My Name Is Martin Shkreli, and I’m Not Afraid to Make Life-saving Medication More Expensive

It’s not unhearddaraprim of for pharmaceutical companies to charge seemingly unreasonable amounts for medication used to treat life-threatening diseases, but there is one company that has been in the news recently. Turing, an American based company formed in early 2015 by Martin Shkreli, acquired the manufacturing licence for Daraprim in August, and recently announced the price of the drug would be going through changes. Keep in mind that Daraprim is on the World Health Organization’s List of Essential Medicines. The original price of Daraprim was $13.50, so you could expect them to raise the price to $20 a pill if they were REALLY struggling, and then reduce it again when they were more financially stable, right? Okay, so they say they’re investing in research and development. $50 might be justifiable, at a push. That’s about 370% of the original price. But that’s not even close to what Turing wanted to charge. The company would have had one pill retailing at $750 – 5555.5% of the original price! It’s hard to see how anyone could do that to anyone without having a very guilty conscience, but Shkreli cared so little that he responded to criticism from the media with quotes from the popular rapper Eminem.  But as the news spread, the backlash was so great that even Shkreli, who is “really good at logic, difficult situations and tough choices” (according to his OKCupid profile), had to back down and lower the price to an as of yet undisclosed reduced price.

One last thing to spend some time thinking about – if this kind of reaction can make Shkreli reduce the price of Daraprim, can the same be done to other companies who charge extreme prices for vital medicines? Could Phizer, who were accused of charging “excessive and unfair” prices for Phenytoin sodium capsules in August 2015, be convinced to lower the prices if people simply stood up and said ‘This is not okay’? If pharmaceutical companies charged fair amounts for their medicines, could the NHS avoid having to cut junior doctors’ wages?



Blackfish- Seaworlds Dark Truth

As my recent posts may have revealed I have a keen interest in the animal Kingdom and the wonders within it. Of course these should be enjoyed but at what point is the line between public enjoyment and animal welfare crossed ?

I recently watched the documentary Blackfish which gives an insight into the controversial captivity of killer whales at SeaWorld- a theme park based around large marine life- and the risk that it poses to both the whales and humans who care for them. The largest SeaWorld tank is just 40 metres deep which to a 10 tonne orca, that would naturally swim up to 100 miles a day, the equivalent of a small swimming pool to us. Un-natural cramped conditions mean that all captive male orcas dorsal fins have collapsed, SeaWorld claim this is natural however just 1 in 5 wild male orcas exhibit this defect. These cramped conditions are also believed to have affected the orca’s behaviour, with many people blaming this for the tragic instances where whales have exhibited aggressive behaviour and injured or even killed their trainers. There’s obviously something wrong and yet SeaWorld continue to defend their actions even to the shocking extent of blaming a trainer, Dawn Brancheau, for her own death after she was pulled under and killed by the orca named Tilikum. SeaWorld are aware that Tilikum has been involved in the death of another trainer previously and has exhibited aggressive behaviour and yet they still breed from the whale and use it in shows, for the sake of profits.

OSHA ( Occupational Safety and Health association ) have been involved in a long standing feud with SeaWorld over both the safety of trainers and the welfare of the animals and as a result of their efforts Seaworld can no longer let trainers in the water with the orcas. This change will prevent further loss of human life but it does not solve the problem of the animal’s welfare and obvious sub standard living conditions. Should keeping whales in captivity be legal? Should keeping any animals in captivity be legal ? A captive orca lives for an average of 9 years, in the wild an orca can live up to 90 years; captive life is clearly doing them harm and lowering their standard of living. Is it not time to change this? Should something not be done?

If someone says the words “animal cruelty” what do you think of? For most people it would be a under-nourished, ill, caged animal such as a dog. If someone says “animal cruelty” to me, I see much more: I see blackfish.

Orcas in captivity infographic

Grimbiosis 1: The Tongue Eating Louse

BlobPerhaps the most strangely cute of all the disgusting parasitic crustaceans, the brutally efficient “tongue eating louse” (Cymothoa exigua) is nonetheless one of the most nightmarish creatures ever discovered. Growing up to just over 2cm in length, this large marine louse is unique in that it is the only known organism with the capacity to completely replace an organ of another creature1.

The disturbing process begins when the louse is newly born, tiny, and immature. The louse is insignificant enough to enter an adult fish, usually a snapper, through its gills. Here, the parasite attaches waits to reach sexual maturity, using the hosts mucus and tiny scraps of food to survive. From there, the female louse move into the mouth of the fish, and secure itself permanently to the fish’s tongue before piercing it and drawing its blood for nutrients. The louse devours the fish’s blood insatiably until the tongue is totally depleted of blood- at which point 90% of the tongue atrophies2, withers, and falls off. From this point onwards, the louse acts as an “organic prosthetic”, performing the same role as the tongue for the fish and, seemingly, leaving the host fairly unharmed- the fish can go on to survive and even thrive, despite its mouth-borne passenger. However, despite researcher’s assurances that the parasite is “benign”, it is hard to believe that the host is not affected by a creature roughly 5% of its size and vaguely resembling an albino Lousewoodlouse living in its mouth.

And then, as if the poor fish has not been violated enough, the louse must then reproduce in order to create even more horrific creatures; meaning that the female will then “do the dirty” with a much younger louse (as a hermaphroditic creature, every individual is born as a male and may only become female after reaching sexual maturity3) inside the fish’s mouth. A few weeks later, the female will then produce a brood of just under 500 hundred eggs, of which around 200 will hatch to produce male lice. Still seem strangely cute?!




1-Brusca & Gilligan, 1983. Available from


2- January C, April 2014, “Isopod got your tongue? (The tongue eating louse)” [ONLINE] Available from [Accessed 17/09/2015]


3- Brusca & Gilligan, 1983. Available from


Also Used:


Human endogenous retroviruses: the hidden heroes of the genome

After once hijacking our DNA and inserting themselves into it, HERVs now play a crucial role in our survival


According to British biologist Sir Peter Medawar, “A virus is a piece of bad news wrapped in protein.” I believe that this opinion is outdated. While it is unlikely that you would find anyone who would disagree that rabies, HIV and Ebola are anything but bad news, not all viruses that interact with the human body are something to fear. There exist some viruses which, rather than causing us harm, are crucial to our existence.

There are retroviruses (viruses which use RNA as their genetic material and, using reverse transcription, convert their RNA into DNA and insert a copy of it into the host cell) living inside us from the moment we are conceived, embedded into the human genome. The genetic material of these viruses, known as HERVs, or human endogenous retroviruses, form part of our DNA. In fact, they are thought to make up about 8% of the human genome1. Their presence can be traced back to our early ancestors² from millions of years ago and these hidden passengers exist without causing us harm.

It is believed that HERVs are descendants of even older exogenous viruses (infectious viruses that can be transmitted horizontally i.e. from human to human; for example HIV) that were once fatal, and evolved to be less harmful so as to not kill the host². Over millions of years, they have lost the ability to transmit to other hosts and are confined to the cell that they originate from.

HERVs form part of our noncoding DNA, which makes up about 98% of our total DNA and is sometimes referred to by those in the scientific community as ‘the dark matter of the genome3’ because there is so much we still do not know about it. These retroviruses are not just passive genetic hitchhikers that have inserted themselves into our genome to continue their germline – some of them are actually crucial to our survival and have important functions that ensure our health in various ways.

Firstly, some endogenous retroviruses protect us from potentially fatal infections. HERV-K protects human embryos by producing a protein which makes the penetration of the embryo by another virus more difficult4. This is a mutually beneficial arrangement; the embryo is protected from infection by viruses such as influenza, increasing its likelihood of survival, and HERV-K has a place to live.

In addition, it seems we owe our placentas to a virus. Placental formation in most mammals is dependent on the ‘syncytin gene’5, which arose from a virus and produces a protein that allows the placenta to fuse to the uterine wall. Since the initial discovery and naming of syncytin in 2000, further discoveries have shown other forms of syncytin in other mammals. The mammals that belong to the order Carnivora have syncytin-Car1. In 2009, a version named syncytin-Ory1, was found in rabbits6.

The version of the rhesus macaquegene which is present in humans (and primates) was described as “the envelope gene of a recently identified human endogenous defective retrovirus, HERV-W” by the team who discovered it in 20007. The discovery of this curious gene explained why, when examining placental tissue from a rhesus macaque, virus particles were seen budding from the tissue (pictured above). It also may explain the way in which placental cells fuse to the uterine wall is unusual in mammalian cells but characteristic of the influences that viruses can have on cells. Viruses use this mechanism because fused cells make it easier for virus particles to spread from one cell to another, but in the case of the placenta, this mechanism makes it easier for nutrients to pass from the mother to her foetus.

Syncytin does this by producing protein that is expressed in the syncytiotrophoblast (epithelial cells between the mother and the developing foetus; the syncytiotrophoblast fuses to the uterine wall and ruptures maternal capillaries to facilitate the exchange of materials). Another form of syncytin, discovered in 2003 and named syncytin 2, is required to suppress the mother’s immune system to prevent it from attacking the foetus8.

Research conducted by Anne Dupressoir et al.9 demonstrated that mice embryos deprived of syncytin 1 died before reaching maturity, proving that it is an essential feature of placenta formation and therefore foetal development for mammalian life forms which have the gene.

Without the existence of the HERV-W retrovirus that gave rise to syncytinjoey in primates, human pregnancy would certainly be a peculiar affair compared to the pregnancy we are familiar with (if primates managed to even survive without HERV-W). A lack of syncytin could have meant that primates never developed placentas. Perhaps this would’ve lead to a pregnancy like the marsupials such as the kangaroo have, culminating in the birth of a tiny, almost foetus-like baby (see the joey pictured above). Surely this would’ve had a huge impact on the development of humans as a species, and the outcome of 65 million years of primate evolution would be completely different.

As the dark matter of the genome and the viruses that live within it are still a rather enigmatic topic, hopefully future research will further highlight how dependent on viruses we are. In the case of HERV-W, it was a stroke of luck for humans that an early primate was infected with it millions of years ago. Such a stroke of luck, in fact, that one might even go as far as to say that HERV-W was a ‘present wrapped in protein’.






1 – Griffiths D J. (June 2001) “Endogenous retroviruses in the human genome sequence” [ONLINE] Genome Biology. Available from: [Accessed: 01 Sep. 15]

2 – Zimmer C. (Feb 2015) “Our Inner Viruses: Forty Million Years In The Making”. National Geographic. Available from:  [Accessed: 01 Sep. 15]

3 – One example of this: [Accessed: 16 Sep. 15]

4 – Coghlan A. (April 2015) “Ancient virus is embryo protector”. New Scientist. Page 10.

5 – Javan R.R. (June 2015) “The Syncytin Gene: Viruses Responsible for Human Life” Available from: [Accessed: 01 Sep. 15]

6- Heidmann O, Vernochet C, Dupressoir A, Heidmann T. (2009) “Identification of an endogenous retroviral envelope gene with fusogenic activity and placenta-specific expression in the rabbit: a new “syncytin” in a third order of mammals.” Retrovirology. Available from: 

7 – Mi S, Lee X, Li X, Veldman G M, Finnerty H, Racie L, LaVallie E, Tang X, Edouard P, Howes S, Keith J C, McCoy John, McCoy Junior (2000) “Syncytin is a captive retroviral envelope protein involved in human placental morphogenesis” Nature. [ONLINE] Available from: [Accessed: 01 Sep. 15]

8 – Blaise S, de Parseval N, Bénit L, Heidmann T (2003) “Genomewide screening for fusogenic human endogenous retrovirus envelopes identifies syncytin 2, a gene conserved on primate evolution”. [ONLINE]  Available from: [Accessed: 01 Sep. 15]

9 – Dupressoir A, Vernochet C, Bawa O, Harper F, Pierron G, Opolon P and Heidmann T (2009) “Syncytin-A knockout mice demonstrate the critical role in placentation of a fusogenic, endogenous retrovirus-derived, envelope gene” [ONLINE:] Available from: [Accessed: 01 Sep. 15]


Also used:

Zimmer C. (February 2012) “Mammals made by viruses” Discover.  Available from: [Accessed: 01 Sep. 15]


Lower R, Lower J and Kurth R (1995) “The viruses in all of us: Characteristics and biological significance of human endogenous retrovirus sequences”. [ONLINE] Available from: [Accessed: 01 Sep. 15]





Amazing Animals-part 4- The Natures Driving Force

It is a both significant and daunting stage in someone’s life when, for the first time, they are deemed ‘responsible’ enough to get behind the wheel of a fossil fuelled tonne of metal, which is capable of doing some serious damage. Being 17 the scary experience of learning to drive is something I’m familiar with, I personally struggled with clutch control but for many it is the system of gears; we often confine gears to the realms of mechanical engineering and technology but they can be seen all around us in nature and in biology. Recent studies at the University of Cambridge have found that some ivy eating insects developed gears millions of years ago and have been using them to propel themselves from the ground at speeds of up to 5m/s, these insects belong to the genus Issus, belonging to the family Issidae of infraorder Fulgoromorpha of suborder Auchenorrhyncha of order Hemiptera.. Could mankind takes some tips from these insects to help 17 year olds everywhere learn to drive a little easier?

Functioning 'mechanical gears' seen in nature for the first time

Ollie Short