Fly-killing fake cow made in Greenwich 'top discovery'
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The creation of an "artificial cow" that kills deadly flies in Africa has been named as one of the ten most important university discoveries by UK academics.
The device, developed at the University of Greenwich, south-east London, was voted the eighth most important university breakthrough of the last 60 years.
It replicates the smell of a cow, attracting the tsetse fly which is then killed. Tsetse flies spread the killer sleeping sickness.
The cow's inventors, Professors Glyn Vale David Hall and Steve Torr, have spent 40 years finding ways of controlling the tsetse fly in Africa.
The one-centimetre-long insect is responsible for spreading sleeping sickness, which kills 30,000 people and two million cattle every year.
'Huge area affected'
Professor Torr, who is still part of the research team said: "Tsetse-transmitted diseases are a dreadful problem in Africa, killing 30,000 people.
"I am thrilled that this research, which tackles a really important issue in the developing world, has been recognised."
Professor Hall said: "Tsetse affects a huge area and a huge number of people - and if this discovery contributes to improving their overall standard of life, it is important."
The scientists have developed a blend of odours which tsetse mistake for the smell of a real cow. The flies are drawn to the 'cow' where they are killed by insecticide.
The technique is now being used in countries such as Uganda, Ethiopia, Kenya, South Africa, Tanzania and Zimbabwe.
Sleeping sickness attacks the nervous system
Sleeping sickness, which is spread through the tsetse fly, is fatal without treatment.
It initially appears as a fever, but later affects the central nervous system manifesting as confusion and poor coordination.
Disturbance of the sleep cycle is also a key symptom of the disease.
Cattle lost to the disease affects the livelihoods of millions locked in poverty throughout Africa.
The tsetse fly exists across 11 million square kilometres of land, an area of land larger than the United States.
Scientists estimate it impacts the lives of up to four million people across Africa.
Dr John Kabayo from Pattec (Pan African Tsetse and Trypanosomiasis Eradication Campaign) coordinates the African effort to eradicate the fly.
He says the work of scientists in the developed world plays a key role.
He said: "There, scientists are better equipped - they have grants, budgets and better equipment to develop the science. The work they do is crucial."
Pattec aims to eradicate the deadly tsetse fly from sub-Saharan Africa by 2031.
File photo of  brucei
Research teams from  the universities of  and  discovered the mechanism the  parasite evolved for "sleeping sickness" disease to circumvent the human immune system.  Their study follows a recent African outbreak of  this parasite causes. The discovery is expected to help develop a cure preventing future deaths.
A , generally responsible for the spread of the condition.
The 1998–2001 sleeping sickness epidemics in  Sudan, Angola, Democratic Republic of Congo, and Uganda caused tens of thousands of deaths.  The parasites are spread by .  It is considered one of the worst epidemics in the last five decades.  As WHO reported, subsequent recent introduction of population screening in rural areas and distribution of more effective drugs had potentially reduced the number of death incidents.  However, the main effect of these measures being a decrease in spreading of the parasite and not in decrease of the death rate, the researchers decided to tackle the puzzle.

The scientists studied the molecules the human immune system activates in response to the attack.  They were looking for the way the parasites inhibit it and lead to the death of the victim.  Of the several known parasite species, the two that can infect humans were chosen to study, called ''Trypanosoma brucei gambiense'' and ''Trypanosoma brucei rhodensiense''.  Several others also exist, but they affect only animals.

Researchers knew that the Trypanosoma attacks typically are repelled by an , more specifically ''trypanosome lytic factor-1'' (TLF-1).  It is generated in the humans' immune system and is toxic to the parasites but not to humans.  It was known that one of the parasites, ''T. b. rhodensiense'', has evolved an inhibitor of the toxic chemical, called Serum Resistance Associated (SRA) protein.  However the other one, ''T. b. gambiense'', was responsible for over 95% of human deaths, and it had been previously unknown why. 

The study showed that a gene mutation has lead to a change in the parasite's surface protein receptor.  It doesn't bind to TLF-1 as well as for other species, leading to a substantial decrease in TLF-1 uptake by the parasite.  The receptor is more strict, causing a lower nutrient intake as well, but it suffices, and the parasite defends against the human immune system. 

As professor and head of the department of biochemistry and molecular biology at UGA (and one of the leaders of the research) Stephen Hajduk explained, "Humans have evolved TLF-1 as a highly specific toxin against African trypanosomes by tricking the parasite into taking up this HDL because it resembles a nutrient the parasite needs for survival. But T. b. gambiense has evolved a counter measure to these human 'Trojan horses' simply by barring the door and not allowing TLF-1 to enter the cell, effectively blocking human innate immunity and leading to infection and ultimately disease."

Based on the results of the research, humans could possibly develop a defense mechanism to keep the parasites from evading the human defense system.  Stephen Hajduk commented, "We believe this research represents a paradigm shift and causes us to think more broadly about how pathogens avoid host defense mechanisms.  It turns out that African trypanosomes have evolved a diversity of ways to avoid human innate and acquired immune systems."

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