A chief weapon cells possess against infection is the ability to commit suicide. Obviously, suicide kills the cell, but it usually kills the invading microbe, as well. Thus, in multicellular organisms, individual cells "take one for the team" -- ending their own lives for the benefit of the organism as a whole, and the cell has multiple suicide options at its disposal.

Apoptosis is the best-known mechanism of cellular suicide. (Note: The second "p" is silent.) While apoptosis is often associated with developmental purposes (e.g., a tadpole losing its tail as it becomes an adult frog), this mechanism also serves an important immune function: Cytotoxic T-cells can trigger apoptosis in body cells which have become infected. For the most part, the death is quick and silent: the DNA is chopped up, and the cell shrivels and fragments into many pieces which are gobbled up by phagocytes.

Pyroptosis is a bit different. (Yes, the second "p" is silent here, too.) Think of "pyromaniacs" -- the people who set fires on purpose. Death by pyroptosis is sort of like that. An infected cell goes out with a bang, triggering inflammation and letting the immune system know that something horrible just happened. It serves as something of a wake-up call, moving the immune system to action.

Or... a cell could eat itself. This option is called autophagy, and like apoptosis, it is often associated with normal developmental processes and fighting infections. The cell fragments into small pieces internally and digests itself from within. Whatever is left over is cleaned up by phagocytes.

Now, researchers report in Nature the discovery of a potential therapeutic agent that triggers autophagy in virus-infected cells.

The authors found that a peptide (short protein) called Tat-Beclin 1 was a strong inducer of autophagy. If applied to HeLa cells infected with three different viruses (Sindbis, Chikungunya, or West Nile -- all of which are transmitted by mosquitoes), the peptide greatly reduced the ability of the viruses to reproduce. The peptide also greatly reduced the ability of HIV to replicate in human macrophage cells. 

Encouraged by these results, the authors moved into a live mouse model, using the Chikungunya and West Nile viruses. The authors wanted to determine if triggering autophagy with Tat-Beclin 1 would rescue mice given a lethal dose of virus. Indeed, it worked, albeit modestly. Both viruses killed 100% of untreated mice. However, 37.5% of Chikungunya-infected and roughly 20% of West Nile-infected mice survived if treated with the therapeutic peptide.

These results clearly imply that autophagy inducing agents can be used as antivirals. Additionally, since autophagy also plays a role in normal developmental processes, the authors hope that autophagy inducing agents could be used to treat a wide variety of medical problems.

Source: Sanae Shoji-Kawata, et al. "Identification of a candidate therapeutic autophagy-inducing peptide." Nature 2013. Published online 30 Jan 2013. doi: 10.1038/nature11866

Background: Susan L. Fink and Brad T. Cookson. "Apoptosis, Pyroptosis, and Necrosis: Mechanistic Description of Dead and Dying Eukaryotic Cells." Infect Immun 2005. April; 73(4): 1907-1916. doi: 10.1128/IAI.73.4.1907-1916.2005

We're all going to die, but some ways are more preferable than others. For instance, a woman in Washington State is suspected of smothering her boyfriend to death with her breasts. Me? I'd prefer that an anvil fall on my head (a la Wile E. Coyote) after my 100th birthday: quick and (probably) painless.

But, most of us won't be that lucky. In fact, each year in the U.S., hundreds of thousands of people die in intensive care units from circulatory shock, a condition in which insufficient oxygen and nutrients are delivered to the body's tissues. Left unchecked, shock can lead to organ dysfunction, which is often followed by that ultimately irreversible symptom: Death.

Shock has multiple causes. Two common types include hemorrhagic shock, which occurs following traumatic blood loss, and septic shock, which occurs following systemic bacterial infection. Both lead to hypovolemia (low blood volume) and hypotension (low blood pressure), which cause organ dysfunction.

Additionally, the intestines play a major role in shock, and it is thought that proteases (digestive enzymes) secreted by the pancreas break through the intestine's mucosal barrier, digesting the intestinal wall. Even worse, the enzymes can enter systemic circulation and damage other organs, greatly exacerbating the problem.

Researchers from UC-San Diego wanted to determine if blocking these enzymes could help rescue rats suffering from shock induced by blood loss, peritonitis (abdominal inflammation due to infection) or endotoxin (a bacterial membrane molecule which causes septic shock). They found that injecting enzyme inhibitors directly into the small intestine greatly increased survival and decreased organ damage. (See figure. Top panel: Normal intestines; middle panel: shock; bottom panel: shock + enzyme inhibitors.) Damage to the lungs and heart was also reduced when the rats were treated with enzyme inhibitors.

Given the success observed in the rat model, the authors hope to see the same in human patients.

Source: F. A. DeLano, D. B. Hoyt, G. W. Schmid-Schönbein. "Pancreatic Digestive Enzyme Blockade in the Intestine Increases Survival After Experimental Shock." Sci Transl Med 5, 169ra11 (2013).

Source and image source: "Blocking Digestive Enzymes May Reverse Shock, Stop Multiorgan Failure." UCSD press release. January 23, 2013.

Fans of The Three Stooges may remember the episode in which Curly asks Moe what he wants to eat. Moe responds, "Four pieces of burnt toast and a rotten egg." Why did he say this? Because Moe had a "tapeworm and it's good enough for him." Little did Moe know that he was actually dispensing profoundly deep immunological wisdom. 

Source: Bonds MH, Dobson AP, Keenan DC (2012). Disease Ecology, Biodiversity, and the Latitudinal Gradient in Income. PLoS Biol 10(12): e1001456. doi:10.1371/journal.pbio.1001456

They say that breaking up is hard to do, but what's infinitely harder is to admit when you're wrong. When somebody publicly issues a heartfelt mea culpa, many people wrongly celebrate with an "I told you so" dance. However, that's not the proper response. Celebrating is okay, as long as we celebrate the "conversion" and welcome the person into the fold. 

I want to start with some apologies. For the record, here and upfront, I apologise for having spent several years ripping up GM crops. I am also sorry that I helped to start the anti-GM movement back in the mid 1990s, and that I thereby assisted in demonising an important technological option which can be used to benefit the environment.

As an environmentalist, and someone who believes that everyone in this world has a right to a healthy and nutritious diet of their choosing, I could not have chosen a more counter-productive path. I now regret it completely.

Wow! That takes guts. He goes on:

What happened...that made me not only change my mind but come here and admit it? Well, the answer is fairly simple: I discovered science, and in the process I hope I became a better environmentalist.

Changing your mind when the data doesn't support your opinion is vital not only to being a good scientist or journalist, but a good human being. Indeed, as RealClearScience assistant editor Ross Pomeroy wrote, it is one of the keys to life. Because many facts have a half-life, all of our opinions should be subject to change. Besides, as astrophysicist Ethan Siegel correctly noted, there is tremendous power in admitting that you're wrong.