Electron micrograph of differentiated human nasal epithelial organoids with cilia of multiciliated cells accentuated in blue.
Credit: Julien Amat, Bao Wang.
You might expect an intelligently designed system, created by an omnibenevolent designer, to work just as effectively for everybody and not badly for some and only just adequately for others. And yet, as so often with creationism, the facts are not at all what the theory predicts. In science this would be called falsification, but for creationists it is just another inconvenient fact to be ignored or blamed on ‘the Fall’ — or even on the victim.
According to a paper just published in Cell Press Blue, the reason some people suffer more from a cold caused by a rhinovirus is not so much because of differences in the virus, but because their bodies react differently. Some take control and prevent the spread of viruses to adjacent cells of the mucous membrane lining the nasal passages, whereas other people’s bodies fail to prevent the virus spreading.
The paper is by a team at Yale School of Medicine, New Haven, CT, USA, led by Associate Professor Dr Ellen F. Foxman, PhD.
By growing organoids in vitro and infecting them with rhinoviruses, the team were able to show that whether the infection spreads depends on how quickly the infected cells are able to mount an interferon response. A good response limits the infection to just a few cells and the cold does not develop beyond a ‘sniffle’. Where the response is weak, the infection spreads and, in cases where the victim has an underlying respiratory condition such as asthma or COPD, the cold can develop into a serious illness.
Why the interferon response differs between individuals is not known with any certainty, but it could be due to a number of factors, including genetics. However, it is known that in patients with pre-existing respiratory conditions, the interferon response is inhibited.
That, of course, begs the question for ID creationists: why a system supposedly designed to protect us gets downgraded when it is most needed, and, if the difference is due to underlying genetics, why some people got better genes in this respect than others. Under the ID creationist paradigm, genes that produce any given output are deemed to hold ‘complex specified genetic information’ and, as such, are evidence for intelligent design.
Leaving aside the question of why any omnibenevolent designer would design viruses to make us sick and then design an immune response to prevent them doing so, we are left with the question of why this immune system does not always work very well and why some people have a worse version than others. If an omnibenevolent designer can design an effective immune system, why did it not give it to everyone? Does it actually want those people to suffer more from the viruses it supposedly designed?
The evolutionary explanation is, of course, straightforward, with none of the theological conundrums that plague creationism. Evolution does not seek out perfection and has no interest in equity. In the environment of an evolutionary arms race with viruses, the results are inevitably suboptimal and unevenly distributed throughout the population unless there is particularly strong selection pressure to drive the ‘best’ solution to fixation. It is also in the survival interests of viruses to tone down their victim’s responses, thereby reducing that selection pressure. The resulting trade-off and compromise is what we see today in the different responses to the same virus.
Rhinoviruses – The Common Cold Viruses. Rhinoviruses are a large group of small, non-enveloped RNA viruses belonging to the family Picornaviridae. They are the single most common cause of the human “common cold”, responsible for around 30–50% of all colds worldwide.The work of the Yale team is explained in a YaleNews item by Karen Guzman.
Key features
- Genome: Single-stranded, positive-sense RNA
- Structure: Non-enveloped, icosahedral capsid
- Size: ~30 nm in diameter
- Replication site: Cytoplasm of infected cells
- Optimal temperature: ~33–35 °C, matching the cooler nasal passages
Diversity
There are over 160 known rhinovirus types, grouped into three main species:
- Rhinovirus A
- Rhinovirus B
- Rhinovirus C (often associated with more severe disease, especially in children)
This extreme diversity is one reason why lasting immunity and an effective vaccine are so difficult to achieve.
Transmission
Rhinoviruses spread easily via:
- Respiratory droplets (coughing, sneezing, talking)
- Direct contact (hands, handshakes)
- Contaminated surfaces (door handles, phones, keyboards)
They can remain infectious on surfaces for several hours.
Infection and symptoms
Rhinoviruses infect epithelial cells lining the upper respiratory tract. Symptoms are caused less by direct cell damage and more by the body’s immune response, especially inflammation triggered by interferons and cytokines.
Typical symptoms include:
- Runny or blocked nose
- Sneezing
- Sore throat
- Cough
- Headache
- Mild fever (more common in children)
Complications
While usually mild, rhinovirus infections can:
- Exacerbate asthma
- Worsen COPD
- Trigger sinusitis or otitis media
- Lead to serious illness in the elderly or immunocompromised
Why colds vary in severity
Disease severity depends largely on the host’s immune response; particularly how rapidly infected cells mount an interferon response to limit viral spread. Genetic factors, age, pre-existing respiratory disease, and immune status all influence outcomes.
Why there is no vaccine
- Over 160 antigenically distinct strains
- Rapid mutation
- Short-lived immunity
- Weak selection pressure for sterilising immunity
Together, these make vaccine development impractical with current technology.
Why the same cold can be a sniffle for some and a crisis for others
It’s not the rhinovirus itself but the body’s early immune response that determines whether the common cold stays mild or flares into something more dangerous, a new study finds.
When Ellen Foxman began her postdoctoral work at Yale School of Medicine (YSM) in 2010, she was interested in what respiratory viruses could reveal about the human immune system. Having a young son diagnosed with asthma around the same time only sharpened this interest.
The number one trigger of asthma attacks is rhinovirus. In the past, people believed asthma attacks were due to allergies, but better virus detection technology showed us years ago that rhinovirus is a major cause.
Associate Professor Ellen F. Foxman, lead author
Department of Laboratory Medicine
Yale School of Medicine
New Haven, CT, USA.
Still, a vexing question remained: Why does the same virus cause only mild sniffles in some people but lead to severe breathing problems in others, particularly people with conditions like asthma or chronic obstructive pulmonary disease (COPD)?
In her latest research, Foxman showed that the answer lies in the body’s response to the virus, not in the inherent power of the virus.
Specifically, she found that the reaction of the cells that form the lining of the nasal passages plays a larger role than was previously understood. These cells have an arsenal of innate defense mechanisms triggered by viruses (also called “innate immunity”), even though they are not part of the traditional immune system. Foxman’s lab identified a switch that determines whether a rhinovirus infection remains a mild cold or escalates into the kind of severe airway inflammation that can land someone in the emergency room.
The findings are published in the journal Cell Press Blue.What’s clear is that it’s not just the virus that determines the disease. There’s something about the human body that’s really driving the disease outcome, but the mechanisms are not well understood. We set out to understand the mechanisms inside virus-infected cells that push the infection in one direction or another.
Associate Professor Ellen F. Foxman.
All in the nose
The body’s first-line antiviral defense in the nose — called the interferon response — usually keeps rhinovirus under control. When the response works properly, fewer than 2% of nasal cells become infected with rhinovirus, and the cold peters out.
For the new study, researchers used a laboratory model that closely mimics the human nasal lining and grew real human nasal cells into organoids that were able to develop cilia and produce mucus, replicating the inside of the nose and lungs. Next, they infected the cells with rhinovirus and used drugs to selectively block different immune signaling pathways, so that they could see what would happen if the interferon response or other defenses are blocked.
They then used single-cell RNA sequencing, which allowed them to see how individual cells responded to infection. Specifically, it revealed which cells were infected, which defensive genes were turned on, and how nearby uninfected cells reacted. The researchers also measured virus levels, cell death, mucus production, and pinpointed the role of inflammatory sensors.
Foxman and colleagues in the lab.
They found that most cold virus infections stay mild because the nasal lining rapidly produces interferons that stop the virus from spreading to other cells. But when that response is weakened or blocked, the body reacts with a more aggressive inflammatory mode that can worsen symptoms and damage airways. Strong, speedy interferon signaling limits infection and keeps the virus and inflammation in check, while weak interferon responses or other factors that promote an aggressive response allow runaway inflammation.
Our experiments with organoids show that a rapid interferon response by the infected cells is extremely effective for shutting down rhinovirus, even without any cells of the immune system present.
Bao Wang, first author. Department of Laboratory Medicine
Yale School of Medicine
New Haven, CT, USA.
Zeroing in on inflammation
Targeting different responses using drugs and genetic changes in organoids helped researchers get a better idea of how the body activates inflammatory signals. These insights may help researchers create or repurpose medications that could reduce dangerous airway inflammation, which could in turn help prevent rhinovirus-induced asthma and COPD attacks.
One very unique aspect of this study was being able to look at thousands of cells working together and how they interact to fight this common infection.
Associate Professor Ellen F. Foxman.
The underlying question, of course, is what would make a person’s interferon response weak in the first place? Why doesn’t everyone’s response simply knock out rhinovirus before it gets a hold?That’s a great question. In our model, we inhibited the response with a drug, but it’s known that in people with chronic airway diseases, the interferon response is lower than in a healthy person. That’s the ‘why’ we just don’t know yet. It’s our next step.
Associate Professor Ellen F. Foxman.
Other study contributors included postdoctoral fellow Julien Amat and research associate Valia Mihaylova in the Foxman Lab at Yale School of Medicine; research scientist Guilin Wang in the Yale Department of Molecular Biophysics and Biochemistry; and senior research scientist Yong Kong in the Department of Biostatistics at the Yale School of Public Health.
Publication:
All of this leaves intelligent design creationists with yet another awkward question they prefer not to ask, let alone answer. If an omnipotent, omnibenevolent designer really did design both rhinoviruses and the human immune system, and if it demonstrably *can* design an immune response that rapidly contains these viruses and prevents serious illness, then why was that effective response not given to everyone? Why should some people be left with a downgraded, sluggish, or easily suppressed version that fails precisely when it is most needed?
The standard theological evasions fare no better here than they do anywhere else. Blaming ‘the Fall’ merely compounds the problem, because it implies either that a perfect design was knowingly made fragile and failure-prone, or that the designer is either unable or unwilling to repair a manifestly defective system. Invoking ‘mysterious ways’ simply concedes the point: that the design is neither optimal nor equitable, and that suffering is an apparently acceptable feature of it.
By contrast, the evolutionary explanation fits the facts without recourse to special pleading. Natural selection does not design for perfection, fairness, or universal robustness; it produces compromises shaped by trade-offs, historical constraints, and shifting selection pressures. In an ongoing arms race with viruses, immune defences evolve unevenly, remain suboptimal, and vary from person to person. That is exactly what we observe.
Once again, the real world stubbornly refuses to conform to the expectations of intelligent design. Instead of a uniformly effective, benevolently engineered immune system, we see a patchwork of variable responses, inherited vulnerabilities, and evolutionary compromises. It is not just inconvenient for creationism — it is flatly incompatible with the idea of an omnipotent, omnibenevolent designer who supposedly could have done better, and demonstrably did not.
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