Enlarge / Diagram of the structure of the virus' spike protein. (credit: McLellan Lab, University of Texas at Austin )

When the COVID-19 pandemic was first recognized for the threat that it is, researchers scrambled to find anything that might block the virus' spread. While vaccines have grabbed much of the attention lately, there was also the hope that we could develop a therapy that would block the worst effects of the virus. Most of these have been extremely practical: identify enzymes that are essential for the virus to replicate, and test drugs that block similar enzymes from other viruses. These drugs are designed to be relatively easy to store and administer and, in some cases, have already been tested for safety in humans, making them reasonable choices for getting something ready for use quickly.

But the tools we've developed in biotechnology allow us to do some far less practical things, and a paper released today describes how they can be put to use to inactivate SARS-CoV-2. This is in no way a route to a practical therapy, but it does provide a fantastic window into what we can accomplish by manipulating biology.

Throw it in the trash

The whole effort described in the new paper is focused on a simple idea: if you figure out how to wreck one of the virus' key proteins, it won't be able to infect anything. And, conveniently, our cells have a system for destroying proteins, since that's often a useful thing to do. In some cases, the proteins that are destroyed are damaged; in others, the proteins are made and destroyed at elevated paces to allow the cell to respond to changing conditions rapidly. In a few cases, changes in the environment or the activation of signaling pathways can trigger widespread protein destruction, allowing the cell to quickly alter its behavior.

Enlarge / While this may look like a set of iridescent satin ribbons, it's actually the scales on the wing of a butterfly. (credit: Don Komarechka )

I don't know how many years I've been putting together image galleries of the Nikon Small World Microscopy contest , but it's been quite a few now, and it's hard not to feel like I'm repeating the same things when I introduce a selection of the images from it. That nature's beauty isn't limited to grand landscapes or charismatic megafauna. That serious science can co-exist with amazing aesthetics. That some of the best scientists also have an eye for the artistic and the desire to capture the worlds they study in compelling ways. That technology and software have revolutionized a technology—the microscope—that has been around for hundreds of years.

All of those things are still true, which is why I keep emphasizing them. But words are just a distraction from the pure artistry of this year's contest winners. So I'll shut up and let you enjoy them.

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  This is a chameleon embryo, which is late enough in development to look a lot like a mature chameleon. Note the loop behind its head is the tip of its tail. [credit: Dr. Allan Carrillo-Baltodano & David Salamanca ]

Enlarge / If you can't socially distance, a face mask helps. (credit: Christopher Furlong / Getty Images )

Many countries that controlled their COVID-19 cases in the spring are now seeing rises in infections, raising the prospect that they'll face a second wave of cases, as many epidemiological models had predicted. But in the United States, the number of cases has never dropped to low levels. Instead, it varied between high levels of infection and very high peaks in cases. Why is everything so different in the states?

While there are plenty of possible reasons, a series of new studies essentially blame all the obvious ones: the United States ended social distancing rules too soon, never built up sufficient testing and contact-tracing capabilities, and hasn't adopted habits like mask use that might help substitute for its failures elsewhere. The fact that some of these studies used very different methods to arrive at similar conclusions suggests that those conclusions are likely to hold up as more studies come in.

Too soon

One of the studies, performed by a US-South African team, looked at the relaxation of social distancing rules in the US. Its authors created a list of restrictions for each state and the District of Columbia and tracked the number of COVID-19 deaths in each state for eight weeks prior to the rules being terminated. The number of deaths was used as a proxy for the total number of cases, as the erratic availability of tests made the true infection rate difficult to determine.

Enlarge / Emmanuelle Charpentier reminds everybody about pandemic safety at the start of a press conference following the announcement of her Nobel Prize. (credit: Pictures Alliance/Getty Images)

On Wednesday, the Nobel Prize Committee awarded the Chemistry Nobel to Emmanuelle Charpentier and Jennifer Doudna, who made key contributions to the development of the CRISPR gene-editing system, which has been used to produce the first gene-edited humans. This award may spur a bit of controversy, as there were a lot of other contributors to the development of CRISPR (enough to ensure a bitter patent fight), and Charpentier and Doudna's work was well into the biology side of chemistry. But nobody's going to argue that the gene editing wasn't destined for a Nobel Prize.

Basic science

The history of CRISPR gene editing is a classic story of science: a bunch of people working in a not-especially-cutting-edge area of science found something strange. The "something" in this case was an oddity found in the genome sequences of a number of bacteria. Despite being very distantly related, the species all had a section of the genome where a set of DNA sequences were repeated, with a short spacer in between them. The sequences picked up the name CRISPR for "clustered regularly interspaced short palindromic repeats," but nobody knew what they were doing there.

The fact that they might be important became apparent when researchers recognized that bacteria that had CRISPR sequences invariably also had a small set of genes associated with them. Since bacteria tended to rapidly lose genes and repeat sequences that weren't performing useful functions, this obviously implied some sort of utility. But it took 18 years for someone to notice that the repeated sequences matched those found in the genomes of viruses that infected the bacteria.

Enlarge / Scientists mixed chitin—an organic polymer found in abundance in arthropods, as well as fish scales—with a mineral that mimics the properties of Martian soil to create a viable new material for building tools and shelters on Mars. (credit: Javier G. Fernandez )

Space aficionados who dream of one day colonizing Mars must grapple with the stark reality of the planet's limited natural resources, particularly when it comes to building materials. A team of scientists from the Singapore University of Technology and Design discovered that, using simple chemistry, the organic polymer chitin —contained in the exoskeletons of insects and crustaceans—can easily be transformed into a viable building material for basic tools and habitats. This would require minimal energy and no need for transporting specialized equipment. The scientists described their experiments in a recent paper published in the journal PLOS ONE.

"The technology was originally developed to create circular ecosystems in urban environments," said co-author Javier Fernandez . "But due to its efficiency, it is also the most efficient and scalable method to produce materials in a closed artificial ecosystem in the extremely scarce environment of a lifeless planet or satellite."

As we previously reported , NASA has announced an ambitious plan to return American astronauts to the Moon and establish a permanent base there, with an eye toward eventually placing astronauts on Mars. Materials science will be crucial to the Artemis Moon Program's success, particularly when it comes to the materials needed to construct a viable lunar (or Martian) base. Concrete, for instance, requires a substantial amount of added water in order to be usable in situ , and there is a pronounced short supply of water on both the Moon and Mars. And transport costs would be prohibitively high. NASA estimates that it costs around $10,000 to transport just one pound of material into orbit.

Enlarge / The spectral signature of phosphine superimposed on an image of Venus. (credit: ALMA (ESO/NAOJ/NRAO), Greaves et al. & JCMT )

Today, researchers are announcing they've observed a chemical in the atmosphere of Venus that has no right to be there. The chemical, phosphine (a phosphorus atom hooked up to three hydrogens), would be unstable in the conditions found in Venus' atmosphere, and there's no obvious way for the planet's chemistry to create much of it.

That's leading to a lot of speculation about the equally unlikely prospect of life somehow surviving in Venus' upper atmosphere. But a lot about this work requires outside input, which today's publication is likely to prompt. While there are definitely reasons to think phosphine is present on Venus, its detection required some pretty involved computer analysis. And there are definitely some creative chemists who are going to want to rethink the possible chemistry of our closest neighbor.

What is phosphine?

Phosphorus is one row below nitrogen on the periodic table. And, just as nitrogen can combine with three hydrogen atoms to form the familiar ammonia, phosphorus can bind with three hydrogens to form phosphine. Under Earth-like conditions, phosphine is a gas, but not a pleasant one: it's extremely toxic and has a tendency to spontaneously combust in the presence of oxygen. And that later feature is why we don't see much of it today; it's simply unstable in the presence of any oxygen.

Enlarge / MOSCOW, RUSSIA - SEPTEMBER 4, 2020: Medical staff with newly delivered boxes containing COVID-19 vaccine in a cold room at No2 Outpatient Clinic in southern Moscow. (credit: Stanislav Krasilnikov / Getty Images )

Russia has been one of the countries hit hard by the COVID-19 pandemic. But its response to that has been a bit... unusual. As many other countries have, Russia worked to develop its own vaccine. But while that development was still in progress, it announced that it wasn't going to wait for detailed safety data , and instead roll the vaccine out to millions. Shortly afterwards, it became clear that the country was actually going to run a standard phase 3 clinical trial , albeit a large one, involving 40,000 people.

It was hard to judge whether any of this was reasonable, because few details of the vaccine itself were available. But that changed somewhat on Friday, as the people who developed the vaccine published the results of the initial clinical trials. And so far, it seems to be about as effective as some of the other ones that have been made it past initial trials.

Two viruses better than one?

As our earlier coverage mentioned, the vaccine is composed of two different engineered viruses. These contain the backbone of an innocuous virus, called an adenovirus, engineered to include the gene that encodes the major surface protein from the SARS-CoV-2 virus. This protein, called Spike, is what the coronavirus uses to latch on to and enter cells. The use of adenovirus allows the immune system to learn to recognize the Spike protein while the body only experiences a harmless adenovirus infection.

Enlarge / FDA Commissioner Stephen Hahn, speaking at the press conference in which he badly mangled statistics. (credit: Pete Marovich/Getty Image )

After several days of rumors with ever-growing hype, the Trump administration announced on Sunday that the Food and Drug Administration was granting an Emergency Use Authorization (EUA) for a COVID-19 treatment. The move was controversial from the start, with reports indicating that the EUA was opposed by a number of health experts, including Francis Collins and Anthony Fauci. The press conference didn't settle matters, with a growing chorus of scientists saying that the data presented in support of the EUA had been misrepresented .

On Monday night, FDA commissioner Stephen Hahn acknowledged that he had made a significant error in presenting the benefits of the treatment, and he followed that with an apology on Tuesday . But Hahn pushed back on indications that the approval of the treatment on the eve of the Republican National Convention was motivated by political pressure.

Wrong kind of risk

The treatment at issue involves taking the antibody-containing plasma from those who have recovered from a SARS-CoV-2 infection (convalescent plasma) and giving it to those currently suffering from COVID-19 symptoms. At Sunday's press conference, the principle justification for allowing this treatment under an EUA was a 35 percent drop in mortality for those receiving plasma in the first three days of treatment—specifically, Hahn said 35 of 100 people "would have been saved" by this treatment.

Enlarge / T-cells attacking a cell recognized as foreign. (credit: NIH )

We're still struggling to understand whether infection with SARS-CoV-2, with our without COVID-19 symptoms, provides protection from further infections. Antibodies are an indicator of immunity and are the easiest aspect of the immune response to track. But data indicates that the generation of antibodies is highly variable , and their production may start fading within months. But there are many other aspects to the immune response, many of them centered on T cells. And here again, the response seems to be extremely complex .

Now, additional studies are coming out looking at other specialized aspects of the immune response. While these results provide some cause for optimism in terms of long-lasting immunity, there remain large numbers of unknowns.

Go with the flow

The two studies we'll look at were enabled by a technique called "flow cytometry" that's proven very useful for studying the immune response. It basically helps researchers get past the biggest issue with these studies: there's an abundance of very similar-looking cells involved in an immune response. While a trained eye can tell a T cell from a macrophage using a microscope, knowing there are T cells doesn't tell us much. Not only would we like to know how many of them there are, we'd need to know what types of T cells are present. T cells may help the production of antibodies, they may kill infected cells, they might be used to remember exposure to pathogens, etc.