When Brain Plague came out (still my favorite book), reviewers sniffed that microbial aliens were “impossible.” They didn’t ask the microbiologists. Today, the microbiologists are homing in on our gut microbiota. “Take me to your leader” may mean taking a look inside your gut.
Why do we eat what we eat–and why does it “taste good”? Increasing evidence suggests that our gut bacteria, which digest much of our food, put out products that act as neurotransmitters that tell us to eat the foods the gut bacteria want. Known neurotransmitters produced by bacteria include glutamate, glutamine, and agmatine (all nitrogen-containing carbon compounds related to amino acids of protein). But research suggests that a large number of other neurotransmitters remain to be discovered.
How could the microbes do this? Either they might cause signals that increase our desire for foods they can digest; or the microbes could produce mild toxins that make us sick, until we consume what they want. It’s well known that the gut has a huge number of connections to the vagus nerve, which leads straight up to the brain.
One candidate (of many) for bacterial Svengalis is the bacteria that ferment chocolate. Chocolate is one of the most complicated foods we eat, the product of bacteria fermentation to begin with. (You cannot eat cocoa until after the beans have rotted three days in the jungle. The cocoa mass gets sent to Europe for fastidious processing.) It’s a mystery why we even like chocolate, which for humans is largely indigestible. But somehow eating cocoa (or dark chocolate with minimal added sugar) is associated with preventing obesity and diabetes. So maybe our gut bacteria know something that’s good for us.
To understand the broader background of Ebola and other viruses, read Michael Spector in the New Yorker. While his title “The Doomsday Strain” is overhype–in fact, I argue, these killer viruses are chronic population regulators–the world he describes, of eat and be infected, is the heart of what’s going on.
What’s unique about Africa is that, as the birthplace of humanity, it’s also the birthplace of the largest number of near-human species on our planet. The nearer-human you are, (1) the closer you compete; (2) the more pathogens–especially viruses–you share. Things like Monkeypox, a cousin of smallpox. Now that we no longer get smallpox vaccinations, monkeypox makes occasional forays into humans–and could evolve into a smallpox-like contagion.
How do viral pathogens evolve? A typical scenario:
–Virus propagates in an adapted host. Most viruses cause mild or no symptoms, because that way they keep their host around the longest. Humans are full of herpes-type viruses you never heard of–because we all have them, and they don’t cause illness.
–Virus jumps from adapted host to non-adapted host. Either the virus fails to grow at all–or else it grows too fast, killing the host before it can transmit to a new one.
–Either the virus burns out quickly in the new host, or it kills off 90% of them. If enough new host survive, they will evolve to adapt to the new virus. Like HIV–there are genetic variants of humans who don’t get AIDS. If this were the state of nature, without technology, these AIDS-resistant people would inherit the earth.
From the standpoint of population: How do viruses relate to their host?
One way they relate is that the virus defends its adapted host population from competitors. When two different monkey populations meet, individuals bite each other, copulate with each other (in secret, sleeping with the enemy), and share bodily fluids in every possible way. Without realizing, in effect they send each other their own viruses–adapted to the donor, possibly deadly to the recipient. In the long run, whoever best withstands the other’s viruses “wins.”
In Africa, an unfortunate effect of “civilized” development has been to increase human-monkey contact–most often by humans consuming near-human primates, aka “bushmeat.” But the bushmeat still sends us their viruses. For most of human history, these viruses helped hold Homo sapiens population in check. Thanks to “civilized” medicine, they no longer do.
Or do they?
Could a bacterium’s defense against bacterial viruses be used to protect a human cell from HIV?
A lot is in the news about people who seemed to be “cured” of HIV (the virus causing AIDS) yet two years later, the virus returns. That’s because the HIV virus hides a DNA copy of its RNA within the human cell’s own DNA chromosomes. The latently infected cells circulate in the bloodstream, undetected, because the hidden viral DNA looks the same as host DNA, to the immune system.
But what if we could cut the embedded DNA copy of HIV’s genome–out of the host cell DNA?
Amazingly, a way to do that has been reported, using a molecular machine used by bacteria to defend themselves from bacterial viruses. This defense is called CRISPR (clustered regularly interspaced short palindromic repeats). It is named for the clusters of short repeated sequences that appear in DNA of the bacterium. Each short sequence has been copied from the viral genome of a previously infecting virus. The genome of the previously infecting virus got recognized by the CAS complex–a protein/RNA machine that makes RNA copies of the infecting DNA sequence. The CAS RNA copies then cause the cell to (1) degrade the viral genomic DNA; (2) make short copies of viral sequence and insert them into host. These short copies (the “palindromic repeats” of CRISPR) then serve to generate future CAS RNAs that recognize the virus when it infects again–a kind of bacterial immune system.
For biotechnology, the CAS machine turns out to be an amazing way to edit vertebrate genomes. We can cut out a gene, for example a cancerous gene. So now, the PNAS researchers report using CAS to edit a small part of an integrated HIV genome, and prevent the integrated viral sequence from generating new phage particles. So far, this has been done in tissue culture. It will remain to be seen whether a delivery method can enable use of CRISPR/CAS to prevent HIV virus production in humans.
Fiction writers used to assume that robots would take us to the stars, or Antarctica, or other future adventures. But today the fastest growing use of robots may be that of caregivers for the elderly. Here in this NYT opinion, a physician argues that robots will be a good thing. Two kinds of robots–one, what you might expect, a robot that takes vital signs and is improbably named GiraffPlus. Another kind however is designed purely for “compassion.” Provides endless patience and limitless consideration, in the absence of that distantly located child with his/her own family.
The author argues that the time has come, and that companion robots will indeed be a good thing. We’ve already seen Robot and Frank, the infinitely self-sacrificing robotic companion. Perhaps its work reflecting how far we want to go down this road? The physician suggests that, with our high geriatric ratio and our declining personal patience, the road already has no exit.
Announcing the fall adventure–yes, it’s true, Ultraphyte is going to Antarctica. The expedition will be led by experienced Antarctic explorer Rachael Morgan-Kiss, of Miami University of Ohio. And yes, I’ll be posting Youtube videos (McMurdo Station has good internet. When the 200-mile winds aren’t blowing.)
Morgan-Kiss has a National Science Foundation grant to study eukaryotic microbes conducting photosynthesis–kinds of algae. See great video of her research. We’ll conduct most of our field work in the Lake Bonney region, including a look at the curious Blood Falls.
Antarctic algae are one of the least understood partners in the global carbon cycle. The more we know about the carbon cycle, the better we can predict climate change. Furthermore, Antarctic climate change is the heavyweight when it comes to long-term impact on sea level.
We’ll get to identify new kinds of algae, with interesting cute little shapes, as well as culture them in the laboratory. Yes, they’re very green.
Getting to Antarctica, and trained to work there, is a major task in itself. Only a few thousand people officially work there, and one assumes that doctors and dentists (and their technology) are scarce. So I have to spend the summer going the round of doctors, opticians, and dentists to fill out a mega-page form. Including EKG stress test–Ultraphyte is in decent shape, from weekly 20-miles running and biking.
Will Antarctica make it into Blood Star Frontier? Yes, toward the end–and will take center stage in book 3, Sun Ice Frontier. Next spring at ICFA and Wiscon, I hope to have more to say about it; and trade notes with Antarctic traveler Stan Robinson.
While we fret over childish court rulings, and homeless children dare to cross our borders, the spread of Ebola virus gets buried. For true heroism, nothing beats Doctors Without Borders–for months, the main source of care and treatment in a growing epidemic. So far the disease has struck Guinea, Liberia and Sierra Leone. Most of our Google news feeds relegate the disease below the first screen on our monitors. But experts say it’s just one plane flight away from Paris. Yes, a place that “matters” (sarcasm).
What makes Ebola virus so deadly? An RNA virus, Ebola has a relatively simple structure, just eight genes encoding proteins. The small RNA is coiled within a flexible tubular protein capsid. The main host cells the virus can infect are white blood cells, liver cells, and endothelial cells–cells that line the blood vessels. That’s quite a deadly combination. By infecting the white blood cells, the Ebola virus disrupts the immune system, avoiding effective defense. Also, the cells carry the virus through the blood, all throughout the body. When the endothelial cells get infected, the blood vessels leak. More from my post in April.
With so much strife in the world, it’s a relief to know that scientists have solved one of nature’s great mysteries: the disco clam. The disco clam, Ctenoides ales, appears to flash lightning bolts within its mouth. Young scientist Lindsey Dougherty at Berkeley has figured out the mechanism of this light display. Note that her research on this project involved “high speed video, transmission electron microscopy, spectrometry, energy dispersive x-ray spectroscopy and computer modeling.” Funded by the National Science Foundation, among several conservation organizations.
So how does it work? Not bioluminescence; that is, there is no biological light organ that emits its own light, like a firefly or the jellyfish Aequorea. Instead, the lip of the clam grows to form a narrow edge that scatters light–only from one side. The edge contains miniature balls of silica (glass) that efficiently reflect and scatter light. So as the lip moves the light appears to flash on and off, like the facets of a disco ball.
Does the clam use this flashing for anything useful? The next stage of research is to figure out if clams use the light signals to communicate. Great possibilities for science fiction.