Links to go viral – 22nd February 2015

“Parasitic Wasps Infected with Mind-Controlling Viruses – Phenomena: The Loom”

Parasitoid wasps are nightmarish critters of death and manipulation. For all the times you’ve been stung by a wasp, just be glad it didn’t lay its carnivorous unborn into your still living flesh. Evolution has ‘gifted’ us a huge number of such insects, which happily prey on as large a number of different bugs to both incubate their eggs and eventually provide the newly hatched young with a live-in shelter to eat their way out of.

“Mike?!” you yell, “Why are you ruining our brains forever with this? Where are the viruses?!”

Worry not, viruses are at work here. In fact, this article deals with just one such virus story (I’ll save the other for a later write-up).

In brief, because you should dive into the linked article:

Wasp injects ladybird (ladybug) with an egg. Ladybird carries around egg, which later hatches and eats its way out of the ladybird. Wasp wraps itself in a cocoon to develop into an adult and the still living (but presumably now-porous) ladybird guards the cocoon from predators. Why? Because a virus, named D. coccinellae Paralysis Virus, or DcPV, that lives in the wasps and their eggs, infects the brain of ladybirds and turns them into zombie guards. Nature. You are scary.

“Experts suspect Ebola virus sometimes spreads by air | CIDRAP”

OK, let’s get serious. A report into what we know about Ebola transmission has been published this week, and the media has leapt on to the authors’ opinion that the virus might spread by air as well as by contact. I don’t see a problem with the media’s interpretation of the report: the news seems to be carrying the salient points made by the piece. But the fact of the matter is that the evidence to back up aerosol transmission of Ebola just isn’t there. We know that people get infected when they come into close contact with the very sick and/or dying: people leaking virus-laden fluid into their immediate surrounding environment.

The possibility of transmission of virus cast into the air by the coughing sick – possible, but paling in comparison to the aforementioned infectious fluid – does not match up to the fear of a ‘Hollywood-style’ virus epidemic. The sick spread the virus to one or two people by close contact, they do not infect dozens by lacing the air with virus particles.

Could the virus evolve to use a different route of transmission though? Suddenly infecting through the air rather than by contact? No. A scene in the movie Outbreak, in which scientists crowd around an electron microscope image of an Ebola-like virus, before and after the “evolution of hair-like molecules” which “enable the virus to spread through the air” is firmly lodged in fiction (for the record, despite being objectively terrible, that movie is ace).

This topic is deserving of full articles to explain this reasoning and the outbreak as it stands, and so I defer to two:

“Microbiology: Ditch the term pathogen : Nature News & Comment”

Finally, because choice of language is more important than we think, a small piece on ditching the term ‘pathogen’. This article isn’t virus-centric, but that’s really the point. We focus on the bugs – the “pathogens” – when we research disease, because we hold them up as the reason for the illness. But in reality, disease isn’t a one-way street. Our immune systems are often responsible for most of the damage done to us during infection, and some people can be asymptomatically infected with viruses, bacteria or fungi, when others become desperately ill.

The term pathogen isn’t going anywhere, but if we think about the pathology of infection a little more holistically, perhaps we’ll make better progress eliminating it.

Links to go viral – 15th February 2015

The tempo of publishing to the site is a little lower than I want at the moment. While I’ll always publish the weekly links, I’ll return to longer writing when stuff ‘behind the scenes’ has calmed down a bit. Now is one of those times, but a more normal service should resume shortly. For this week, I’ve a report, a video and a podcast to feed your audio-visual thirst for virology:

“WHO Ebola Situation Report – 11 February 2015”

News of Ebola’s ‘death’ may have been greatly exaggerated – including by yours truly. For the second consecutive week in a row the number of new cases has risen in all three afflicted countries. We’ll have to pay careful attention to disease trends from here on. Extinguishing the last embers of this outbreak may require even more water than anticipated.

“Viral Supercomputer Simulations – Vincent Racaniello – YouTube”

Ever looked at a 3D reconstruction of a virus particle and found the whole thing boringly static? No me neither, BUT this video demonstrates just how fluid a poliovirus particle in motion may be. The second half of the video looks behind the curtain of such simulations. No wizards here (well, not magic ones anyway…), just massive supercomputer CPU arrays. It’s all really cool (literally and figuratively).

I’ll admit, I generally think of (and refer to) virus capsids as protein shells – but rigid and brittle these particles are not. Perhaps coats is a better metaphor, something protective but allowing for motion.

“TWiV 321: aTRIP and a pause — This Week in Virology with Vincent Racaniello — Overcast”

Speaking of language and its careful use, I only just got around to listening to the linked episode of This Week in Virology, featuring guest Paul Duprex of the National Emerging Infectious Diseases Institute in Boston. The episode focuses upon the debate surrounding so-called “gain of function” experiments. A previous example of such an experiment would be the adaption of influenza to transmit between ferrets, in order to understand the mechanics of virus evolution and transmission in new hosts.

Proponents of such work say it’s necessary to understand and combat the results of phenomena occuring in wild flu infections. Opponents suggest that such work may create new pandemic viruses that would endanger global human health if they were accidentally released. Given the nature of the debate, the rhetoric is being horribly ratcheted up by those against this work.

Whilst sometimes wishing it had a bit more teeth, I appreciate both Paul Duprex’s defence of the work and his calls for the return to reasoned debate, because there’s one to be had. To quote: “if it’s a fight, no one’s gonna win”. I think he’s probably right.

Links to go viral – 8th February 2015

Carl Zimmer’s been on fire recently. Here are two great articles of his to get your teeth into this week:

 

“How The Measles Virus Became A Master of Contagion – Phenomena: The Loom”

Measles virus is in the news recently for all the wrong reasons, but how can the virus make such a roaring comeback in developed countries if vaccination campaigns slip? The answer: it is insanely contagious. And it needs to be – once you’ve had the virus you are immune for life – so if susceptible humans are around to be infected, the virus needs to get at them to survive and continue spreading. The article also touches on a cool thought that seems paradoxical to how well the virus can spread: because it can only infect people and not animals, it’s a great candidate for eradication from the planet.

“Our Inner Viruses: Forty Million Years In the Making – Phenomena: The Loom”

When it comes to transmission between hosts, measles is at the ‘hit-and-run’ end of the spectrum: infect human and get out before the immune system kills every last one of you. On the complete opposite end of the spectrum we have endogenous retroviruses.

Retroviruses, like HIV, bury themselves in your DNA. Every time an infected cell divides into two, you get twice as many copies of virus. But when such viruses get into sperm or egg cells, things get weird. If the infected sperm or egg goes on the make a new lifeform, every cell in the new life’s body will contain of copy of the virus! Surely this must be rarity, right? Nope. In human beings, this has probably occurred more than 30 times. But as the article concludes, apes (including humans), may have finally had enough of picking up these stowaways.

 

For a third story, this week saw a ‘great’ example of the science media hype machine in action, not helped by the study authors’ press release one bit. Here are 5 tweets from Stephen Curry regarding both the study and one example of an accompanying news report that deftly summarised the article I had planned to write this week. Curses.

Drug trials are useless without patients: Ebola and Brincidofovir

Excellent news reported in the New York Times today – Ebola drug trial is halted due to lack of patients. The quicker this virus leaves the West African region alone, the better. But this news is also a somber reflection on drug and vaccine development. As I wrote before, medical trials in countries with declining disease are doomed to fail. You cannot work out if a treatment works if you don’t have the patients to treat.

Before I go any further, I’ll reiterate: of course it’s excellent news that this horrendous virus is finally leaving the people of Liberia alone (and soon Guinea and Sierra Leone). But when the virus comes back in the future1, having new and effective weapons against it could prevent outbreaks happening again at this scale.

Before the 2014 outbreak in West Africa, news of Ebola vaccines was confined to the academic literature. Once the outbreak was in full force we finally decided to pay attention and fire up the drug pipeline. We needed candidate vaccines and drugs ready to go into the field at the beginning.

I admit the example of ZMapp, an experimental antibody cocktail against Ebola, was such a drug candidate. ZMapp was shown to protect rhesus macaques against the virus (albeit during the outbreak) and saw action in the field. The fact that the drug is so difficult to make in large quantities was probably tolerated by its manufacturers because the world had never seen such a large Ebola outbreak. Either way, we still don’t definitively know if it works in people because too few received it.

This newest drug trial closure is different. We’ve known about this one – Brincidofovir – for some time. Brincidofovir is a potent DNA virus growth inhibitor. It’s currently being stockpiled by the U.S. to counteract a smallpox bioterrorism threat. The fact that it works against Ebola in dishes of cells is an oddity (Ebola has a genome made of RNA, not DNA) that we don’t understand. But we know it works.

I’m not angered by the failings of the current trials. Logistics and manufacturing mean that responding to such an unforeseen virus outbreak without a whole bunch of candidate drugs was always going to prove difficult.

But we need to be ready next time. We don’t have time to run the compulsory safety trials while the virus is raging. We need a list of potential drugs and vaccines that we already know are safe in humans. Only then can we ethically test whether they work during the timeframe of an outbreak. And this preparation should also apply to other emerging virus diseases.

If we fail next time, then there’ll be reason to be angry.


  1. The virus is thought to persist in insectivorous bats in the wild. When a virus persists in an animal reservoir, the only way to effectively eliminate it is to vaccinate or kill enough of that species. Both are extremely difficult and undesirable courses of action. With the virus persistent in bats, there is always the potential for human infection in the future.

Links to go viral – 1st February 2015

This week’s selection of fascinating virology links:

 

In Sierra Leone’s Chaotic Capital, Ebola Found Fertile Ground – National Geographic

The story of poverty, population density and a deadly pathogen. Whilst more about Freetown, Sierra Leone than the Ebola virus, this is one of those articles that blossoms understanding in the minds of those fortunate enough to be on the other side of the planet. The virus is fascinating and deadly, but it’s the human side of the equation that is by far the most complicated. The photography is really great here too, but just a warning that some photos early on in the article are harrowing.

 

“Explainer: is the Ebola virus mutating? – The Conversation”

It’s an absolute truism: yes, it’s mutating because it’s a virus. Connor Bamford slams the recent lazy headlines about the virus mutating with a comprehensive explanation of what we mean by mutation, what the likely consequences of this are, why you shouldn’t worry about it and why we need to continue tackling Ebola as we currently are.

 

“Mystery childhood paralysis stumps researchers – Nature News & Comment”

A virus to keep on the radar: the snappily named Enterovirus D68. The circulation of this virus increased in the US last year, coincident with strange cases of fever, respiratory illness and paralysis in children and young adults. There is no smoking gun connecting the virus to these cases of paralysis at the moment, so why mention them in the same breath?

The most important reason is the timing of the cases – the virus could be isolated from some of the people suffering from sudden onset paralysis – but correlation is not causation, and assuming the virus is responsible could prevent us treating people if it’s not actually the cause. The second reason suspicion is being cast on the virus is due to our history with one of its close relatives – Poliovirus.