) to provide the energy the cell needs. Ribosomes are the cell’s factories – they make all the various substances that the cell needs. The nucleus contains the instructions the cell needs to function, stored on a molecule called DNA. More about that in another post.

The structure of a virus is very different to a cell. To start with, they are much, much smaller. Viruses are about 1000 times smaller than human cells. The goal of a virus is simply to reproduce – to make as many copies of itself as it possibly can. That is literally all they exist to do. The structure of a virus is a lot simpler than that of a cell, as shown in the diagram below:

Structure of a virus. A nanometre is one billionth of a metre
Influenza viruses seen with an electron microscope. You can clearly see the spikes on the envelopes of each virus.

As with cells, there are lots of types of virus and some look different to the one in the diagram. But they all have certain structures in common. All viruses have a protective capsule, called the envelope, which protects the contents. On the surface of the virus there are protein molecules sticking out – these are called spikes, and help the virus attach itself to a cell.

Inside the envelope is a strand of either DNA or RNA. These are molecules which carry all the information the virus needs to make copies of itself. Basically, the DNA or RNA is an instruction manual for making more viruses.

But, viruses have a problem. They don’t have any organelles, and they need them in order to reproduce. They need a nucleus to process the DNA or RNA (a bit like reading the instructions). They need mitochondria to provide energy, and they need ribosomes to make and assemble the new viruses. They solve the problem by taking getting inside a cell (called the host), taking over its organelles and using them to make new viruses. Here’s how its done:

  1. Attachment. The spikes on the surface of the virus stick to the surface of the cell. Have you ever been for a walk in long grass in summer, and come back with those spiky seeds stuck to your clothes? It’s a bit like that.
  2. Penetration. Once the virus has attached itself to the cell surface, it can penetrate the cell membrane and get inside.
  3. Uncoating. The envelope of the virus breaks apart, releasing the contents into the cell.
  4. Biosynthesis. Synthesis is basically a scientific word for making something. Biosynthesis is when the virus takes over the cell’s organelles and uses them to make everything needed for a new virus.
  5. Assembly. The virus uses the cell’s organelles to put the new viruses together.
  6. Release. The virus destroys the cell membrane so that the cell bursts open and releases the new viruses. They then go on to infect other cells.

So, how do viruses make us ill? Partly by the damage they do to our cells, but also as a result of the things our body does to fight them off. More of that in a later post.

I really hope you have found this post useful. Coming up tomorrow: how viruses change, and how viruses move from animals into humans. If you have any questions you’d like me to try and answer, please send them to me by comment, email or Facebook!