Time and husband makes wife have interracial sex videoagain, Martin Moore’s children get sick with a cold. He hauls them to their doctor, who then informs him that there’s nothing to be done aside from taking them home and waiting it out.

The experience is maddening for Moore — especially because he’s a virologist. For everything that virologists have learned about rhinoviruses — the cause of the majority of colds — they have not invented a vaccine for them.

In 2013, Moore wondered if he could make one. He consulted a rhinovirus expert for some advice. Instead, the expert told him, “Oh, there will never be a vaccine for rhinovirus — it’s just not possible.”

“I thought, ‘Well, let’s look into that,’” recalled Moore, an associate professor at Emory University and a research scholar at Children’s Healthcare of Atlanta.

Three years later, Moore and his colleagues now have a vaccine that has shown promising results in trials on macaques. The monkeys were able to produce antibodies against many types of rhinoviruses. Moore and his colleagues are now following up on those results with more research and hope to move soon to human trials.

They’re not alone, however. Other research groups, based at universities and at pharmaceutical companies, are making advances with vaccines of their own. After decades of disappointment and resignation, scientists think the common cold may at last be beatable.

“There’s a huge amount going on,” said Gary McLean, of Imperial College London, who is working on another vaccine.

Rhinoviruses were discovered in the early 1960s, and soon afterward a number of researchers tried to make vaccines against them. They soon discovered that rhinoviruses were a wily foe. They’ve evolved into many different forms, and so antibodies to one form (known as a serotype) usually don’t work against any others.

The last report on a human cold vaccine trial was published in 1975. Since then, there’s been nothing.

In recent years, however, some scientists have been trying to drum up interest again in a vaccine. They’ve demonstrated that the rhinovirus is not as harmless as it once seemed. “It’s getting more respect as a pathogen,” said Dr. James Gern, a pediatrician at the University of Wisconsin School of Medicine who studies colds.

Colds take an enormous economic toll on families. Between sick days and parents staying home to care for their children, colds drain an estimated $25 billion a year from workplace productivity in the United States.

Colds can also cause more physical harm than scientists previously appreciated. When most people get a cold, the rhinoviruses stay in their nose. But Gern and others have discovered that some types of rhinovirus can invade deep into the lungs. Many cases of childhood pneumonia turn out to be caused by rhinoviruses.

Rhinoviruses are especially dangerous for people who already have certain chronic disorders such as asthma, cystic fibrosis, or chronic obstructive pulmonary disease. Even a mild cold can trigger runaway inflammation in their lungs. It turns out that the majority of asthma attacks are brought on by rhinoviruses.

“Rhinovirus can cause more disease in certain people, and when I say ‘certain people,’ I mean a lot of people,” said Gern.

If someone with COPD ends up in the hospital due to a cold-triggered attack, doctors can try to tamp down the inflammation, but the best treatments are not very effective. “A vaccine would stop all that in its tracks before it gets started,” said McLean.

Over the past decade, McLean and others at Imperial have been studying colds in mice to find new inspirations for a vaccine. They exposed the animals to different parts of rhinoviruses to see how their immune systems responded.

The cold vaccines that scientists had tested in the 1960s and 1970s had prompted the immune system to make antibodies only to the proteins on the surface of the virus shells. When the vaccinated volunteers got infected again, those antibodies could grab onto the rhinoviruses and summon the immune system to destroy them.

The problem with this approach is that each serotype has surface proteins with different shapes. Antibodies that can grab onto one serotype slip off another.

But our immune system can also fight rhinovirus in another way — after they’ve invaded our cells. Once viruses have worked their way inside, their shells break open and they dump out internal proteins and genes. The cells then use these molecules to make new viruses.

It turns out that cells can grab some of these molecules and push them to their surface. It’s as if they’re pushing a home invasion alarm. Immune cells can learn to recognize these viral proteins. They instruct infected cells to kill themselves and slow down an infection.

McLean and his colleagues set out to build a new vaccine based on this alarm defense. They whipped up batches of internal proteins from rhinoviruses and injected them into mice. The scientists found that the immune system of the mice could learn to recognize the proteins. If they mixed rhinoviruses with mouse blood, immune cells aggressively attacked infected cells.

What’s especially exciting about this approach is that the proteins from one type of rhinovirus can trigger a response to other types as well. That’s because the internal proteins they’re targeting are pretty much the same from one type to another. It’s probably impossible for them to evolve into different shapes, because they’d stop doing their essential work.

When Martin Moore got into the cold vaccine game, he didn’t try to find a new strategy the way the Imperial scientists did. Instead, he tried to update an approach that had been pioneered by University of Virginia scientists in the 1970s.

The Virginia team had picked out 10 different serotypes and combined them into one shot.

“It produced some antibody, but it wasn’t great,” said Bruce Hamory, one of the Virginia researchers. “If you challenged someone with a strain that wasn’t in the vaccine, there was no cross-protection.”

But Moore decided the idea was sound. The only problem was that scientists in the 1970s just didn’t have the tools to make it work. In the 21st century, those tools were now at hand.

A lot of other scientists didn’t share Moore’s optimism. “It was definitely a risk,” he said. “We broke the bank, people left the lab. You name it. But I just felt this is what I needed to do.”

To make a new vaccine, Moore needed a lot of rhinoviruses. He also needed a lot of different types of rhinoviruses. So far, scientists have identified 160 types from people with colds.

To get his hands on the pathogens, Moore contacted James Gern. He knew that Gern has gathered rhinoviruses from his patients for over two decades in order to do research on colds.

“We probably have one of the world’s biggest collections of kid snot,” said Gern.

Out of his snot collection, Gern and his colleagues can isolate many different types of rhinoviruses. They can then extract the genes for those viruses and store them. When they want to study a particular type, they simply inject the genes into human cells and let them churn out new viruses. This gene-based method lets them make viruses much faster than in the 1970s, and they can be sure they’re making exactly the type they want.

For a trial vaccine, Moore decided to ramp up Hamory’s 10-type vaccine to 50. He and his colleagues packed a large number of each type of rhinovirus into a single shot.

They injected the vaccine into macaques and then later drew blood from the monkeys. When they mixed the viruses into the blood, they got a strong antibody response to 49 out of the 50 types. Moore and his colleagues published the results in Nature Communications, and they’re now moving forward with some additional studies that they hope will open the way to a human trial.

Meanwhile, the Imperial team has filed a patent on its internal-protein vaccine and is also moving in the same direction. “To convince people to part with large sums of money, you need a lot of preclinical data. And we’ve got about as much as we can at the moment,” said McLean.

It’s still an open question which strategy will win out. It’s even possible that both will fail. McLean and his colleagues still need to show that a vaccine using a single protein can protect against the full range of rhinoviruses that cause the most colds.

McLean also wonders how well Moore’s 50-type vaccine would work in the real world. “It’s a great paper, but it’s not showing anything new except for being able to pack in 50 types of the virus into one little injection,” said McLean. “Great, you’re going to get 50 immune responses. That’s going to work for those 50, but it might not work for an extra 30.”

Gern agrees that’s a concern. “If it really takes 130 types, that’s a lot of manufacturing that would go into one vaccine,” he said. He says it might make sense for now to tailor Moore’s vaccine for just one group of people.

Only certain types of rhinovirus appear to pose the biggest risk to people with COPD, for example. Scientists might start by testing a cold vaccine for COPD. If that works, they could think about scaling up to a cold vaccine for more people.

After giving up on a cold vaccine 40 years ago, Hamory likes to hear people talk this way again. “I’m tremendously excited,” he said. “I think it’s absolutely spectacular that people are going back to an important problem that’s laid fallow for so many years.”