A Team of Israeli Students Just Created Honey Without Bees
The bee-free honey on the left, and the Israeli team that won the iGEM competition.
Can you make honey without honeybees? According to 12 Israeli students who took home a gold medal in the iGEM (International Genetically Engineered Machine) competition with their synthetic honey project, the answer is yes, you can.
The honey industry faces serious environmental challenges, like the mysterious Colony Collapse Disorder.
For the past year, the team from Technion-Israel Institute of Technology has been working on creating sustainable, artificial honey—no bees required. Why? As the team explains in a video on the project's website, "Studies have shown the amazing nutritional values of honey. However, the honey industry harms the environment, and particularly the bees. That's why vegans don't use honey and why our honey will be a great replacement."
Indeed, honey has long been a controversial product in the vegan community. Some say it's stealing an animal's food source (though bees make more honey than they can possibly use). Some avoid eating honey because it is an animal product and bees' natural habitats are disturbed by humans harvesting it. Others feel that because bees aren't directly killed or harmed in the production of honey, it's not actually unethical to eat.
However, there's no doubt that the honey industry faces some serious environmental challenges. Colony Collapse Disorder, a mysterious phenomenon in which worker bees in colonies disappear in large numbers without any real explanation, came to international attention in 2006. Several explanations from poisonous pesticides to immune-suppressing stress to new or emerging diseases have been posited, but no definitive cause has been found.
There's also the problem of human-managed honey farms having a negative impact on the natural honeybee population.
So how can honey be made without honeybees? It's all about bacteria and enzymes.
The way bees make honey is by collecting nectar from flowers, transporting it in their "honey stomach" (which is separate from their food stomach), and bringing it back to the hive, where it gets transferred from bee mouth to bee mouth. That transferal process reduces the moisture content from about 70 percent to 20 percent, and honey is formed.
The product is still currently under development.
The Technion students created a model of a synthetic honey stomach metabolic pathway, in which the bacterium Bacillus subtilis "learns" to produce honey. "The bacteria can independently control the production of enzymes, eventually achieving a product with the same sugar profile as real honey, and the same health benefits," the team explains. Bacillus subtilis, which is found in soil, vegetation, and our own gastrointestinal tracts, has a natural ability to produce catalase, one of the enzymes needed for honey production. The product is still currently under development.
Whether this project results in a real-world jar of honey we'll be able to buy at the grocery store remains to be seen, but imagine how happy the bees—and vegans—would be if it did.
In this week's Friday Five, an old diabetes drug finds an exciting new purpose. Plus, how to make the cities of the future less toxic, making old mice younger with EVs, a new reason for mysterious stillbirths - and much more.
The Friday Five covers five stories in research that you may have missed this week. There are plenty of controversies and troubling ethical issues in science – and we get into many of them in our online magazine – but this news roundup focuses on scientific creativity and progress to give you a therapeutic dose of inspiration headed into the weekend.
Here is the promising research covered in this week's Friday Five:
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- How to make cities of the future less noisy
- An old diabetes drug could have a new purpose: treating an irregular heartbeat
- A new reason for mysterious stillbirths
- Making old mice younger with EVs
- No pain - or mucus - no gain
And an honorable mention this week: How treatments for depression can change the structure of the brain
Researchers at Stanford have found that the virus that causes Covid-19 can infect fat cells, which could help explain why obesity is linked to worse outcomes for those who catch Covid-19.
Obesity is a risk factor for worse outcomes for a variety of medical conditions ranging from cancer to Covid-19. Most experts attribute it simply to underlying low-grade inflammation and added weight that make breathing more difficult.
Now researchers have found a more direct reason: SARS-CoV-2, the virus that causes Covid-19, can infect adipocytes, more commonly known as fat cells, and macrophages, immune cells that are part of the broader matrix of cells that support fat tissue. Stanford University researchers Catherine Blish and Tracey McLaughlin are senior authors of the study.
Most of us think of fat as the spare tire that can accumulate around the middle as we age, but fat also is present closer to most internal organs. McLaughlin's research has focused on epicardial fat, “which sits right on top of the heart with no physical barrier at all,” she says. So if that fat got infected and inflamed, it might directly affect the heart.” That could help explain cardiovascular problems associated with Covid-19 infections.
Looking at tissue taken from autopsy, there was evidence of SARS-CoV-2 virus inside the fat cells as well as surrounding inflammation. In fat cells and immune cells harvested from health humans, infection in the laboratory drove "an inflammatory response, particularly in the macrophages…They secreted proteins that are typically seen in a cytokine storm” where the immune response runs amok with potential life-threatening consequences. This suggests to McLaughlin “that there could be a regional and even a systemic inflammatory response following infection in fat.”
It is easy to see how the airborne SARS-CoV-2 virus infects the nose and lungs, but how does it get into fat tissue? That is a mystery and the source of ample speculation.
The macrophages studied by McLaughlin and Blish were spewing out inflammatory proteins, While the the virus within them was replicating, the new viral particles were not able to replicate within those cells. It was a different story in the fat cells. “When [the virus] gets into the fat cells, it not only replicates, it's a productive infection, which means the resulting viral particles can infect another cell,” including microphages, McLaughlin explains. It seems to be a symbiotic tango of the virus between the two cell types that keeps the cycle going.
It is easy to see how the airborne SARS-CoV-2 virus infects the nose and lungs, but how does it get into fat tissue? That is a mystery and the source of ample speculation.
Macrophages are mobile; they engulf and carry invading pathogens to lymphoid tissue in the lymph nodes, tonsils and elsewhere in the body to alert T cells of the immune system to the pathogen. Perhaps some of them also carry the virus through the bloodstream to more distant tissue.
ACE2 receptors are the means by which SARS-CoV-2 latches on to and enters most cells. They are not thought to be common on fat cells, so initially most researchers thought it unlikely they would become infected.
However, while some cell receptors always sit on the surface of the cell, other receptors are expressed on the surface only under certain conditions. Philipp Scherer, a professor of internal medicine and director of the Touchstone Diabetes Center at the University of Texas Southwestern Medical Center, suggests that, in people who have obesity, “There might be higher levels of dysfunctional [fat cells] that facilitate entry of the virus,” either through transiently expressed ACE2 or other receptors. Inflammatory proteins generated by macrophages might contribute to this process.
Another hypothesis is that viral RNA might be smuggled into fat cells as cargo in small bits of material called extracellular vesicles, or EVs, that can travel between cells. Other researchers have shown that when EVs express ACE2 receptors, they can act as decoys for SARS-CoV-2, where the virus binds to them rather than a cell. These scientists are working to create drugs that mimic this decoy effect as an approach to therapy.
Do fat cells play a role in Long Covid? “Fat cells are a great place to hide. You have all the energy you need and fat cells turn over very slowly; they have a half-life of ten years,” says Scherer. Observational studies suggest that acute Covid-19 can trigger the onset of diabetes especially in people who are overweight, and that patients taking medicines to regulate their diabetes “were actually quite protective” against acute Covid-19. Scherer has funding to study the risks and benefits of those drugs in animal models of Long Covid.
McLaughlin says there are two areas of potential concern with fat tissue and Long Covid. One is that this tissue might serve as a “big reservoir where the virus continues to replicate and is sent out” to other parts of the body. The second is that inflammation due to infected fat cells and macrophages can result in fibrosis or scar tissue forming around organs, inhibiting their function. Once scar tissue forms, the tissue damage becomes more difficult to repair.
Current Covid-19 treatments work by stopping the virus from entering cells through the ACE2 receptor, so they likely would have no effect on virus that uses a different mechanism. That means another approach will have to be developed to complement the treatments we already have. So the best advice McLaughlin can offer today is to keep current on vaccinations and boosters and lose weight to reduce the risk associated with obesity.