The Misconception of Unset Jelly

As an experimental cook, the conventional fruit which are set in jelly on top of a cake are not good enough. So, fuelled by the desire to find the most original combination of fruit that could adorn a cake creation whilst smothered in jelly, I managed to find a few unusual possibilities, until I met my nemesis: fruit, which no matter how long the jelly sat in the fridge, prevented it from setting.

This post looks at why, and the slight misconception which surrounds the idea that some fruit prevent jelly from setting.

An Introduction to Gelatine

What is gelatine?

Gelatine is a mild tasting protein that is derived from collagen in animal tissue, which in turn is a hard, insoluble, fibrous protein [1]. Collagen is the connective tissue protein that provides strength to muscles and tendons and resiliency to an animal’s skin and bones, meaning that in humans it makes up one third of the total protein content [1]. Furthermore, since it is a structural protein, collagen is found in many parts of an animal’s body as it helps to maintain the structure and shape.

Where does gelatine come from?

Most gelatine is manufactured from pig skin because around 30% of its weight is collagen [2]. Firstly, the pig skin is soaked in dilute hydrochloric acid for roughly 24 hours. This step leads to the unravelling of the crosslinking protein bonds in collagen, resulting in the free protein chains then being extracted. These are filtered, purified and dried into sheets or granules (powder) that contain around 90% gelatine, 8% water and the remaining 2% is salts and glucose [2].

How does gelatine work?

Gelatine has claimed the prize of being different to all other proteins typically used in a kitchen setting, partially because it is the only protein that has the power to thicken liquids. This is why gelatine thickened sauces are ‘crystal clear and syrupy’ rather than opaque and creamy like sauces which use starch or flour as the thickening agent [2]. Gelatine’s unique properties arise from that fact its response to heat is not one that is usually demonstrated by proteins. Normally, food proteins respond to heat by unravelling (meaning they lose their tertiary and potentially secondary structures), and then bonding to one another to coagulate into a firm, solid mass. This is demonstrated by an egg frying since the albumin (liquid protein of the white) firms up into a solid mass of egg white as it is heated. However, gelatine proteins do not readily form bonds with one another, meaning that although heat initially causes them to unravel and disperse like any other protein, the gelatine proteins never form new bonds. This results in the liquid that they are dispersed in remaining as a fluid. Furthermore, because gelatine proteins are also long and stringy, they tend to become interwoven and this leads to the hot liquid in which they are suspended to thicken, although not completely solidify when warm. As the gelatine gradually cools down, the protein strands line up next to each other and twist into long ‘ropes’ and turn the liquid into a firm gel [2].

Plot Twist from an Innocent Addition

Learning from my past experiences, the following fruit should not be added if you wish for your jelly to achieve its intended state:

  • Pineapple
  • Kiwi
  • Figs
  • Papaya
  • Pawpaw
  • Mango
  • Guava
  • Ginger root

There are, as always, some exceptions to this rule, however I will come onto this later.

An unexpected culprit

You may have noticed that some of the aforementioned fruit are quite acidic, such as kiwi, and for me, initially, this was why the jelly did not set. However, it was as I did more research that I realised this was not the case.

As far as I am aware, when we study enzymes at school, whether at GCSE or A Level, enzymes seem to take on the role of the keys to existence, the Gods of all things bright and biological, or words to that effect. Or an effect slightly less exaggerated.

And yes, I do not dare disagree with the importance of their function as biological catalysts, whether it be in the baby food industry, slimming food industry or even saving the world by being a part of biological washing powders which require a lower temperature.

However, enzymes are the reason behind your cake masterpiece having a ‘soggy top’ as a result of the jelly not setting, which would lead to a piercing ice-blue stare from Paul Hollywood himself, an ‘It’s a little informal’ comment from the Queen of baking, Mary Berry, and may even provoke Shakespeare’s ‘God has given you one face, and you make yourself another’ exclamation.

Why are enzymes the downfall of jelly?

The listed fruit contain enzymes, in particular, proteases. Pineapple, kiwi, papaya, pawpaw and mango all contain actinidin, papaya and pawpaw also contain papain, pineapple also has bromelain, figs contain ficain and ginger contains zingibain.

The reason that jelly sets is because the collagen proteins in the gelatine form a tangled mesh as a result of being interwoven, meaning that water molecules are trapped, as well as other components of the liquid, and this provides the gelatine its semisolid state when it cools [3].


Fig 1. The long gelatine molecules as seen in set jelly [4].

The proteases in the fruit act on gelatine protein, and this can be thought of as the proteases acting as scissors and ‘cutting up’ the long strands of gelatine protein into smaller pieces, so that they can no longer interweave and create a network to trap water and other liquid molecules, meaning the jelly does not set [4]. This is shown in figure 2 and figure 3.


Fig 2. Scissors representing enzymes (proteases) acting on gelatine [4].


Fig 3. Shorter gelatine molecules after protease action [4].

In addition, it is important to note that pineapple and kiwi contain far more proteases than the other listed fruit. The reason for this difference is unknown, however it may be linked to the idea of repelling pests. As a basic concept, animals and bacteria are made up of proteins meaning that essentially the high levels of proteases in the fruit will digest any of the pests trying to feed on the fruit [4].

Moreover, I should address the exception that I mentioned earlier in the post. The fruit has to be fresh in order for it to ‘rain unset jelly on your cake parade’. For example, canned pineapple will not ruin your showstopper. This is because during the canning process, the pineapple is heated to kill bacteria so that the pineapple can be in the can for a long period of time and not decay [4]. This process also denatures the enzymes which means that they no longer act on the gelatine protein and prevent the jelly form setting. The high heat causes the bonds in the protein of the enzyme to vibrate meaning the bonds break (hydrogen bonds break first). Since hydrogen bonds are an essential part of the tertiary structure of the protein (which create a fibrous chain or globular chain) and the secondary (which is responsible for the protein either being an alpha helix or beta pleated sheet), the two structures of the enzyme are lost. This results in the active site of the enzyme no longer being complementary to the substrate (the gelatine protein molecule), so that no enzyme-substrate complexes form, meaning the gelatine is not catabolised. As a result, the jelly sets in its normal fashion.

Overall, for me the misconception lies in the fact that the fruit which should not be added fresh are rather acidic, especially kiwi. This always seemed to mean that it is the acidic conditions that the prevent the jelly from setting rather than the presence of certain enzymes.






Other websites used



Oxytocin: Liquid Trust


I was listening to a Bryson Tiller song this morning and being the cynic of love that I am, I cringed at the lines ‘Love holds me together’. As much as I hate clichés like these however, those lyrics may hold some truth in them. Patty Van Cappellen, associate director of the Interdisciplinary and Behavioral Research Center at Duke University in Durham, NC, and colleagues found that men given oxytocin nasal spray reported a greater sense of ‘being whole’. Afterwards, those who received the oxytocin were more likely to say spirituality was important in their lives, and that they felt connected to other living things, agreeing with statements like “All life is interconnected”.


Oxytocin is also known for its role in maternal bonding, and there is strong evidence that the hormone is important for social bonding, empathy
, trust, and sexual pleasure, hence why it is often dubbed the love hormone.


So looks like all those soppy love songs were on to something that science has only recently begun to explore. So what does this mean for us? Is oxytocin the real life version of Amortentia and therefore the love potion to solve all our relationship woes? Not so fast says Dr Radulovic (well actually I’m saying it, but you get what I mean).


Jelena Radulovic, senior author on the study and a professor at Northwestern University’s medical school claims that:


“The love drug also plays an important role in intensifying negative emotional memories and increasing feelings of fear in future stressful situations.”


This is because the hormone actually strengthens social memories, whether it be positive or nightmarish. The scientists discovered that oxytocin strengthens negative social memory and future anxiety by triggering an important signalling molecule – ERK (extracellular signal regulated kinases) – that becomes activated for six hours after a negative social experience. Although the experiment was conducted on mice, it’s safe to assume that oxytocin might have played a role in those cringe-bombs every time you remember that moment when you were depants in front of your crush.


“Love is essentially a biochemical cocktail, and a poorly understood one at that”


~Jessica Hullinger


Research also links oxytocin to increased trust, social bonding and even a predisposition to donate to charity, thus earning its nickname ‘Liquid Trust’.

Speaking from personal, one of the most common ways to incite an oxytocin release is by hugging for more than 5 seconds. It’s these positive influences that make researchers hopeful that it could help treat mental health disorders, including autism, social anxiety disorder and schizophrenia.

Despite oxytocin’s dark side, it is undeniably an important hormone especially with its many roles in building trusting relationships, increasing one’s sense of interconnectedness and an overall kumbaya feeling, and could potentially even be used to treat schizophrenia.


My verdict? Go ahead and hug somebody today.

GoF (pt2)

Before I revisit GoF (which I guess is admittedly, something of a hobbyhorse of mine), I must plug the BDG’s recent podcast on Euthanasia. Many thanks to the large (14+?)  group that gathered to eat my doughnuts and then discuss a difficult topic.

Anyway … on to a topic which I think  in some ways just as important but sadly, one that frankly, I don’t see is being discussed particularly rationally. Why is GoF so important an issue for me? I think it indicates a growing divide between scientists who do science, scientists who now no longer do science but earn a dollar commenting on science and politicians who have never done science but control the purse strings.

OK, GoF stands for Gain of Function and research using this technique has become increasingly controversial and something of a scientific football. Essentially, molecular biologists tinker with a pathogen’s genes and enable that pathogen to do “more”. That could include a wider host range (a non-human to human virus), different transmissibility (non-airborne to airborne) and so on.

Why are these experiments performed? Current medical countermeasures are often insufficient largely because of resistance mechanisms. There is, therefore, a continual need to develop new antiviral drugs and additional options, such as immunotherapy. GoF studies, which enhance viral yield and immunogenicity, are clearly going to aid the development of vaccines and other antivirals. How do we begin to study pathogens that only infect humans and have no animal models?

A recent PNAS paper (Menachery et al) describe a methodology involving a number of approaches to assess the ability of SARS-CoV–like viruses to infect human cells and cause disease in mouse models. The authors’ results suggest that a bat SARS-like virus, WIV1-CoV, can infect human cells but is attenuated in mice. Moreover, they indicate that additional changes in the WIV1-CoV genome would be required to increase the pathogenesis of the virus for mice. Vincent Racaniello (Professor in Microbiology at Columbia and one of the hosts of the fabulous TWiV podcast) was asked to write a commentary on the paper (see below) and again, criticised the current pause on GoF experiments. Essentially, Racaniello (and many others) want these studies to go ahead but more importantly want a balanced and informed debate to decide on the future of these experiments. Ideally, out of a series of debates and what would undoubtedly be some heated exchanges, a set of criteria would be agreed such that a panel could approve (or not) each and every GoF based on merit and potential risk. I won’t try and summarise Racaniello’s commentary, it is one I whole heartedly agree with. My worry is that large swathes of what might be considered “pure research” are already difficult to get funded because of a sometimes rather uninformed group of politicians who control the purse-strings. GoF undoubtedly has risks but surely the most prudent course of action would be to debate, discuss and then reach a decision. Pausing potentially valuable research without any plan to evaluate its benefits is surely rather reactionary?

Sadly, Wain-Hobson and others who stress some rather apocalyptic scenarios, currently have the upper hand. The sometimes angry exchanges between various camps may well be exciting but ultimately, given no international/multidisciplinary meeting is on the cards, it’s all rather sad.

Anyway, Racaniello’s commentary:

“The current government pause on these gain-of-function experiments was brought about in part by several vocal critics who feel that the risks of this work outweigh potential benefits. On multiple occasions these individuals have indicated that some of the SARS-CoV work discussed in the Menachery et al. article is of no merit. … These findings provide clear experimental paths for developing monoclonal antibodies and vaccines that could be used should another CoV begin to infect humans. The critics of gain-of-function experiments frequently cite apocalyptic scenarios involving the release of altered viruses and subsequent catastrophic effects on humans. Such statements represent personal opinions that are simply meant to scare the public and push us toward unneeded regulation. Virologists have been manipulating viruses for years—this author was the first to produce, 35 y ago, an infectious DNA clone of an animal virus—and no altered virus has gone on to cause an epidemic in humans. Although there have been recent lapses in high-containment biological facilities, none have resulted in harm, and work has gone on for years in many other facilities without incident. I understand that none of these arguments tell us what will happen in the future, but these are the data that we have to calculate risk, and it appears to be very low. As shown by Menacherry et al. in PNAS, the benefits are considerable.

A major goal of life science research is to improve human health, and prohibiting experiments because they may have some risk is contrary to this goal. Being overly cautious is not without its own risks, as we may not develop the advances needed to not only identify future pandemic viruses and develop methods to prevent and control disease, but to develop a basic understanding of pathogenesis that guides prevention. These are just some of the beneficial outcomes that we can predict. There are many examples of how science has progressed in areas that were never anticipated, the so-called serendipity of science. Examples abound, including the discovery of restriction enzymes that helped fuel the biotechnology revolution, and the development of the powerful CRISPR/Cas9 gene-editing technology from its obscure origins as a bacterial defense system.

Banning certain types of potentially risky experiments is short sighted and impedes the potential of science to improve human health. Rather than banning experiments, such as those described by Menachery et al., measures should be put in place to allow their safe conduct. In this way science’s full benefits for society can be realized, unfettered by artificial boundaries.”

Casadevall.A., 2014 mBio 5(4) “Risks and benefits of gain-of-function experiments with pathogens of pandemic potential, such as influenza virus: a call for a science-based discussion.”

Menachery.V.D., Yount Jr. B.L., Sims.A.C., Debbink.K., Agnihothram.S.S., Gralinski.L.E., Graham.R.L., Scobey.T., Plante. J.A., Royal.S.R., Swanstrom.J., Sheahan.T.P., Pickles.R.J., Corti.D., Randell.S.H., Lanzavechia.A., Marasco.W.A., & Baris.R.S. 2016 PNAS “SARS-like WIV1-CoV poised for human emergence.”

Zika – Pt 1, some background

The rapid spread of Zika virus through the Americas, together with the association of infection with microcephaly and Guillain-Barré syndrome, propelled a somewhat unknown virus onto numerous front pages. The WGS Biology Discussion Group (BDG) recently discussed some of the background for its first podcast  to this flavivirus but a little more background may help set the context of what is going to be an intriguing story for months to come.
Zika virus was first identified in 1947 in a sentinel monkey that was being used to monitor for the presence of yellow fever virus (another flavivirus) in the Zika Forest of Uganda. At this time cell lines were not available for studying viruses, so serum from the febrile monkey was inoculated intracerebrally into mice. All the mice became sick, and the virus isolated from their brains was called Zika virus. The same virus was subsequently isolated from Aedes africanus mosquitoes in the Zika forest.

Serological studies done in the 1950s showed that humans carried antibodies against Zika virus, and the virus was isolated from humans in Nigeria in 1968. Subsequent serological studies revealed evidence of infection in other African countries, including Uganda, Tanzania, Egypt, Central African Republic, Sierra Leone, and Gabon, as well as Asia (India, Malaysia, Philippines, Thailand, Vietnam, Indonesia).

Zika virus moved outside of Africa and Asia in 2007 and 2013 with outbreaks in Yap Island and French Polynesia, respectively. The first cases in the Americas were detected in Brazil in May 2015. The virus circulating in Brazil is an Asian genotype, possibly imported during the World Cup of 2014. As of this writing Zika virus has spread to 23 countries in the Americas.

The virus
Zika virus is a member of the flavivirus family, which also includes yellow fever virus, dengue virus, Japanese encephalitis virus, and West Nile virus. The genome is a ~10.8 kilobase, positive strand RNA enclosed in a capsid and surrounded by a membrane. The envelope (E) glycoprotein, embedded in the membrane, allows attachment of the virus particle to the host cell receptor to initiate infection. As for other flaviviruses, antibodies against the E glycoprotein are likely important for protection against infection.

Zika virus is transmitted among humans by mosquito bites. The virus has been found in various mosquitoes of the Aedes genus, including Aedes africanusAedes apicoargenteusAedes leuteocephalusAedes aegyptiAedes vitattus, and Aedes furcifer.Aedes albopictus was identified as the primary vector for Zika virus transmission in the Gabon outbreak of 2007. Whether there are non-human reservoirs for Zika virus has not been established.

Signs and Symptoms
Most individuals infected with Zika virus experience mild or no symptoms. About 25% of infected people develop symptoms 2-10 days after infection, including rash, fever, joint pain, red eyes, and headache. Recovery is usually complete and fatalities are rare.

Two conditions associated with Zika virus infection have made the outbreak potentially more serious. The first is development of Guillain-Barré syndrome, which is a progressive muscle weakness due to damage of the peripheral nervous system. The association of Guillain-Barré was first noted in French Polynesia during a 2013 outbreak.

Congenital microcephaly has been associated with Zika virus infection in Brazil. While there are other causes of microcephaly, there has been a surge in the number of cases during the Zika virus outbreak in that country. Whether or not Zika virus infection is responsible for this birth defect is not known. One report has questioned the surge (1) in microcephaly, suggesting that it is largely attributed to an ‘awareness’ effect.

Current epidemiological data are perhaps insufficient to prove a link of microcephaly with Zika virus infection. However the evidence establishing a causal relationship between Zika and microcephaly is growing as has the body of evidence that demonstrates that Zika could be one of the few pathogens able to cross the placental barrier and infect a foetus.

Given the serious nature of Guillain-Barré and microcephaly, it is prudent for pregnant women to either avoid travel to areas that are endemic for Zika virus infection, or to take measures to reduce exposure to mosquitoes.

There are currently no antiviral drugs or vaccines that can be used to treat or prevent infection with Zika virus. We do have a safe and effective vaccine against another flavivirus, yellow fever virus. Substituting the gene encoding the yellow fever E glycoprotein with that from Zika virus might be a good approach to quickly making a Zika vaccine. However testing of such a vaccine candidate might require several years.

Mosquito control is the only option for restricting Zika virus infection. Measures such as wearing clothes that cover much of the body, sleeping under a bed net, and making sure that breeding sites for mosquitoes (standing water in pots and used tires) are eliminated are examples. Reducing mosquito populations with insecticides may also help to reduce the risk of infection.

Oxitec first unveiled (2) its large-scale, genetically-modified mosquito farm in Brazil in July 2012, with the goal of reducing “the incidence of dengue fever,” as The Disease Daily reported (3). Dengue fever is spread by the same Aedes mosquitoes which spread the Zika virus — and though they “cannot fly more than 400 meters,” WHO stated, “it may inadvertently be transported by humans from one place to another.” By July 2015, shortly after the GM mosquitoes were first released into the wild in Juazeiro, Brazil, Oxitec proudly announced (4) they had “successfully controlled the Aedes aegyptimosquito that spreads dengue fever, chikungunya and zika virus, by reducing the target population by more than 90%.”

Closing thoughts
It is not surprising that Zika virus has spread extensively throughout the Americas. This area not only harbours mosquito species that can transmit the virus, but there is little population immunity to infection. Infections are likely to continue in these areas, hence it is important to determine whether or not Zika virus infection has serious consequences. Moreover evidence suggests that humans may act as an amplifying host for Zika (unlike Dengue for example) and thus person-mosquito-person transmission may be very common, hence a rapid spread into and throughout urban areas.

Recently, Zika virus was identified in multiple US states, including Texas, New York, and New Jersey, in international travellers returning to the US . Such isolations are likely to continue as long as infections occur elsewhere. Whether or not the virus becomes established in the US is a matter of conjecture. West Nile virus, which is spread by culecine mosquitoes, entered the US in 1999 and rapidly spread across the country. In contrast, Dengue virus, which is spread by Aedes mosquitoes, has not become endemic in the US.

What I have been fascinated by is the tone adopted by different public health and microbiology “camps”. Articles by numerous highly specialised scientists have both urged caution before we conclusively state that “Zika causes microcephaly” and warned us that Zika is the new Ebola only much much worse. Personally, I always thought that good science is evidence-based and a good scientist attempts to educate not frighten and always, ALWAYS adopts a moderate open-minded approach. Based on some of the salaries that contributors to the popular press on both sides of “the pond” enjoy, I’ve clearly been doing it wrong for years.



The Rise and Demise of Antibiotics

On the 20th of January Dr Chris Morris from the University of East Anglia delivered a talk to a keen audience of WGS Biologists and general science enthusiasts alike.

Dr Morris explained the ingenious method which he hopes will eventually lead to a new breed of antibiotics. Antibiotics in circulation today use a variety of methods to kill the bacterial cell causing infection – prevent the construction of the cell wall of the bacteria, stopping protein synthesis, prevent the bacteria multiplying, or allow the host’s defence mechanism to deal with it. The new method proposed by Dr Morris and his team was simple in concept, but as he later explained was much more complex in practise.

Segments of sense (coding strand) DNA are surrounded by a capsule of nanoparticles measuring between 1 and 100 nanometers in size. This capsule locates the bacteria being targeted by electrostatic forces of attractions and locks onto the bacteria cell surface. When attached, it punches a hole and the sense DNA fragment is released into the cell. Once inside the cell, the DNA segment knocks out a transcription factor – a protein that binds to specific DNA sequences, thereby controlling the rate of transcription of genetic information from DNA to messenger RNA – resulting in the repair response gene being switched off. The repair response to the hole formed in the surface of the bacterial cell no longer occurs, and thus by lysis the cell is destroyed. I believe it’s fair to say the audience were stunned by Dr Morris’ astounding method of puncturing the cell, and preventing the repair response as a way to remove bacterial infections.

Dr Morris also detailed some of the remaining hurdles to be overcome. One problem that continues is the control of the size of the nano particles and prevent the coagulation of them. Dr Morris is hopeful with more years of testing and hard work this form of antibiotic may one day be prescribed to patients fighting bacterial infections. His team’s method also raises the obvious question, is there any way we could apply this to the fight against viral infections?

Isabelle Hall

The chemistry of Christmas crackers

Christmas has now just about finished for another year and I’m sure at some point over the festive period we all ate too much, drank too much and of course pulled a few Christmas crackers. Despite wondering if you’ll get a mini tape measure or tiny pack of cards, I doubt you’ve ever put much thought into what’s in a cracker. The distinctive bang comes from silver fulminate, AgCNO. Fulimates contain the fulimate ion, CNOand are referred to as friction explosives. This is what makes them perfect for crackers, as they produce the distinctive bang, a tiny explosion, when pulled. The silver fulminate is coated on a piece of card, this runs next to another piece of card which is abrasive- a bit like sandpaper. When the cracker is pulled the two bits of card are pulled apart, rubbing together, creating friction and igniting the silver fulminate. The tube around this amplifies the sound making it louder. Apart from its use here in Christmas crackers silver fulminate has very few other uses, it is extremely explosive and sensitive, so much so that a few grams would self detonate due to the force of its own weight.

I hope you had a cracking Christmas and a great new year!


Influenza – The Virus That Gets Away With Murder

The ‘flu season is quickly approaching, but I bet most people don’t have it marked in their diaries because no one dies of the ‘flu anymore, right? Wrong! Every year around 8,000 people die of the ‘flu in Britain, and that number is slowly rising. [1] This year, in a three week period after January the 23rd, 28,000 people died of the ‘flu – in the same three week period for the last five years the average has been 21,000 – this is a huge increase of a third. [2]

What does this murderous virus look like?Image result for influenza virus

Influenza, aka the ‘flu’, is caused by a virus which under an electron microscope looks like a ball of strands of nucleic acid enclosed in a protective coat that is spiked with antigens. This gives it the very iconic shape that all biologists associate with this underestimated virus.

What symptoms does the ‘flu virus cause?

In the next few months, people all over the country will be complaining to their doctors (or friends and family) that they have a fever, sore throat, headache, and are really tired. [3] Little do these people know, but they have probably been infected with the ‘flu. These symptoms are due to the body’s reaction to the virus infiltrating the cells in the throat, hijacking the DNA into producing more ‘flu viruses, and these viruses violently bursting from the infected cells. [4]

The sore throat experienced is due to the violent nature of this bursting from the cells. Many of the throat cells are damaged as this happens, and each generation of viruses infiltrates more and more cells and they reproduce rapidly.

Headaches can be due to the body producing mucus in the nose to try to stop any more infectious microorganisms entering the body. This mucus blocks the sinuses, which increases the pressure inside the head.

A fever is a very clever defence mechanism because the high temperature is not so high that it permanently damages (or ‘denatures’) human enzymes, but is high enough to denature the virus’ enzymes – slowing it down enough to allow the body’s white blood cells to swoop in and destroy it.

Symptoms of the ‘flu are very similar to the symptoms experienced during a rhinovirus infection (the common cold) but ‘flu symptoms are actually much worse. Many people, therefore, are tempted to dismiss ‘flu symptoms as a bad cold. This is actually their second mistake, but I’ll come back to the first mistake a bit later.

So why now?

Why is the ‘flu season so late in the year? Most diseases pop up in the summer months when the temperatures are warm and humid, and parasites, bacteria, and viruses can thrive…. but the ‘flu virus is weird – it prefers the winter months when temperatures are cold and all life seems to slow down.

A study carried out in October 2007 showed that guinea pigs were more likely to infect other guinea pigs in colder temperatures.[6] In addition, the ‘flu virus was also able to stay alive for different amounts of time in different conditions.

Why should this be? In cold temperatures, the protective coat on the virus hardens until it becomes rubbery. [5] This gives it the protection it needs to not only spread from person to person, but also to survive for 22 hours more than if temperatures were hotter. As temperatures rise, at around 90 degrees Fahrenheit the virus’ protective coat melts into a liquid and the virus then has very little protection from the elements. In this state, the virus is only able to stay alive for 1 hour. [6] It would seem a poor evolutionary step to develop this way, but the virus must give up its protective coat so that it can infect the host – the virus is only able to infect cells when its coat is in this liquid state.[5]

How does the virus travel from person to person?

The spread of this virus is by droplet. When an infected person coughs, sneezes or even talks, the virus can be projected from the mouth into the air, contained in droplets. In cold conditions, its outer coat protects the virus from some soaps and external conditions that could damage it. However, once a floating, infected droplet has been inhaled or swallowed by another person, the virus takes only 1 to 4 days to cause symptoms. [3]

You’ve got the ‘flu – what now?

If symptoms are not severe, keeping warm and hydrated at home can often be enough, with a few pain medications for aches. If the symptoms are severe, there are antiviral treatments available that stop the virus multiplying and help the body to battle the infection. [3]

So, what is the first mistake people make?

The first mistake many people make when it comes to the ‘flu is not taking it seriously enough. A ‘flu vaccination is available and should be taken by elderly people, young children, pregnant women and the immunosuppressed, as they may not be able to battle the virus by themselves. Unfortunately, the vaccination itself can give symptoms of the ‘flu because it contains live virus particles, but the strain of ‘flu causing infections may be different each year, and so it’s sensible to have the vaccination repeated each year with the current version of the virus so that your immune system is ready.

Can the ‘flu be prevented?

The good news is that preventing the spread of the ‘flu is simple. Washing hands regularly with soap is very important, as it removes any virus particles from your hands so they can’t be transferred to surfaces. [7] Staying away from infected people (or non-infected people if you have symptoms) and being very careful with hygiene are also crucial in the battle with the ‘flu.


The influenza virus kills thousands of people each year and yet most people consider it to be only mildly worse than the common cold. This ‘flu virus really is the virus that gets away with murder and if it is possible to minimise the amount of people who die from this virus yearly by preventing the spread of it, I think we should try.


[1] PUBLIC HEALTH ENGLAND. (2014) Public Health England and the NHS prepare for unpredictable flu season. [Online] Available from: [Accessed: 26th October 2015]


[2] CHRIS COOK. (2015) Death rate up by a third in January. [Online] Available from: [Accessed: 26th October 2015]


[3] NHS CHOICES. (2015) Flu. [Online] Available from: [Accessed: 26th October 2015]


[4] RUSSEL MCLENDON. (2013) How does the flu work? [Online] Available from: [Accessed: 26th October 2015]


[5] NIH NEWS. (2008) NIH Scientists Offer Explanation for Winter Flu Season. [Online] Available from: [Accessed: 26th October 2015]


[6] SITNFLASH. (2014) The Reason for the Season: why flu strikes in winter. [Online] Available from: [Accessed: 26th October 2015]

[7] CENTERS FOR DISEASE CONTROL AND PREVENTION. (2015) CDC Says “Take 3” Actions to Fight The Flu. [Online] Available from: [Accessed: 26th October 2015]