Higher and higher still, the cotton bollworm moth caterpillar climbs, its tiny body ceaselessly scaling leaf after leaf. Reaching the top of a plant, it will die, facilitating the spread of the virus that steered the insect there.

One virus behind this deadly ascent manipulates genes associated with caterpillars’ vision. As a result, the insects are more attracted to sunlight than usual, researchers report online March 8 in Molecular Ecology.

The virus involved in this caterpillar takeover is a type of baculovirus. These viruses may have been evolving with their insect hosts for 200 million to 300 million years, says Xiaoxia Liu, an entomologist at China Agricultural University in Beijing. Baculoviruses can infect more than 800 insect species, mostly the caterpillars of moths and butterflies. Once infected, the hosts exhibit “tree-top disease,” compelled to climb before dying and leaving their elevated, infected cadavers for scavengers to feast upon.
The clever trick of these viruses has been known for more than a century, Liu says. But how they turn caterpillars into zombies doomed to ascend to their own deaths wasn’t understood.

Previous research suggested that infected caterpillars exhibit greater “phototaxis,” meaning they are more attracted to light than uninfected insects. Liu and her team confirmed this effect in the laboratory using cotton bollworm moth caterpillars (Helicoverpa armigera) infected with a baculovirus called HearNPV.

The researchers compared infected and uninfected caterpillars’ positions in glass tubes surrounding a climbing mesh under an LED light. Uninfected caterpillars would wander up and down the mesh, but would return to the bottom before pupating. That behavior makes sense because in the wild, this species develops into adults underground. But infected hosts would end up dead at the top of the mesh. The higher the source of light, the higher infected hosts climbed.

The team moved to the horizontal plane to confirm that the hosts were responding to light rather than gravity, placing caterpillars in a hexagonal box with one of the side panels illuminated. By the second day after infection, host caterpillars crawled to the light about four times as often as the uninfected.

When the researchers surgically removed infected caterpillars’ eyes and put the insects in the box, the blinded insects were attracted to the light a quarter as often as unaltered infected hosts. That suggested that the virus was using a caterpillar’s vision against itself.

The team then compared how active certain genes were in various caterpillar body parts in infected and uninfected larvae. Detected mostly in the eyes, two genes for opsins, the light-sensitive proteins that are fundamental for vision, were more active after an infection with the virus, and so was another gene associated with vision called TRPL. It encodes for a channel in cell membranes involved in the conversion of light into electrical signals.

When the team used the gene-editing tool CRISPR/Cas9 to shut off the opsin genes and TRPL in infected caterpillars, the number of hosts attracted to the light in the box was cut roughly in half. Their height at death on the mesh was also reduced.

Baculoviruses appear capable of commandeering the genetic architecture of caterpillar vision, exploiting an ancient importance of light for insects, Liu says.

Light can cue crucial biological processes in insects, from directing their developmental timing, to setting their migration routes.

These viruses were already known to be master manipulators in other ways, tweaking their hosts’ sense of smell, molting patterns and the programmed death of cells, says Lorena Passarelli, a virologist at Kansas State University in Manhattan, who was not involved with the study. The new research shows that the viruses manipulate “yet another physiological host process: visual perception.”

There’s still a lot to learn about this visual hijacking, Passarelli says. It’s unknown, for instance, which of the virus’s genes are responsible for turning caterpillars into sunlight-chasing zombies in the first place.

More than 2,000 years ago, Hippocrates, the Greek physician often considered the father of modern medicine, identified what came to be known as the clitoris, a “little pillar” of erectile tissue near the vagina’s entrance. Aristotle then noticed that the seemingly small structure was related to sexual pleasure.

Yet it wasn’t until 2005 that urologist Helen O’Connell uncovered that the “little pillar” was just the tip of the iceberg. The internal parts of the organ reach around the vagina and go into the pelvis, extending a network of nerves deeper than anatomists ever knew.

It took millennia to uncover the clitoris’s true extent because sexism has long stymied the study of female biology, science journalist Rachel E. Gross argues in her new book, Vagina Obscura. Esteemed men of science, from Charles Darwin to Sigmund Freud, viewed men as superior to women. To be male was to be the ideal standard. To be female was to be a stunted version of a human. The vagina, the ancient Greeks concluded, was merely a penis turned inside out, the ovaries simply interior testicles.

Because men mostly considered women’s bodies for their reproductive capabilities and interactions with penises, only recently have researchers begun to truly understand the full scope of female organs and tissues, Gross shows. That includes the basic biology of what “healthy” looks like in these parts of the body and their effects on the body as a whole.

Vagina Obscura itself was born out of Gross’ frustration at not understanding her own body in the wake of a vaginal infection. After antibiotics and antifungal treatments failed due to a misdiagnosis, her gynecologist prescribed another treatment. As Gross paraphrases, the doctor told her to “shove rat poison up my vagina.” The infection, it turned out, was bacterial vaginosis, a hard-to-treat, sometimes itchy and painful condition caused by an overgrowth of bacteria that normally reside in the vagina. (The rat poison was boric acid, which is also an antiseptic. “It’s basically rat poison,” the doctor said. “You’re going to see that on the internet, so I might as well tell you now.”)
The book’s exploration of female anatomy begins from the outside in, first traversing the clitoris’s nerve-filled external nub to the vagina, ovaries and uterus. The last chapter focuses on gender affirmation surgery, detailing how physicians have transformed the field for transgender people. (Gross is up-front that words such as women and men create an artificial binary, with seemingly more objective terms like “male” and “female” not performing much better in encompassing humankind’s diversity, including intersex and transgender people.)

Throughout this tour, Gross doesn’t shy away from confronting the sexism and prejudices behind controversial ideas about female biology, such as vaginal orgasms (versus coming from the clitoris) and the existence of the G-spot (SN: 4/25/12). Both “near-mystical” concepts stem from the male perspective that sexual pleasure should be straightforward for women, if only men could hit the right spot. Nor are the more appalling offenses swept under the rug, including racism, eugenics and female genital cutting. Footnotes throughout the book detail Gross’ efforts to navigate controversial views and stigmatizing or culturally charged terminology.

To lift readers’ spirits, she finds the right spots to deliver a dose of wry humor or a pun. She also shares stories of often forgotten researchers, such as lab technician Miriam Menkin, who showed in 1944 that in vitro fertilization is possible (SN: 8/12/44). Yet Menkin’s role in describing the first instance of a human egg being fertilized in a lab dish has largely been erased from IVF’s history (SN: 6/9/21). There’s also plenty of opportunity to marvel at the power of the female body. Despite the long-held notion that a person is born with all the eggs they’ll ever have, for example, researchers are now discovering the ovary’s regenerative properties.

Studying female bodies more closely could ultimately improve quality of life. Chasing cells capable of producing more eggs might bring about discoveries that could restore the menstrual cycle in cancer patients rendered infertile by chemotherapy or make menopause less miserable. Patients with endometriosis, a painful disorder in which uterine tissue grows outside the uterus, are often dismissed and their symptoms downplayed. Some doctors even recommend getting pregnant to avoid the pain. But people shouldn’t have to suffer just because they aren’t pregnant. Researchers just haven’t asked the right questions yet about the uterus or endometriosis, Gross argues.

Vagina Obscura reinforces that female bodies are more than “walking wombs” or “baby machines.” Understanding these organs and tissues is important for keeping the people who have them healthy. It will take a lot of vagina studies to overcome centuries of neglect, Gross writes. But the book provides a glimpse into what is possible when researchers (finally) pay attention.

You can never have too much ice cream, but you can have too much ice in your ice cream. Adding plant-based nanocrystals to the frozen treat could help solve that problem, researchers reported March 20 at the American Chemical Society spring meeting in San Diego.

Ice cream contains tiny ice crystals that grow bigger when natural temperature fluctuations in the freezer cause them to melt and recrystallize. Stabilizers in ice cream — typically guar gum or locust bean gum — help inhibit crystal growth, but don’t completely stop it. And once ice crystals hit 50 micrometers in diameter, ice cream takes on an unpleasant, coarse, grainy texture.

Cellulose nanocrystals, or CNCs, which are derived from wood pulp, have properties similar to the gums, says Tao Wu, a food scientist at the University of Tennessee in Knoxville. They also share similarities with antifreeze proteins, produced by some animals to help them survive subzero temperatures. Antifreeze proteins work by binding to the surface of ice crystals, inhibiting growth more effectively than gums — but they are also extremely expensive. CNCs might work similarly to antifreeze proteins but at a fraction of the cost, Wu and his colleagues thought.

An experiment with a sucrose solution — a simplified ice cream proxy — and CNCs showed that after 24 hours, the ice crystals completely stopped growing. A week later, the ice crystals remained at 25 micrometers, well beneath the threshold of ice crystal crunchiness. In a similar experiment with guar gum, ice crystals grew to 50 micrometers in just three days.
“That by itself suggests that nanocrystals are a lot more potent than the gums,” says Richard Hartel, a food engineer at the University of Wisconsin–Madison, who was not involved in the research. If CNCs do function the same way as antifreeze proteins, they’re a promising alternative to current stabilizers, he says. But that still needs to be proven.

Until that happens, you continue to have a good excuse to eat your ice cream quickly: You wouldn’t want large ice crystals to form, after all.