Rosa Rubicondior: Malevolent Design - Science is Close To Combatting Another Of Creationism's Divine Malevolence's Nasties

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Scientists develop first-of-its-kind antibody to block Epstein-Barr virus - Fred Hutch

A recent paper in the Cell Press journal Cell Reports Medicine by researchers at the Fred Hutch Cancer Center in Seattle reports the development of monoclonal antibodies against Epstein-Barr virus (EBV), a pathogen carried by an estimated 95% of the global human population. The mere existence of such a virus, together with the fact that human scientists have now produced what looks like a promising way of blocking it, should be acutely embarrassing to any creationist prepared to follow the evidence where it leads.

For devotees of creationism’s putative intelligent designer, EBV is an awkward example of its supposed handiwork. It is superbly adapted for what it does: infecting human cells, evading immune defences, and contributing to a range of diseases, including several cancers. If one were looking for something that appears exquisitely “designed” to do harm, EBV would be a strong candidate.

It is especially effective at finding and entering its target cells. The viral glycoprotein gp350 helps it bind to receptors on human cells, while gp42 helps it fuse with and enter them. In other words, it possesses precisely the sort of functional complexity that Intelligent Design advocates such as William Dembski and Michael Behe habitually point to as evidence of design. By their own argument, a system so finely tuned to perform a specific task should count as “specified complexity” or even “irreducible complexity”. The problem, of course, is that the task in question is the infection of human beings by a cancer-associated virus.

Creationists who lean on these arguments are therefore trapped by them. If complexity and functional integration are proof of a designer, then they must also account for the obvious implication: a designer responsible for EBV would have to be, at best, indifferent to human suffering and, at worst, positively malevolent. To escape that conclusion, they usually have to abandon Intelligent Design’s own logic and retreat instead to the theological fallback of “The Fall” and “sin” from the Abrahamic creation myths. In doing so, they quietly concede that their alleged scientific proof of design proves far more than they want it to.

This paper adds a further layer of discomfort. Human scientists have begun to do what any competent and benevolent designer should have done in the first place: devise antibodies capable of blocking the virus from infecting human cells. The study reports monoclonal antibodies against gp350 and gp42, with one anti-gp42 antibody preventing infection in mice with human immune systems. So the obvious question for intellectually honest creationists is this: if human science can engineer a way to interfere with such a pathogen, why was an all-powerful designer unable, or unwilling, to equip us with protection from the outset?

Predictably, most will not confront that question. They will retreat into the familiar refuge of mystery: “we cannot know the mind of God”. But that is precisely where religion and science part company. Science does not declare a problem solved by calling it unknowable. It treats mysteries as challenges to be investigated, understood and, where possible, overcome. That is exactly what these researchers have done with EBV.

What is Epstein–Barr virus (EBV)?

EBV is an extremely common human virus — also known as human herpesvirus 4. Most people are infected at some point in their lives, often in childhood, and after the initial infection the virus remains latent in the body and can later reactivate. It spreads mainly through saliva. [1]
Many infections cause few or no symptoms, but when primary infection occurs in teenagers or young adults, EBV commonly causes infectious mononucleosis — in the UK usually called glandular fever — with fatigue, fever, sore throat, and swollen lymph nodes. [1]
EBV is more than just a cause of glandular fever. It can also cause complications affecting the liver and spleen, and in some cases the brain, spinal cord and nerves, particularly in people with weakened immune systems. [2]
It is strongly implicated in several cancers. EBV was the first virus shown to be linked to a human cancer, and it is now associated with Burkitt lymphoma, some Hodgkin lymphomas, nasopharyngeal carcinoma, some gastric cancers, and post-transplant lymphoproliferative disorders. [3]
EBV is also implicated in autoimmune disease, although the strength of evidence varies. The clearest current evidence is for EBV as a major trigger of multiple sclerosis. It has also been linked to diseases such as systemic lupus erythematosus, but those links are still being worked out in more detail. [4]
Why EBV matters medically: because it infects so many people, persists for life, and is linked not only to an acute illness but also to cancer, immune dysfunction, and serious disease in immunocompromised patients. That is why vaccines, antivirals and antibody-based therapies against it are of such interest. [1]

An account of the scientists’ work is given in a news release from the Fred Hutch Cancer Center:

Scientists develop first-of-its-kind antibody to block Epstein-Barr virus
SEATTLE – February 17, 2026 – Fred Hutch Cancer Center scientists reached a crucial milestone in blocking Epstein-Barr virus (EBV), a pathogen estimated to infect 95% of the global population that is linked to multiple types of cancer, neurodegenerative diseases and other chronic health conditions.
Using mice with human antibody genes, the research team developed new genetically human monoclonal antibodies that prevent two key antigens on the surface of the virus from binding to and entering human immune cells. Published in Cell Reports Medicine, the study highlights one of the newly identified monoclonal antibodies that successfully blocked infection in mice with human immune systems when they were challenged with EBV.

Finding human antibodies that block Epstein-Barr virus from infecting our immune cells has been particularly challenging because, unlike other viruses, EBV finds a way to bind to nearly every one of our B cells. We decided to use new technologies to try to fill this knowledge gap and we ended up taking a critical step toward blocking one of the world’s most common viruses.

Dr. Andrew T. McGuire, PhD, corresponding author
Vaccine and Infectious Disease Division
Fred Hutchinson Cancer Center
Seattle, WA, USA.

A new scientific approach yields answers to a puzzling challenge

A key challenge in the study was to pursue human monoclonal antibodies that could successfully halt EBV infection without triggering an anti-drug response to the antibodies themselves, a common response among patients treated with antibodies raised in other animals. The researchers targeted two antigens, gp350, which helps EBV bind to cell receptors, and gp42, which allows EBV to enter and infect human cells through a process called fusion. Using an innovative mouse model carrying human antibody genes, the effort yielded two monoclonal antibodies against gp350 and eight against gp42.

Not only did we identify important antibodies against Epstein-Barr virus, but we also validated an innovative a new approach for discovering protective antibodies against other pathogens. As an early-career scientist, it was an exciting finding and has helped me appreciate how science often leads to unexpected discoveries.

Crystal B. Chhan, first author
Vaccine and Infectious Disease Division
Fred Hutchinson Cancer Center
Seattle, WA, USA.

With help from Fred Hutch’s Antibody Tech Core, further analysis found sites of vulnerability that could be useful in future vaccine development. In the final step of the study, the research team discovered that one of the monoclonal antibodies against gp42 successfully prevented infection of EBV. Another monoclonal antibody against gp350 provided partial protection.

Hope for patients at the highest risk of Epstein-Barr virus

More than 128,000 people in the U.S. undergo solid organ and bone marrow transplant annually. However, there are no specific therapies to prevent EBV from infecting or reactivating in patients undergoing immunosuppression for transplant procedures. Post-transplant lymphoproliferative disorders (PTLD) are an aggressive and sometimes life-threatening lymphoma that can develop after immune suppression and is most often caused by unchecked EBV infection.

Post-transplant lymphoproliferative disorders (PTLD), most of which are EBV-associated lymphomas, are a frequent cause of morbidity and mortality after organ transplantation. Preventing EBV viremia has strong potential to reduce the incidence of PTLD and limit the need to reduce immunosuppression, thereby helping preserve graft function while improving overall patient outcomes. Effective prevention of EBV viremia remains a significant unmet need in transplant medicine.

Associate Professor Rachel Bender Ignacio, MD, MPH
Immunology and Vaccine Development Program
Vaccine and Infectious Disease Division
Fred Hutchinson Cancer Center
Seattle, WA, USA.

Transplant recipients may experience infection if their donor was exposed to EBV and passed on latent virus through the donor cells, or for transplant patients who already have had EBV infection, immunosuppression may cause latent virus in their bodies to replicate unchecked. Children undergoing immunosuppression for transplant could especially benefit from a specific therapy to prevent EBV, as a higher proportion of children have not yet been exposed to EBV.

The next mile

The scientists envision a future therapy in which an infusion of these monoclonal antibodies could prevent PTLD by blocking EBV infection and activation in the patient populations who face the highest risk of EBV-related complications.

Fred Hutch has filed for intellectual property rights covering monoclonal antibodies identified in the study, and McGuire and Chhan are working with scientific collaborators and an industry partner to advance a potential therapy for immunocompromised patients. A potential therapy could be tested for safety in healthy adult volunteers and, if acceptable, proceed to clinical trials in the relevant patient population.
There’s momentum to advance our discovery to a therapy that would make a huge difference for patients undergoing transplant. After many years of searching for a viable way to protect against Epstein-Barr virus, this is a significant stride for the scientific community and the people at the highest risk of complications from this virus.

Dr. Andrew T. McGuire, PhD.

Publication:
Chhan, Crystal B.; Lang, Kevin; Davis, Amelia R.; Wan, Yu-Hsin; Aldridge, Nicholas T.; Kher, Gargi; Scharffenberger, Samuel C.; Hardy, Samantha R.; Iureniev, Roman; Giltiay, Natalia V.; Edwards, Kristina R.; Radtke, Stefan; Kiem, Hans-Peter; Pancera, Marie; McGuire, Andrew T. (2026)
Transgenic mouse-derived human monoclonal antibodies targeting EBV gp350 and gp42 provide basis for therapeutic development
Cell Reports Medicine 7(2), DOI: 10.1016/j.xcrm.2026.102618

Highlights

Transgenic mice were used to make genetically human EBV mAbs against gp350 and gp42
mAbs potently neutralize EBV infection by blocking receptor-ligand interactions
mAbs prevent EBV infection following EBV challenge in humanized mice

Summary
Epstein-Barr virus (EBV) causes infectious mononucleosis and contributes to neurodegenerative disorders and malignancies, particularly in immune-compromised hosts. Transplant patients face high risk of post-transplant lymphoproliferative disease, a life-threatening EBV-driven lymphoma. There are no EBV-specific vaccines or treatments; however, neutralizing antibodies against EBV glycoproteins may offer utility as therapeutic agents. EBV entry into B cells involves gp350, which binds complement receptors, and gp42, which engages HLA class II to trigger fusion. Most existing monoclonal antibodies (mAbs) against these antigens are non-human, limiting clinical use. Using a transgenic mouse model, we generate two gp350 and eight gp42 genetically human neutralizing mAbs that block receptor binding. Structural analyses reveal extended sites of vulnerability relevant to vaccine development. Delivery of a gp42 mAb protects humanized mice from EBV challenge, while a gp350 mAb provides partial protection. These mAbs highlight the utility of transgenic mice to produce therapeutic mAbs for preventing EBV-driven disease.

Graphical abstract

Chhan, Crystal B.; Lang, Kevin; Davis, Amelia R.; Wan, Yu-Hsin; Aldridge, Nicholas T.; Kher, Gargi; Scharffenberger, Samuel C.; Hardy, Samantha R.; Iureniev, Roman; Giltiay, Natalia V.; Edwards, Kristina R.; Radtke, Stefan; Kiem, Hans-Peter; Pancera, Marie; McGuire, Andrew T. (2026)
Transgenic mouse-derived human monoclonal antibodies targeting EBV gp350 and gp42 provide basis for therapeutic development
Cell Reports Medicine 7(2), DOI: 10.1016/j.xcrm.2026.102618

Copyright: © 2026 The authors.
Published by Cell Press (Elsevier Inc). Open access.
Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)

So, far from supporting any notion of a benevolent, intelligent designer, EBV does the exact opposite. It is a virus exquisitely adapted to invade human cells, persist for life, and contribute to serious disease, including cancer. If creationists wish to treat functional complexity as evidence of design, then they must also accept the obvious implication: the “designer” of something like EBV would have to be either indifferent to human suffering or actively malevolent. EBV is not a showcase for intelligent design; it is a powerful illustration of why that argument collapses under its own logic.

What this study actually showcases is not divine ingenuity but human ingenuity. By identifying monoclonal antibodies against the viral glycoproteins gp350 and gp42, and showing that at least one anti-gp42 antibody could block infection in mice with human immune systems, the researchers have taken a real, testable step towards preventing or treating an infection carried by most of humanity. That is how science works: not by declaring a mystery sacred and unknowable, but by identifying a problem, understanding its mechanism, and then trying to solve it.

And that is the sharpest contrast of all between science and creationism. Creationist dogma asks people to admire harmful complexity as if it were evidence of supernatural wisdom, then retreat into theology when that claim becomes morally embarrassing. Science does not need such evasions. It explains why viruses like EBV exist, how they work, and how they might be defeated. In that sense, every genuine medical advance is also a quiet refutation of the creationist habit of mistaking ignorance for explanation.

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