Rhinoviruses are the predominant cause of the common cold and also exacerbate asthma. Photo from Thinkstock. 
 
 The vaccine tested by Emory/CHOA researchers does not cover all known rhinoviruses, but it does stimulate antibodies against 50 of them. 
 
 Scientists are making the case that a vaccine against rhinoviruses, the predominant cause of the common cold, is achievable. 
 
 The quest for a vaccine against rhinoviruses may have seemed quixotic, because there are more than 100 varieties circulating around the world. Even so, the immune system can handle the challenge, researchers from Emory University School of Medicine and Children’s Healthcare of Atlanta say. 
 
 Vaccines that combine dozens of varieties of rhinovirus at once are effective in stimulating antiviral antibodies in mice and monkeys, the researchers report in Nature Communications. The paper was also posted on Biorxiv before publication. 
 
 “We think that creating a vaccine for the common cold can be reduced to technical challenges related to manufacturing,” says Martin Moore, PhD, associate professor of pediatrics at Emory University School of Medicine. 
 
 Rhinoviruses are the most common cause of the common cold; other viruses such as respiratory syncytial virus, parainfluenza virus and adenoviruses can cause them too. Rhinoviruses also exacerbate asthma attacks. Although they come in many varieties, rhinoviruses do not drift to the same degree that influenza viruses do, Moore says. 
 
 Researchers showed in the 1960s that it was possible to vaccinate people against one variety of rhinovirus and prevent them from getting sick when challenged with samples of the same virus. The trouble was the sheer diversity of rhinoviruses – or that’s how it appeared at the time. 
 
 “It’s surprising that nobody tried such a simple solution over the last 50 years. We just took 50 types of rhinovirus and mixed them together into our vaccine, and made sure we had enough of each one,” Moore says. “If we make a vaccine with 50 or 100 variants, it's the same amount of total protein in a single dose of vaccine. The variants are like a bunch of slightly different Christmas ornaments, not really like 50 totally different vaccines mixed.” 
 
 A mixture of 25 types of inactivated rhinovirus can stimulate neutralizing antibodies against all 25 in mice, and a mixture of 50 types can do the same thing in rhesus macaques. In this paper, antibodies generated in response to the vaccine were tested for their ability to prevent the virus from infecting human cells in culture. However, the vaccines were not tested for their ability to stop animals from getting sick. 
 
 “There are no good animal models of rhinovirus replication,” Moore says. “The next step would be human challenge models with volunteers, which are feasible because the virus is not very pathogenic.” 
 
 Emory has optioned the vaccine technology to a startup company, Meissa Vaccines, Inc., which is pursuing a product development plan with support from the National Institute of Allergy and Infectious Diseases’ vaccine manufacturing services. 
 
 The co-first authors of the paper are assistant professor of pediatrics Sujin Lee, PhD, and research specialist Minh Trang Nguyen. The research was supported by the National Institute of Allergy and Infectious Diseases (R01AI087798, U19AI095227) and a pilot grant from the Emory/Children’s/Georgia Tech Center for Childhood Infections and Vaccines. Experiments with rhesus macaques were performed at Yerkes National Primate Research Center. 
 
 Moore co-founded and serves as chief scientific officer for Meissa Vaccines, Inc. Lee, Nguyen and Moore are co-inventors in a patent application describing the rhinovirus vaccine reported in the Nature Communications paper. ||||| Sore throat and runny nose are usually the first signs of a cold, followed by coughing and sneezing. Most people recover in about 7-10 days. You can help reduce your risk of getting a cold: wash your hands often, avoid close contact with sick people, and don’t touch your face with unwashed hands. 
 
 Common colds are the main reason that children miss school and adults miss work. Each year in the United States, there are millions of cases of the common cold. Adults have an average of 2-3 colds per year, and children have even more. 
 
 Most people get colds in the winter and spring, but it is possible to get a cold any time of the year. Symptoms usually include: 
 
 sore throat 
 
 runny nose 
 
 coughing 
 
 sneezing 
 
 headaches 
 
 body aches 
 
 Most people recover within about 7-10 days. However, people with weakened immune systems, asthma, or respiratory conditions may develop serious illness, such as bronchitis or pneumonia. 
 
 Help reduce your risk of getting a cold by washing hands often with soap and water. Practice good cough and sneeze etiquette: always cough and sneeze into a tissue or your upper shirt sleeve, completely covering your mouth and nose. 
 
 How to Protect Yourself 
 
 Viruses that cause colds can spread from infected people to others through the air and close personal contact. You can also get infected through contact with stool (poop) or respiratory secretions from an infected person. This can happen when you shake hands with someone who has a cold, or touch a surface, like a doorknob, that has respiratory viruses on it, then touch your eyes, mouth, or nose. 
 
 You can help reduce your risk of getting a cold: 
 
 Wash your hands often with soap and water. Wash them for 20 seconds, and help young children do the same. If soap and water are not available, use an alcohol-based hand sanitizer. Viruses that cause colds can live on your hands, and regular handwashing can help protect you from getting sick. 
 
 Wash them for 20 seconds, and help young children do the same. If soap and water are not available, use an alcohol-based hand sanitizer. Viruses that cause colds can live on your hands, and regular handwashing can help protect you from getting sick. Avoid touching your eyes, nose, and mouth with unwashed hands. Viruses that cause colds can enter your body this way and make you sick. 
 
 Viruses that cause colds can enter your body this way and make you sick. Stay away from people who are sick. Sick people can spread viruses that cause the common cold through close contact with others. 
 
 How to Protect Others 
 
 If you have a cold, you should follow these tips to help prevent spreading it to other people: 
 
 Stay at home while you are sick 
 
 Avoid close contact with others, such as hugging, kissing, or shaking hands 
 
 Move away from people before coughing or sneezing 
 
 Cough and sneeze into a tissue then throw it away, or cough and sneeze into your upper shirt sleeve, completely covering your mouth and nose 
 
 Wash your hands after coughing, sneezing, or blowing your nose 
 
 Disinfect frequently touched surfaces, and objects such as toys and doorknobs 
 
 There is no vaccine to protect you against the common cold. 
 
 How to Feel Better 
 
 There is no cure for a cold. To feel better, you should get lots of rest and drink plenty of fluids. Over-the-counter medicines may help ease symptoms but will not make your cold go away any faster. Always read the label and use medications as directed. Talk to your doctor before giving your child nonprescription cold medicines, since some medicines contain ingredients that are not recommended for children. Learn more about symptom relief of upper respiratory infections, including colds. 
 
 Antibiotics will not help you recover from a cold caused by a respiratory virus. They do not work against viruses, and they may make it harder for your body to fight future bacterial infections if you take them unnecessarily. Learn more about when antibiotics work. 
 
 When to See a Doctor 
 
 You should call your doctor if you or your child has one or more of these conditions: 
 
 symptoms that last more than 10 days 
 
 symptoms that are severe or unusual 
 
 if your child is younger than 3 months of age and has a fever or is lethargic 
 
 You should also call your doctor right away if you are at high risk for serious flu complications and get flu symptoms such as fever, chills, and muscle or body aches. People at high risk for flu complications include young children (younger than 5 years old), adults 65 years and older, pregnant women, and people with certain medical conditions such as asthma, diabetes and heart disease. 
 
 Your doctor can determine if you or your child has a cold or the flu and can recommend therapy to help with symptoms. 
 
 Causes of the Common Cold 
 
 Many different respiratory viruses can cause the common cold, but rhinoviruses are the most common. Rhinoviruses can also trigger asthma attacks and have been linked to sinus and ear infections. Other viruses that can cause colds include respiratory syncytial virus, human parainfluenza viruses, adenovirus, human coronaviruses, and human metapneumovirus. 
 
 Know the Difference between Common Cold and Flu 
 
 The flu, which is caused by influenza viruses, also spreads and causes illness around the same time as the common cold. Because these two illnesses have similar symptoms, it can be difficult (or even impossible) to tell the difference between them based on symptoms alone. In general, flu symptoms are worse than the common cold and can include fever or feeling feverish/chills, cough, sore throat, runny or stuffy nose, muscle or body aches, headaches and fatigue (tiredness). Flu can also have very serious complications. CDC recommends a yearly flu vaccination as the first and best way to prevent the flu. If you get the flu, antiviral drugs may be a treatment option. ||||| Cell lines and viruses 
 
 H1-HeLa (CRL-1958) and WI-38 (CCL-75) cells were obtained from the American Type Culture Collection (ATCC) and cultured in minimal essential media with Richter’s modification and no phenol red (MEM) (Thermo Fisher) supplemented with 10% fetal bovine serum. The cell lines were not authenticated but are not commonly misidentified (International Cell Line Authentication Committee). We tested HeLa-H1 cells using the LookOut Mycoplasma detection kit (Sigma), and these were mycoplasma negative. HRV-7 (VR-1601), HRV-9 (VR-1745), HRV-11 (VR-1567), HRV-13 (VR-286), HRV-14 (VR-284), HRV-16 (VR-283), HRV-19 (V4-1129), HRV-24 (VR-1134), HRV-29 (VR-1809), HRV-30 (VR-1140), HRV-31 (VR-1795), HRV-32 (VR-329), HRV-36 (VR-509), HRV-38 (VR-511), HRV-40 (VR-341), HRV-41 (VR-1151), HRV-49 (VR-1644), HRV-53 (VR-1163), HRV-56 (VR-1166), HRV-58 (VR-1168), HRV-59 (VR-1169), HRV-60 (VR-1473), HRV-64 (VR-1174), HRV-66 (VR-1176), HRV-68 (VR-1178), HRV-75 (VR-1185), HRV-76 (VR-1186), HRV-77 (VR-1187), HRV-78 (VR-1188), HRV-80 (VR-1190), HRV-81 (VR-1191), HRV-85 (VR-1195), HRV-88 (VR-1198), HRV-89 (VR-1199), HRV-96 (VR-1296), and HRV-100 (VR-1300) prototype strains were purchased from ATCC. HRV-1B, HRV-10, HRV-21, HRV-28, HRV-33, HRV-34, HRV-39, HRV-45, HRV-50, HRV-51, HRV-54, HRV-55 and HRV-94 strains were obtained from the Centers for Disease Control and Prevention. The HRVs in the study are species A, with the exception of HRV-14 (B), and represent A species broadly20,21. 
 
 HRV propagation and titration 
 
 HRV stocks were generated in H1-HeLa cells. Approximately 0.5 ml of HRV was inoculated onto subconfluent H1-HeLa monolayer cells in a T-182 flask. After adsorption for 1 h at room temperature with rocking, 50 ml of HRV infection medium (MEM supplemented with 2% FBS, 20 mM HEPES, 10 mM MgCl 2 , 1 × non-essential amino acids (Gibco catalog 11140-050)) was added and the infection was allowed to proceed at 32 °C in a 5% CO 2 humidified incubator until the monolayer appeared to be completely involved with cytopathic effect (CPE), 1 to 3 days post-infection. The cells were scraped, and the cells and medium (∼50 ml) were transferred to two pre-chilled 50 ml conical polypropylene tubes and kept on ice while each suspension was sonicated using a Sonic Dismembrator Model 500 (Fisher Scientific) equipped with a ½-inch diameter horn disrupter and 1/4-inch diameter tapered microtip secured on a ring stand. Sonication was performed by an operator in a closed room with ear protection, at 10% amplitude, 1 s on/1 s off intervals and 1 pulse per 1 ml of material. Sonication yielded higher titres than freeze–thaw. The suspension was clarified by centrifugation at 931g for 10 min. The supernatant was transferred to cryovials, snap-frozen in liquid nitrogen and stored at −80 °C. For comparing HRV yield in H1-HeLa and WI-38 cells, T-75 flasks of subconfluent cells were infected at a multiplicity of infection of 0.1 TCID 50 per cell, and 20 ml of culture medium were discarded before scraping the cells in the remaining 5 ml followed by sonication. For all stocks, TCID 50 ml−1 titres were determined by infecting subconfluent H1-HeLa cells in 96-well plates with serially diluted samples, staining the cells 6 days post-infection with 0.1% crystal violet/20% methanol, scoring wells for CPE and calculating the end point titre using the Reed and Muench method38. 
 
 HRV purification 
 
 HRV stock was collected from H1-HeLa cell monolayers as described above and clarified by brief centrifugation at low speed to remove large cellular debris (931g, 10 min, 4 °C). To remove excess albumin from the crude virus stock by affinity chromatography, the supernatant was loaded onto a HiTrap Blue HP column (GE Healthcare) using an ÄKTA Purifier system (GE Healthcare) according to the manufacturer specifications. Flowthrough was subsequently loaded through a HiTrap Capto Core 700 column (GE Healthcare) to refine the virus prep by size exclusion chromatography. The flowthrough from the HiTrap Blue HP and the HiTrap Capto Core 700 was captured using the ÄKTA Purifier system (GE Healthcare) with a 20 mM sodium phosphate buffer (pH 7.0). Flowthrough from size exclusion chromatography was dialyzed overnight with 0.1 M Tris-HCl buffer (pH 8.0), then loaded onto a HiTrap Q XL column (GE Healthcare) and separated into fractions by ion exchange chromatography. Virus-containing fractions were eluted using the ÄKTA Purifier system (GE Healthcare) with a 0.1 M Tris-HCl buffer (pH 8.0) and a sodium chloride gradient. Fractions showing high absorption peaks at 280 nM were collected and analysed for viral titre by TCID 50 end point dilution assay, and fraction purity visualized on a 10% SDS-PAGE gel by silver stain (Thermo Fisher Scientific; Supplementary Fig. 6 and Supplementary Table 4). Fractions of HRV-16, HRV-36 and HRV-78 of high virus titre and purity were combined for formalin inactivation as described below. 
 
 Mice and RMs 
 
 All experiments involving animals were performed at Emory University and the Yerkes National Primate Research Center in accordance with guidelines established by the Animal Welfare Act and the NIH Guide for the Care and Use of Laboratory Animals. Animal facilities at Emory University and the Yerkes Center are fully accredited by the Association for Assessment and Accreditation of Laboratory Animal Care International (AAALAC). The Institutional Animal Care and Use Committee (IACUC) of Emory University approved these studies. Pathogen-free, 6–7-week female BALB/c mice were purchased from the Jackson Laboratory (Bar Harbor, ME, USA). Mice were randomly assigned to groups based on the sequential selection from an inventory, and investigators were not blinded to outcome assessment. No statistical methods were used in predetermining sample sizes. 
 
 Young adult (3–5 kg, 2–4 years of age, 2 females and 2 males) Indian RMs (Macaca mulatta; RM) were maintained according to NIH guidelines at the Yerkes National Primate Research Center. Handling and movement of RMs was performed by qualified personnel who have received specific training in safe and humane methods of animal handling at the Yerkes National Primate Research Center. The initial exclusion criterion was pre-existing nAb against HRV. The studies were performed in strict accordance with US Department of Agriculture regulations and the recommendations in the Guide for Care and Use of Laboratory Animals of the NIH. The RMs were allocated in an un-blinded manner to two vaccine groups (25-valent and 50-valent), one male and one female per group. No statistical methods were used in predetermining sample sizes. 
 
 Vaccination 
 
 Before immunization, all HRV types were inactivated by addition of 0.025% formalin followed by incubation with stirring for 72 h at 37 °C, as previously described for HRV vaccine33. Complete inactivation of infectivity was confirmed by end point TCID 50 titration in H1-HeLa cells. Formalin inactivation by this method resulted in greater immunogenicity in mice than alternative inactivation by β-propiolactone, suggesting formalin inactivation preserved antigenic determinants. Mice were vaccinated i.m. with inactivated HRV strains mixed with 100 μg of Alhydrogel adjuvant 2% (aluminium hydroxide wet gel suspension, alum; Sigma catalog A8222 or Invivogen catalog vac-alu) according to instructions of the manufacturers. The total volume per mouse was 100 μl, administered in 50 μl per thigh. Mice were given a second identical vaccination (boost) at the time indicated in figure legends. RMs were vaccinated i.m. with inactivated HRV strains mixed with 500 μg of Alhydrogel adjuvant 2%. The total volume per RM was 1 ml, administered in one leg. RMs were boosted with an identical vaccination at four weeks. 
 
 Serum collection 
 
 In mice, peripheral blood was collected into microcentrifuge tubes from the submandibular vein. Samples were incubated at room temperature for 20 min to clot. The tubes were centrifuged 7,500g for 10 min to separate serum. The serum samples were pooled from mice of each group and stored at −80 °C until used. Phlebotomy involving RMs was performed under either ketamine (10 mg kg−1) or Telazol (4 mg kg−1) anaesthesia on fasting animals. Following anaesthesia with ketamine or Telazol, the animals were bled from the femoral vein. Yerkes blood collection guidelines were followed and no more than 10 ml kg−1 per 28 days of blood was collected. After collecting blood in serum separating tube, samples were incubated at room temperature for 30 min. The tubes were centrifuged at 2,500g for 15 min to separate serum. The serum samples from individual RM were stored at −80 °C until used. 
 
 Serum neutralization assay 
 
 H1-HeLa cells were seeded in 96-well plates to attain 80–90% confluence in 24 h. Due to the limited volume of mouse serum per bleed and the number of nAb assays required, we pooled mouse sera. After separating serum from whole blood, equal volumes of sera per mouse were pooled from each group, before heat inactivation. Levels of nAb against the indicated HRV types in the vaccines used in mice were measured in pooled sera. Heat-inactivated (56 °C, 30 min) serum samples were twofold serially diluted in MEM and added to 500 TCID 50 ml−1 HRV of each type to be tested, in an equal volume. The virus and serum mixtures were incubated at 37 °C for 1 h. Then, 50 μl of the serum–virus mixture was transferred onto H1-HeLa cell monolayers in 96-well plates in triplicate, and plates were spinoculated at 2,095g for 30 min at 4 °C. For each type, a no-serum control was added to test the input 500 TCID 50 . We tested pooled HRV-16 anti-sera against HRV-16 in each assay as a standard. After spinoculation, 150 μl of HRV infection medium were added to each well. The 96-well plates were incubated for 6 days at 32 °C and 5% CO 2 and then stained with crystal violet as described above. Wells were scored for the presence or absence of CPE. Neutralizing antibody end point titres and 95% confidence intervals were determined by the method of Reed and Muench38, as previously described for HRV14,38. The 95% confidence interval indicates variability of three technical replicates within a single nAb experiment. An example of the nAb assay and titre calculation is provided in Supplementary Fig. 7. 
 
 Data availability 
 
 Primary data that support the findings of this study are available from the corresponding author on request. ||||| Time and again, 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.” 
 
 This article originally published at STAT here
– When an expert in rhinoviruses told Martin Moore in 2013 that there would never be a vaccine for the common cold, the Emory University professor thought to himself, "Well, let's look into that." Three years later, it appears his probing against the odds has paid off: Per a study published last month in the journal Nature, mice and macaque monkeys given a vaccine developed by Moore and his team have been able to work up antibodies against a variety of rhinoviruses, which most often are the cause of the common cold, Mashable reports. Not that Moore is the sole pioneer on this landscape: Other researchers at colleges and with pharma companies have been toiling away in labs seeking a similar remedy for the coughing, sneezing, and sniffling that the CDC notes is the main reason why kids miss school and grownups call in sick to work. Per an Emory press release, even though scientists in the '60s were able to develop a vaccine effective against one type of rhinovirus, it didn't work against the many other varieties that exist; Mashable pegs that figure at more than 160. So Moore mixed together 50 different rhinoviruses—gathered from immunologist James Gern, who keeps what he calls "one of the world’s biggest collections of kid snot"—into one vaccine, "like a bunch of slightly different Christmas ornaments." Post-vaccine, the monkeys had developed antibodies in their blood for 49 out of the 50 viruses; similar results were found in the mice. Moore is hoping to eventually test the vaccine out on humans. "We think that creating a vaccine for the common cold can be reduced to technical challenges related to manufacturing," he says. (Here's why colds are more common when the mercury drops.)