Unlike its predecessors, this round up doesn’t feature on a Friday. It features on a day when I’ve struggled to concentrate ever since I got in to work. I don’t want to launch into a full length blog when I’m not achieving anything else (what can I say, my Mum never let me go to Brownies if I hadn’t been at school either…) but equally having all of these tabs open is probably preventing me from achieving anything else.
So, without further ado and in no particular order:
- Tamsin Edwards writes a thoughtful piece in the Guardian about whether scientists should air their political viewpoints
- Scientists at Bristol University discover that the four kinds of virus causing Dengue Fever may be quite different to one another
- Six Turkish academics have been charged with terrorism after what appears to amount to nothing more than secularism
- Scientists from the United Arab Emirates have identified a mutation that gives plants reduced susceptibility to two fungal pathogens, Botrytis cinerea and Alternaria brassicicola.
- In case you missed it, scientists produced the world’s first synthetically grown beef burger this week. New Scientist unpacks the story.
- Groups in Australia and New Zealand have identified a potential new insectide, produced by bacteria. Along the way they showed that the bacteria keep this toxin in a special vesicle, allowing it to build up to high levels without damaging the micro-organism.
Posted in Biology, Genetics, Round Up, Science
Tagged artifical meat, biology, Dengue Fever, epidemiology, fungi, genetics, lab-grown burger, mutant, plant pathology, policy, science, virology, viruses
A quick microbiology primer before we begin, for the uninitiated or those who don’t have a 14 year old in their lives to ask.
Microbe is a catch-all terms that we use to describe microscopic organisms. These may or may not be pathogenic (disease-causing). They include, but are not limited to:
- Bacteria (like E. coli and S. aureus, which cause food poisoning)
- Fungi (like athlete’s foot and brewer’s yeast)
- Protists (like Plasmodium, which causes malaria and Naegleria, which you might have seen in an episode of House)
We probably shouldn’t include viruses (like the common cold) or prions (like variant CJD) in there because they’re not really classified as organisms: they’re not alive, simply inert particles that harness other living things to replicate themselves. As my year 8s would tell you, they don’t do MRS NERG (movement, reproduction, sensitivity, nutrition, excretion, respiration or growth). Continue reading
Every couple of years or so it seems the world is gripped by a new epidemiological scare: CJD, SARS, Avian flu, Swine flu… This year’s new panic seems to be over coronavirus, one of the many viruses that can be responsible for the common cold (or even SARS). The coronaviruses are RNA viruses with a massive genome (26-32kb: which is frankly ridiculous) and a protective envelope, covered in viral spike peplomers which lead to their name. The particular strain of interest right now presents as pneumonia, with renal failure in some patients, and is referrred to as hCoV-EMC.
The key ingredients for a global pandemic are that it occurs across a wide area and that it is able to spread from person to person. Various zoonotic diseases are able to be passed from animals to humans (see rabies, swine flu and bird flu), but this only becomes a global risk when individual humans are seen to pass the disease to one another. In the last two months there have been nine reported infections with a novel strain of coronavirus, in Qatar, Saudi Arabia and Jordan, five of which were fatal. Because three patients in Qatar and two patients in Jordan were closely associated, there is a very real chance that human-to-human transmission has occurred (although they may have simply been exposed to the same source). This, combined with the currently-reported very high death rate (i.e. more than 50%) is really very concerning.
SARS (severe acute respiratory syndrome) is also caused by a coronavirus, and there has been some concern that we could be facing a pandemic of similar size and severity. It was this fear that led to a recent paper in mBio investigating the receptor sites of the virions. The particular receptor utilised by the SARS-causing coronavirus (angiotensis-converting enzyme 2, or ACE2) is limited to humans, meaning that zoonotic transfer was unlikely. It has previously been shown that SARS-CoV infection can be blocked with an anti-ACE2 antibody. What Muller et al have demonstrated in this paper is that the anti-ACE2 antibody works in kidney cells from monkeys, humans and swine to block infection with SARS-CoV, but that the same is not true of the new coronavirus currently making the headlines. This is apparently because the ACE2 enzyme isn’t actually involved in CoV-EMC replication, as it is in the SARS-responsible CoV.
This is actually slightly worrying and depressing news. While it’s interesting that the two viruses are unlikely to utilise the same receptor, and therefore have similar epidemiology, from the point of view of fighting the disease, this makes it an unknown quantity. Given that the Müller et al suggest it may utilise a broadly conserved receptor present across the animal kingdom. From the point of view of preventing repeated infection, or multiple posts, this could be very serious indeed.
Müller, MA et al (2012) mBio 3 (6):e00515-12
Today I am at home, theoretically packing my van in order to start moving house at 10am. What this actually means, of course, is that I’m enjoying the chance to still be in my bedroom at 8:30am with a cup of tea and the science news, including this super interesting story.
A collaboration of scientists from Edinburgh, Cambridge, Cork, Utah and Seattle funded by the BBSRC have discovered firstly that the flu virus has one more gene than they were expecting, and secondly that the allelic differences in this gene control how the host (i.e. you and me) respond to contracting the virus. Now you may be thinking ‘The influenza A virus genome is only 14000 bases long! [because you’re a massive geek like me and know things like that…] How can it possibly a) code for 13 genes in the first place and b) have a spare one hiding that nobody has noticed?!” Continue reading