Rhinovirus and the Common Cold Explained

The Centers for Disease Control and Prevention (CDC) says more than 200 respiratory viruses can cause a cold, and that rhinoviruses are the most common cause in the United States. Adults average two to three colds a year, and children often get more. Yet there is no vaccine, and the antiviral that came closest was never licensed in the United States. The obstacle is not neglect. Rhinovirus is a small, fast-changing, many-faced virus, and the misery it brings is partly the work of your own immune response. This article explains how rhinovirus gets into cells, why it prefers the nose, why vaccines keep failing, and what controlled trials say about the remedies on the pharmacy shelf.

Educational content, not medical advice. Talk to your doctor before changing any medication, treatment, or routine. Information here reflects current research but every person's situation differs.

What rhinovirus is, and how many kinds there are

Rhinovirus belongs to the family Picornaviridae, a group of small RNA viruses whose name combines "pico," meaning very small, with RNA. Its genome is a single strand of positive-sense RNA about 7,200 bases long. Positive-sense means the strand can be read directly by a cell's protein-making machinery, much as a recipe card can be cooked from without being rewritten. The genome is translated into one long chain of protein, which is then cut into 11 final proteins. Four of them, VP1 to VP4, form the outer shell, called the capsid, with 60 copies of each.

The species are named A, B, and C. According to a 2013 review in Clinical Microbiology Reviews, species A has 74 serotypes and species B has 25 among the original 99 strains, and at least 50 types of species C have since been identified. A serotype is a variant distinguished by how antibodies recognize it. In 2009, a team led by Ann Palmenberg completed genome sequences for all 99 known strains, published in Science, and found a structure in all of them that may explain their rapid translation inside cells.

Species C deserves special mention. It was recognized as a separate species by the International Committee on Taxonomy of Viruses in 2009, and it was first grown in the laboratory only in 2011, which helps explain why culture-based methods missed it for so long.

Feature	Rhinovirus A	Rhinovirus B	Rhinovirus C
Known types (2013 review)	74	25	At least 50
Grown in lab culture	Yes	Yes	First in 2011
Seasonal pattern	Early fall peak and a smaller spring peak in temperate climates (A and B combined)	Same	Fall or winter in most temperate and subtropical regions

On receptors, the 2013 review notes that the "major group," more than 90 percent of known serotypes, uses ICAM-1, and the "minor group" uses LDLR. That review listed the receptor for species C as unknown. It was identified two years later, as described below.

How the virus gets in: a key and a lock

Every virus needs a way to attach to a cell, and the receptor it chooses defines much of its behavior. Think of the capsid as a ring of keys and the receptor as a lock on the cell surface. Most rhinoviruses carry keys that fit ICAM-1, a protein on the surface of cells lining the airway. ICAM-1 normally helps immune cells stick to blood vessel walls during inflammation, so the virus is borrowing a doorway that exists for the body's own defense.

Once the virus is attached, it delivers its RNA into the cell. The cell treats it as its own instructions, builds viral proteins, and assembles new virus particles, which are released to infect neighboring cells. For a broader tour of that process, see how viruses work from infection to replication.

A minority of types use a different receptor, LDLR, which normally handles cholesterol particles. And species C uses CDHR3, a protein that is highly expressed in the cells lining the airway. In a 2015 PNAS study, Yury Bochkov and colleagues showed that expressing CDHR3 allowed otherwise resistant cells to bind and replicate species C. A variant of the protein with tyrosine at position 529, which is linked to asthma risk, bound the virus and produced progeny virus about 10 times more efficiently than the standard version.

Why the nose, and what temperature has to do with it

One of the best-known facts about rhinovirus is that it grows well at nasal temperature, around 33 to 35 degrees Celsius, cooler than the roughly 37 degrees at the core of the body. The picture is more nuanced than the usual retelling. The 2013 review notes that early studies suggested 33 degrees as optimal, but that a 1999 study of eight strains found minimal differences between 33 and 37 degrees, and some types grew equally well or better at 37.

A 2015 PNAS study by Ellen Foxman and colleagues in the laboratory of Akiko Iwasaki offers a mechanism. Working in primary mouse airway cells with a mouse-adapted rhinovirus, they found that at 37 degrees the cells mounted stronger antiviral responses, with more type I and type III interferons (signaling proteins that put neighboring cells on alert). When the interferon pathway was blocked, the virus grew better at 37 degrees. The authors concluded that rhinovirus replicates preferentially at nasal temperature partly because infected cells mount a weaker defense when cool.

Two cautions apply. The experiment used mouse cells, and a result in mouse cells does not guarantee the same size of effect in people. And the study does not say that chilling yourself causes colds. It says something about how quickly cells in a cooler nose raise their defenses once infected.

Your cold: virus damage or immune response?

For many years, textbooks said cold symptoms come mostly from the immune system rather than from the virus. The truth is mixed. The 2013 review concludes that rhinovirus pathogenesis, drawn mostly from laboratory cell data and experimental infection of healthy adults, involves both direct viral effects and tissue damage due to the host immune response. In other words, do not picture a virus quietly destroying your nose, and do not picture your immune system as the sole culprit either.

The timeline of a typical cold is reasonably well documented.

Event	Typical timing	Source
Incubation	Average of about 2 days	Jacobs et al., 2013
Virus shedding	From about 1 day before symptoms to about 6 days after, highest in the first 2 days	Jacobs et al., 2013
Symptom peak	Within 2 to 3 days of infection	CDC
Duration	CDC: usually less than a week; the 2013 review gives a range of 7 to 14 days	CDC; Jacobs et al., 2013

The two duration figures differ because they describe different things. A cold's worst days are over quickly, but a lingering cough or stuffy nose can persist into the second week. The overlap between the shedding window and the symptom peak explains why people are most contagious just when they feel worst, and why they can pass the virus on before feeling sick at all.

Sneezing, a runny nose, and congestion are the body's attempt to flush and wall off the infection. Our explainer on why we sneeze covers the reflex, and the broader response is described in how the immune system fights viruses step by step. When a fever does accompany an infection, it is part of a defensive response, as covered in why fevers help fight infections.

How it spreads: contact, droplets, and what a card game showed

CDC states that most respiratory viruses spread through droplets from coughs or sneezes, or by touching a contaminated surface and then your eyes, nose, or mouth. Rhinovirus is no exception, and the review summarizes experiments that show which route matters more than people assume.

• In an experimental study, aerosol transmission occurred in 56 percent of 18 volunteers who played cards for 12 hours with infected subjects while kept from touching them.
• In a study of 24 couples, transmission occurred in 9 couples over contact periods of 63 to 149 hours.
• The virus survives on undisturbed skin for about 2 hours.

The takeaway is that the hands-versus-air argument does not have a single winner. Both contact and aerosol spread occur. A related finding on prevention is also humbling. In a challenge study, ethanol hand sanitizer removed detectable virus from fingertips more effectively than soap and water, at 80 percent versus 31 percent efficacy. But a trial in natural settings of hand treatment showed no difference in rhinovirus infection. Cleaning your hands removes the virus from your hands, which does not guarantee fewer colds in daily life.

Why a rhinovirus vaccine does not exist

A vaccine needs a stable target: a part of the virus that looks similar across strains, so that antibodies made against it protect against many of them. The influenza vaccine is updated every year precisely because its target changes, but it can be updated because there are only a few lineages to track. Rhinovirus offers no such shortcut.

The 2013 review states that more than 100 serotypes exist, that antigenic sites vary greatly in sequence, and that there is little cross-neutralization among serotypes. That last phrase is the crux. An antibody that neutralizes type 14 does little to type 89, so immunity to one cold does not carry over to the next. A vaccine would have to cover all of them at once, which is like trying to build one key that opens more than 100 different locks. As of that review, no rhinovirus vaccine had been tested in clinical trials.

The answer to "why can't we just make a cocktail of all the types?" is practical rather than theoretical. A multivalent product would need to include every circulating type, and the number of types keeps growing as new ones are identified. The target is also a moving one, since the virus evolves.

The picture for antivirals is similar. Pleconaril, an oral drug that binds the capsid, shortened illness by one day compared with placebo in a phase 3 trial, according to the same review, but licensing in the United States was withheld because of safety concerns. A drug that gives a one-day benefit for a mild illness has to clear a high safety bar, and this one did not.

Rhinovirus, asthma, and the children who get it worst

For most healthy adults a cold is a nuisance. For people with asthma or other airway disease, the same virus can be a trigger for serious illness. The 2013 review states that about two-thirds of respiratory virus-associated asthma exacerbations are due to rhinovirus. It also cites studies finding that children with rhinovirus-associated wheezing in outpatient settings were 10 times more likely to have asthma at age six, and that infants hospitalized with rhinovirus-associated wheezing had about four times the childhood asthma risk of those whose wheezing had other viral causes. These are associations. They do not show that the virus causes asthma, because children who are already prone to airway disease may be the ones who wheeze with a cold.

The genetics point in a similar direction. A 2014 genome-wide association study in Nature Genetics by Klaus Bønnelykke and colleagues compared 1,173 children with recurrent, severe asthma exacerbations between ages two and six against 2,522 controls and identified CDHR3 as a new susceptibility gene. Later work connected the dots with the virus. A 2018 study in the American Journal of Respiratory and Critical Care Medicine reported that the asthma risk allele was associated with more respiratory illnesses, specifically those involving species C. A 2025 study in Virology Journal of 11,756 respiratory specimens from hospitalized children found species C to be the dominant rhinovirus species linked to wheezing, and the same variant was associated with a higher risk of infection with it.

The story is not finished. A 2026 study in Microbiology Spectrum compared airway cell cultures from children and adults and found similar CDHR3 levels, similar viral replication, and comparable innate immune responses. The authors concluded that those factors alone are unlikely to explain why species C causes more severe disease in young children, and suggested that immature antibody responses and other developmental differences may matter more. If you are interested in other viruses that affect the lower airway, our article on RSV is a good companion, as is the piece on seasonal coronaviruses.

Stress and colds: a classic experiment

One of the most cited studies in the field asked whether psychological stress changes susceptibility. In 1991, Sheldon Cohen, David Tyrrell, and Andrew Smith reported in the New England Journal of Medicine on 394 healthy adults who completed stress questionnaires and then received nasal drops containing one of five respiratory viruses, while another 26 received saline. Participants were quarantined and monitored.

Infection and clinical cold rates rose with stress in a dose-response pattern. Infection rates ranged from about 74 to 90 percent, and clinical colds from about 27 to 47 percent. The link held after adjustment and across all five viruses, and smoking, alcohol, exercise, diet, sleep, white cell counts, and personality traits did not explain it. The authors concluded that higher stress was associated with greater risk mainly because of higher infection rates, not because of more symptoms after infection. Note that the viruses were not all rhinoviruses, so the study speaks to respiratory viruses in general. For background on the hormonal side, see cortisol and the stress response.

What the evidence says about remedies

The table below summarizes leading systematic reviews, with the caveats the authors themselves state. This is a summary of research, not a recommendation to take anything.

Remedy	Review	Main finding	Key caveat
Zinc	Singh and Das, Cochrane, 2013 (16 therapeutic trials, 1,387 participants)	Shortened symptom duration by about 1 day (mean difference -1.03 days, 95% CI -1.72 to -0.34) when started within 24 hours	Very high heterogeneity (I-squared 89%); bad taste and nausea more common
Vitamin C	Hemila and Chalker, Cochrane, 2013 (29 comparisons, 11,306 participants)	No reduction in colds in the general community (risk ratio 0.97, 95% CI 0.94 to 1.00); colds 8% shorter in adults and 14% shorter in children with regular use	No consistent effect when started after symptoms began
Echinacea	Karsch-Volk et al., Cochrane, 2014 (24 trials, 4,631 participants)	No statistically significant prevention in any of 12 comparisons measuring incidence; one of seven treatment trials showed a benefit	Preparations differ widely
Antihistamines	De Sutter et al., Cochrane, 2015 (18 trials, 4,342 participants)	Short-lived benefit on days 1 and 2 (45% vs 38% with placebo), none by days 3 to 4	Authors considered the improvements clinically non-significant; sedation
Saline nasal irrigation	King et al., Cochrane, 2015 (five trials)	Possible benefit, but evidence is low quality	Most outcomes showed no difference

Zinc

The zinc review is the most encouraging, and also the most uncertain. Zinc given within 24 hours of the first symptoms shortened colds on average, and the authors suggested lozenges at 75 milligrams a day or more if zinc is used at all. For prevention, two trials with 394 participants gave an incidence rate ratio of 0.64, but the authors said there was insufficient data for a firm recommendation. Adverse events were more common with zinc, including a bad taste (odds ratio 2.31) and nausea (odds ratio 2.15). The 2013 review also reports that zinc is thought to block rhinovirus binding to ICAM-1 and to decrease histamine release, although a mechanism proposed in a laboratory is not proof of one in a nose. A Cochrane update that appeared in 2015 is listed in the database as withdrawn.

Vitamin C

Linus Pauling's name is attached to the idea that vitamin C prevents colds, and the evidence has not supported it for the general public. The Cochrane review found a risk ratio near 1.0 in community trials of 10,708 participants. But in five trials of 598 marathon runners, skiers, and soldiers on subarctic exercises, the risk ratio was 0.48 (95% CI 0.35 to 0.64), a halving of cold risk under brief extreme physical stress. For regular users, colds were modestly shorter. Seven therapeutic trials, where vitamin C was started after symptoms began, showed no consistent effect on duration or severity. The authors concluded that routine supplementation is not justified for the general population.

Antihistamines, saline, and honey

The antihistamine story shows how a mechanism can sound better than the clinical result. First-generation antihistamines (the sedating kind) cut sneezing and runny nose in some trials. The 2013 review cites reductions in sneeze and runny-nose scores of up to 50 and 62 percent for clemastine and brompheniramine given over four days, with no difference in other symptoms. The Cochrane review, across 18 trials, found benefits that did not persist beyond the first days and that the authors deemed clinically non-significant.

Saline nasal irrigation looks safe and plausible, but the Cochrane review judged the evidence low quality: one larger pediatric trial found reductions in nasal secretion and obstruction scores, which the authors noted may have minimal clinical significance. For cough in children, a separate Cochrane review (Oduwole and colleagues, 2018) found that honey probably reduces cough frequency compared with no treatment or placebo, with moderate-certainty evidence, and that it showed no clear advantage beyond three days. That review concerned cough in children, not colds as a whole.

Antibiotics do nothing for a cold

Antibiotics act on bacteria, and a cold is a viral illness, so they have no role in treating one. The scale of misuse is documented. A 2016 CDC-led study in JAMA analyzed 184,032 US outpatient visits from 2010 to 2011 and estimated that acute respiratory conditions accounted for 221 antibiotic prescriptions per 1,000 people each year, of which only 111 were appropriate. Across all conditions, about 506 prescriptions per 1,000 people were written and an estimated 353 were appropriate, which means about 30 percent were not. The consequences are covered in how antibiotic resistance spreads and why antibiotics are running out.

The cost of the common cold

The best-known cost estimate is old, and it covers more than rhinovirus. In a 2003 study in Archives of Internal Medicine, A. Mark Fendrick and colleagues surveyed 4,051 US households between November 2000 and February 2001. About 72 percent of respondents reported a non-influenza viral respiratory infection in the past year, averaging 2.5 episodes. Extrapolated to the population, that is roughly 500 million episodes a year, with a total economic impact estimated at about $40 billion annually, made up of $17 billion in direct costs and $22.5 billion in indirect costs such as lost work.

Three caveats matter. The survey measured non-influenza viral respiratory infections, which include rhinovirus but also other viruses. The figure is in 2000s dollars. And it relied on self-reports. It is best read as an order-of-magnitude estimate that shows how a mild illness, repeated across a population, adds up.

Comparing rhinovirus with flu and COVID-19

Feature	Rhinovirus	Influenza	SARS-CoV-2
Virus family	Picornaviridae	Orthomyxoviridae	Coronaviridae
Genome	Single-strand RNA, positive-sense	Single-strand RNA, negative-sense, segmented	Single-strand RNA, positive-sense
Main receptor	ICAM-1, LDLR, or CDHR3 depending on type	Sialic acid	ACE2
Typical illness site	Nose and throat; can reach the lower airway in some people	Upper and lower airway	Upper and lower airway
Vaccine	None	Yes, updated regularly	Yes
Serotype diversity	More than 100 serotypes	A few circulating lineages	Variants

The rhinovirus entries on receptors come from the sources discussed above. The comparison with influenza and SARS-CoV-2 reflects standard virology textbooks. For a deeper look at the flu, see our influenza explainer.

What people get wrong about colds

Cold weather does not directly cause colds. The seasonal pattern is real. The 2013 review describes an early fall peak and a smaller spring peak in temperate climates, and CDC notes you can catch a cold at any time of year. The cause of the pattern is not settled. Cooler nasal temperatures may slow the cell's early antiviral response, according to the mouse-cell study, and behavior changes that bring people together indoors likely matter, but neither explanation has been proven to account for the whole pattern.

A cold is not weakness in your immune system. Having several a year is normal for adults, in the range of two to three according to CDC. Frequency probably reflects how many different serotypes you meet as much as how strong your defenses are.

Antibiotics are not a safety net. A cold that lingers or worsens may signal a complication, such as a middle ear or sinus infection, which CDC lists as mild complications. Those are decisions for a clinician, not a reason to demand antibiotics.

Rhinovirus is not always mild. CDC lists asthma attacks, bronchitis, bronchiolitis, and pneumonia among potentially severe complications of common cold viruses. People with airway disease, infants, and those with weakened immunity deserve extra caution.

The takeaway

Rhinovirus is hard to beat because it is a swarm rather than a single enemy: more than 100 serotypes, little cross-neutralization, a capsid that antivirals struggle to hit safely, and a preference for the cooler nose where defenses start slowly. What medicine can offer is modest. Zinc may trim about a day off a cold at the cost of side effects, vitamin C helps mostly under extreme physical stress, and antibiotics do nothing. The clearest finding of recent years is the link between CDHR3 and species C, which turned a vague association between colds and childhood asthma into a specific molecular mechanism that may one day be a target.

Frequently Asked Questions

Q: Why can't scientists make a rhinovirus vaccine? A: Rhinovirus has more than 100 serotypes, the antigenic sites vary greatly, and antibodies against one type provide little cross-neutralization against others. A vaccine would need to cover every circulating type at once. As of a 2013 review, none had been tested in clinical trials.

Q: Can you catch the same cold twice? A: Repeated colds are expected because immunity to one serotype does little against others. The same type can in principle return, but studies cited here do not quantify how long protection to a specific serotype lasts, so no precise figure can be given. Adults average two to three colds a year, according to CDC.

Q: Does cold weather or wet hair cause colds? A: No direct evidence supports wet hair as a cause. Infection requires exposure to the virus. A 2015 mouse-cell study suggests cooler nasal temperatures may slow the cell's antiviral response, but it did not test whether chilling the body makes people more likely to catch a cold.

Q: Does zinc actually work? A: A 2013 Cochrane review found that zinc started within 24 hours of symptoms shortened colds by about one day on average, but the trials varied widely and bad taste and nausea were more common. It found insufficient data to recommend zinc for prevention. Talk to a clinician before taking supplements, particularly over long periods.

Q: Does vitamin C prevent colds? A: Not in the general population, according to a 2013 Cochrane review of 29 comparisons with 11,306 participants. The exception was people under brief, extreme physical stress, such as marathon runners and soldiers on subarctic exercises, where the risk ratio was 0.48. Started after symptoms began, it showed no consistent effect.

Q: Why is rhinovirus linked to asthma attacks? A: Rhinovirus accounts for about two-thirds of virus-associated asthma exacerbations, according to a 2013 review. Species C binds CDHR3, and a CDHR3 variant tied to asthma risk raises binding of the virus about 10-fold in cell experiments. Researchers are still working out why young children are affected most.

Q: Does stress make colds more likely? A: In a 1991 quarantine study of 394 adults exposed to five respiratory viruses, higher psychological stress scores were associated with higher infection rates (about 74 to 90 percent) and clinical colds (about 27 to 47 percent) in a dose-response pattern. It shows an association with susceptibility to respiratory viruses in general.

Sources

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