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Winter bugs: A yearly battle for dominance

By Jonathan Ball
Professor of molecular virology, University of Nottingham

image captionViral particles are shed when we sneeze

Suffering from a post-festive slump? Sadly, the same could not be said for flu and noroviruses.

Why norovirus and flu infections peak during winter is unclear.

A recent paper suggests that a combination of factors influence the seasonal pattern of influenza virus infections - factors that have also been implicated in norovirus spread.

As the weather becomes more inclement, people huddle together, contact becomes more frequent and viruses can spread more readily.

Also, specific changes in the environment - decreased temperature and humidity - make it easier for the virus to spread, presumably because these conditions support virus persistence.

It might even be that seasonal fluctuations weaken our own defences in the face of this contagious onslaught. Decreased daylight hours lower vitamin D levels - which is essential for a properly functioning immune system.

Whatever the reason, every winter a wave of nausea and malady ripples through our communities.

But why are we continually susceptible to the effects of these debilitating and sometimes deadly foes, despite being armed with an excellent means of defence. What is so special about these marauding infections that make repeat attacks so frequent?

To answer this we need to look at how our body defends itself and what the viruses do to by-pass this protection.

As soon as an infection occurs, specialised cells within us deploy a range of weapons to seek and destroy the virus.

Special proteins called antibodies - made by a type of white blood cell called a B-cell - lock onto the surface of the virus to prevent them from infecting cells. These antibodies also tag the virus so that other blood cells can consume them.

Additional components of the immune system recognise cells already infected and quickly destroy them before they release their cargo of newly-made germs.

Once the conflict is won and the virus has been cleared, a small number of these specialist cells persist.

Each is equipped with a high definition photographic memory of the virus it helped destroy and it is primed and ready to prevent subsequent infection - but only if it encounters the same virus.

This specificity means that the immune system targets foreign invaders without harming the body's normal cells. This specificity is essential but it is also its Achilles' heel - because these viruses are masters of disguise.

When they infect, norovirus and flu replicate at an incredible rate - producing billions of new viruses every day.

And as the viruses replicate they mutate. Each new virus harbours small but often advantageous changes in its genes and these accumulate as the virus passes from one person to the next.

During this process of transformation - or genetic drift - the virus alters its appearance and the immune memory cells struggle to recognise it. The virus escapes detection and is free to infect once more.

But not all of the immune cells are fooled by the new disguise and they offer at least some protection, which limits the severity of the infection.

It is this continual process of genetic drift gives rise to the seasonal epidemics of flu and norovirus.

The animal swap-shop

But flu has another more insidious trick up its sleeve - one that leads to deadly outbreaks of disease.

Flu virus is found throughout nature and different strains can infect a variety of hosts including humans, dogs, horses, swine, bats and birds.

Following years of transmission in each of these hosts the viruses become very different from one another.

This means that the immune cells from, let's say, humans are unable to recognise a virus that has been infecting birds - they offer no protection.

Occasionally, one of these animal viruses is able to jump into humans - either directly or through an intermediate host, such as a chicken or a swine.

Swine have long been suspected as the ideal mixing vessel for the emergence of new influenza strains.

New viruses are formed when two different strains infect the same cell and exchange whole genes - a process known as genetic shift.

Then, as the new virus replicates it mutates further and, if luck is on its side, some of these mutations allow it to spread from human to human - a new influenza pandemic is born.

Sweet resistance

But just as the genetic material of the virus dictates the next wave of infections, so our own genetic make-up can influence our susceptibility to these.

Studies of norovirus epidemics and human volunteer experiments (yes, there really are people willing to do this) showed that some individuals had natural resistance and this appeared to run in families - it was inherited.

In order to gain entry into the cells of the gut, norovirus locks onto sugar molecules present on the surface of these cells.

Not just any sugar. The virus interacts with specific types of sugar that are also present on the surface of red blood cells - those that give rise to the various blood groups.

And here is the twist - gut cells in around 20% of Caucasians lack these key sugars because of a fault in a gene called Fut2.

These individuals are highly resistant to common strains of norovirus.

Norovirus and influenza can strike at any time, but as many of us can vouch, this Christmas has been a particularly good time for these malevolent marauders.

If you were one of the lucky few to escape their attentions this time, just remember how rapidly these viruses can change.

What goes around comes around - if not this bleak midwinter then perhaps the next.

More on this story

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  • How close is a vaccine for the winter vomiting bug?