How are bacteria and viruses different?

In my last post I discussed how our bodies protect us from the threat of attack from our surroundings. Two of these threats take the form of bacteria and viruses. But is there any major difference between these two invaders? In short, yes – and we’ll explore what this difference is during the rest of this post.

Let’s start by thinking about bacteria, and how they differ from the cells from which our bodies are made. By contrast with the sprawling metropolis of cells that form our body, a bacterium (we talk of a single bacterium, but many bacteria) is just a single cell. And unlike the cells of our body, which rely on each other for survival, a bacterium is a self-contained living entity. Inside that single cell is all the machinery needed for the bacterium to survive, along with that all-important element of life: a genome; the genome contains all the information needed to instruct the formation of a new bacterium, allowing the continuation of life. A bacterium feeds, grows, reproduces and dies, mirroring our own existence, but at the level of a single cell. However, bacterial cells have distinct differences from other cells, the cells of our bodies included. For example, the building materials used to construct a bacterial cell wall are quite different from the materials that encapsulate each of our cells. These differences are important, as we’ll see a little later.

So what of a virus? In short, a virus is nothing more than a neatly-packaged instruction manual. A bacterium contains its own instruction manual – its genome – but also all the molecular machinery needed to read and make use of that instruction manual: it can use its genome to maintain its own existence (and does so very effectively). By contrast, a virus simply contains a set of instructions – its own genome – but none of the machinery to bring those instructions to life. So how does it survive? Well, in the absence of its own set of molecular machinery, it steals a set from elsewhere – namely, from a living organism like us. When a virus infects us, it hijacks the molecular machinery found in each of our cells; this machinery stops reading the information stored in our own genome, and starts to read the viral genome instead.

When a viral genome is ‘read’ by a cell, two things happen: the cell makes more copies of the viral genome, and more packaging to wrap it in. The virus is basically hijacking a living cell and using the cell as a photocopier to generate multiple copies of itself. So why is this such a problem? In some cases, it isn’t: some viruses infect us without there being any adverse effects – and, indeed, without us ever being aware that the infection has happened. Others, however, are much less forgiving. In some instances, once the hijacked cell has made copies of the viral genome and new packaging to wrap it in, the cell bursts, releasing its newly-built viral cargo, but also killing the cell in the process.

By contrast with viruses, bacteria seem almost to be tame, and certainly don’t hijack our cells to drive forward their existence in the same ruthless way that some viruses do. Indeed, some bacteria are entirely harmless to humans: we have 1.5 kilos of bacteria in our gut alone, which carry out a range of useful functions. Other bacteria are less accommodating, however, and release toxins, substances that our bodies find poisonous. It is these toxins that cause our bodies to react in ways we associate with ‘being ill’ – for example, the bouts of diarrhoea and vomiting that we could all live without.

So how do we defend ourselves against these particularly harmful invaders? The key issue for our own wellbeing is that we want to eliminate the alien intruders without damaging our own cells. A bottle of bleach might well do serious damage to some invading bacteria, but it would do just as much damage to our own cells too. Not an ideal solution. The problem is compounded when it comes to viruses: the ideal solution would be to switch off their means of reproducing – but as that means of reproducing is us – our own cells – we’re left having to find other solutions. The key is to find a way of discriminating between ‘them’ and ‘us’. So what options are there?

I mentioned earlier how bacteria are encased by cell walls that are made from different building materials than those that are used to build our own cells. This is just the kind of difference that can be exploited to our benefit. Some antibiotics – naturally-occurring or man-made chemicals that destroy bacteria – can selectively target and destroy bacterial cell walls (having much the same effect as a sledgehammer on a brick wall) while leaving our own cells intact.

Viruses are somewhat trickier beasts to overcome; as I mention above, if we were to target the machinery they use to reproduce, we’d be targeting our own cells. Instead, we need to find ways of stopping the virus getting into the cell in the first place. Typically, the first step in a virus attacking a cell is its attachment to the outside of that cell. If we can prevent the virus from clinging on to the cell surface, we can stop it from subsequently getting inside to wreak its usual havoc. And this is exactly what some vaccines do: they stimulate the production of antibodies, which essentially act as cellular bodyguards, getting in the way of the virus and its intended target.

We don’t have antibiotics and vaccines to protect us against infection by all bacteria and viruses, but only those that have the potential to do us particular harm, and which could overwhelm our immune system before it had chance to respond. Other bacteria and viruses – the ones that cause us merely some annoyance and discomfort (such as the viruses that cause the common cold) – are removed through the protective action of our immune system, as explained in my previous post.

The eagle-eyed amongst you will have noted an important point above: antibiotics and vaccines attack bacteria and viruses in different ways. This is why there’s no point taking antibiotics to treat a viral infection: the antibiotic just won’t work; they’re designed to do a completely different job. You wouldn’t eat a peppermint and expect it to relieve a headache; equally, you shouldn’t take an antibiotic and expect it to cure a viral infection. So, your GP diagnoses you with a viral infection, don’t think they’re neglecting you if they don’t immediately write you a prescription for an antibiotic; to do so will be of no benefit to you at all. In fact, taking antibiotics unnecessarily can do more harm than good, as I’ll explain in a future post. 

How does our immune system work?

Each day of our lives is a battle for survival against an army of invaders so vast in size that it outnumbers the human population hugely. Yet, despite its vastness, this army is an invisible threat, each individual so small that it cannot be seen with the naked eye. These are the microbes – among them the bacteria and viruses – that surround us every day, and could in one way or another kill us were it not for our immune system, an ingenious defence mechanism that protects us from these invisible foes.

Our immune system is a multi-layered operation, much like the fortifications mounted to protect medieval castles. Our first line of defence – the equivalent of a castle moat – is our skin, a physical barrier that separates the hordes of microbes in our environment from the cells of our bodies that lie beneath. However, our skin does not keep us sealed off completely from our surroundings; indeed, some gaps in our defences are essential for our survival. And two gaps are very obvious: our nose and mouth. 

Every minute of every day we inhale air deep into our lungs. But along with the oxygen molecules we so desperately need come other less desirable particles, including viruses and fungal spores. Fortunately, we have another barrier in place to prevent these less desirable particles getting where we don’t want them. The lining of our lungs is covered by a layer of mucus, which traps many of these particles. Under this layer of mucus lie millions of tiny finger-like protrusions that bend from side-to-side, generating a Mexican wave-like movement that wafts this detritus-laden mucus up and out of our lungs, to be expelled (to put it as delicately as I can) every time we cough up phlegm or blow our noses.

Our requirement for food also leaves us exposed to the threat of invasion, this time via our digestive system. Once again, though, we are primed to defend ourselves. The inside of our stomach isn’t the most hospitable of places: it is highly acidic – perfect for aiding the digestion of food, but not a great place for many bacteria to set up home.

Despite the best efforts of these first lines of defence, however, the most determined invaders succeed in their mission and infect us. But this isn’t the end of the fight as far as our bodies are concerned: when our outer defences are breached a whole army of cells are in place to protect us. These cells are our white blood cells. 

The white blood cells operate as two separate battalions. One battalion is on the constant look-out for any general signs of trouble. In this respect, it acts a bit like a bouncer in a nightclub, who is primed to respond quickly and decisively to any one of a number of general ‘alarm’ signals - be it signs of a scuffle on the dance floor, or signs of inebriation from a late-night reveller. Whenever the alarm is raised inside the body, our first battalion is called to arms, and responds equally quickly and decisively, often simply by ‘eating’ whatever intruder first raised the alarm. 

This approach lacks what one might call any refinement: it is a fairly indiscriminate one-size-fits-all strategy. By contrast, the second battalion acts in a much more specific way, more akin to a group of snipers, each waiting for their particular target. This second battalion has two regiments – the B cells and T cells: B cells police the areas of the body outside of individual cells, including the blood; by contrast, T cells monitor the inside of cells. So how is the specificity of this second battalion achieved?

To answer this question, let’s focus on the B cell. B cells produce special Y-shaped molecules called antibodies. An antibody is like one half of a two-piece jigsaw: its specific shape allows it to recognise – and bind to – something with a complementary shape (just like neighbouring pieces of  a jigsaw fit together because their shapes are complementary). In the case of antibodies, however, the other piece of the jigsaw is a foreign object, such as a bacterium. The binding of an antibody to a foreign particle is one of the general alarm signals that call our first battalion to arms. So, the two battalions of white blood cell work together, with the second ‘sniper’ battalion often helping to focus the activity of the first on a particular invader.

Of central importance to the operation of our immune system is the fact that each B cell produces a uniquely-shaped antibody. Consequently, each antibody will recognize something different. This is important when we consider that our bodies face many different sources of danger, including many thousands of different microbes: we need lots of different antibodies to recognise them all. 

When we get infected by a specific type of bacteria, however, our bodies won’t be facing just one or two cells, but a whole army. We need lots of antibody to tag all of these invaders for destruction – but there’s no way we can always keep in circulation enough B cells to produce all the antibodies we need to destroy all the different microbes we might ever encounter. Instead, our immune system has a clever way of ensuring that large numbers of a particular antibody are only produced when actually needed. So how does this happen?

B cells circulate throughout our bodies in a continual surveillance mission, waiting until they encounter a foreign particle that can bind to their particular antibody (which, at this point in time, is protruding from the B cell like a probe). As soon as recognition happens, the B cell rapidly proliferates, stimulating the production of many copies of its particular antibody, which is now available in sufficient quantities to ‘tag’ many members of the invading army. This rapid proliferation is the reason why it feels like our ‘glands are up’ when we’re fighting infection: these ‘glands’ are our lymph nodes, specific areas around our bodies where B cells accumulate while they undergo proliferation; this accumulation occurs to such an extent that the lymph nodes actually swell.

The ingenuity of our immune system doesn’t end with the way it can detect many different foreign particles: it ‘remembers’ if it has encountered a particular invader before, and responds all the more rapidly (and effectively) if it encounters the same invader again. This memory is exploited by various vaccines, which ‘trick’ the immune system into thinking it is being attacked by a fully-fledged threat (when, in fact, it isn’t). When the body is subsequently exposed to the real threat, however, our immune system can mount a full-scale attack on the invader much more quickly than it could have done if encountering the invader for the first time. Indeed, the priming of our immune system by vaccines is essential to defend us against particularly nasty invaders, which could kill us if the immune system hadn’t already been primed.

This post leaves a number of questions unanswered. For example, is there a difference between bacteria and viruses, and what does this mean for how we defend ourselves against them? We’ll explore these questions in my next post.

How do organisms evolve?

The world around us has been in a state of constant change for millions of years: mountains have been thrust skywards as the plates that make up the Earth’s surface crash against each other; huge glaciers have sculpted valleys into the landscape; arid deserts have replaced fertile grasslands as rain patterns have changed. But the living organisms that populate this world are just as dynamic: as environments have changed, so too has the plethora of creatures inhabiting them. But how do creatures change to keep step with the world in which they live? The answer lies in the process of evolution.

Many organisms are uniquely suited to their environment: polar bears have layers of fur and fat to insulate them from the bitter Arctic cold; camels have hooves with broad leathery pads to enable them to walk on desert sand. These so-called adaptations – characteristics that tailor a creature to its environment – do not develop overnight: a giraffe that is moved to a savannah with unusually tall trees won’t suddenly grow a longer neck to be able to reach the far-away leaves. Instead, adaptations develop over many generations. This process of gradual change to make you better suited to your environment is called what’s called evolution.

So how does this change actually happen? In previous posts I’ve explored how the information in our genomes acts as the recipe for the cells, tissues and organs from which we’re constructed. If we are somehow changing to suit our environment, then our genes must be changing too. But there isn’t some mysterious process through which our genes ‘know’ how to change: if an organism finds its environment turning cold, its genome won’t magically change so that it now includes a new recipe for the growth of extra fur to keep it warm. Instead, the raw ‘fuel’ for genetic change is an entirely random process: the process of gene mutation.

In my last post, I considered how gene mutation alters the DNA sequence of a gene, and so alters the information stored by that gene. If you change a recipe when cooking, the end product will be different. And so it is with our genome: if the information stored in our genome – the recipe for our existence – changes, then we must change in some way too. 

I mentioned above how the process of mutation is random. A mutation may be introduced when an incorrect DNA ‘letter’ is inserted into a growing chain as a chromosome is being copied: instead of manufacturing a stretch of DNA with the sequence ATTGCCT, an error may occur at the second position, to give AATGCCT. But it’s just as likely that an error could have been introduced at the sixth position instead of the second, with ATTGCCT becoming ATTGCGT. Such mutations are entirely down to chance.

And this is where we encounter something of a paradox. Though the mutations that occur in our genes to fuel the process of evolution do so at random, evolution itself is anything but random. So how can we reconcile this seeming conflict?

To answer this question, let’s imagine a population of sheep, all of whom have a woolly coat of similar thickness. Quite by chance, a gene in one of the sheep in the population picks up a mutation so that offspring of that sheep develop a slightly thicker coat. However, the thick-coated sheep is in a minority: most of the population carry the normal, non-mutated gene, and so have coats of normal thickness. Now, the sheep population live in a fairly temperate environment in which a slightly thicker or slightly thinner coat makes little difference to an individual’s chance of survival. So, it’s just as likely that our thick-coated sheep will reproduce – and pass on its mutated gene to the next generation – as it is that the normal-coated sheep will reproduce, and pass on their non-mutated gene. When we look at the population as a whole, we don’t see any real change, as the balance between normal-coated and thick-coated sheep is staying firmly tipped towards coats of a normal thickness. 

However, over a period of years, the climate grows chilly. As this change occurs, the thick-coated sheep – a minority in the population as a whole – find themselves at a distinct advantage. Their thicker coats keep them warmer than their thinner-coated cousins, who find themselves increasingly susceptible to cold-induced disease; in other words, in the population as a whole, the thick-coated sheep have a greater chance of survival. Vitally, this increased chance of survival makes it more likely that they, rather than the thinner-coated sheep, will pass their genes on to the next generation. And so we see the prevalence of the mutated ‘thick coat’ gene increasing as time goes on, and see a greater proportion of the sheep population sporting thicker coats. 

Over time, what started out as a little quirk – a thicker woolly coat – goes from being an anomaly to being the norm, a defining characteristic of a species. When this happens – when a change becomes pervasive – the species is said to have evolved.

Charles Darwin is famed for introducing the world to the process of evolution in his book On the Origin of Species by Natural Selection; what we have seen here is the process of natural selection in action: in a population with different coat thicknesses, environmental conditions are favouring those sheep with the thicker coat. As a consequence, it is more likely that their genes are passed on to the next generation. We’re seeing a random event – the mutation that generated the ‘thick coat’ version of the gene – having a non-random consequence, all thanks to environmental pressures.

This exploration of evolution shows how life is driven by an elegant interplay between the recipe for our existence – our genomes – and the environment in which we live. In biological terms, nothing much happens in a single lifetime: it seems almost as unchanging as a single frame in a film. It is only by playing the film of life through many frames, over many generations, that the real beauty of this interplay is revealed.