Rosa Rubicondior: Malevolent Designer - How A Common Virus Sneaks Past Our Immune System And Causes Birth Defects

Scientists Uncover How a Common Herpes Virus Outsmarts the Immune System | School of Medicine | University of Pittsburgh.

Intelligent (sic) Design creationists have painted themselves into a corner.

Two of their most prominent arguments—irreducible complexity (Michael J. Behe) and complex specified information (William A. Dembski)—are intended to demonstrate the involvement of an intelligent designer in the natural world. But when these same criteria are applied to harmful parasitic organisms, such as the common herpesvirus (cytomegalovirus), which is the leading infectious cause of birth defects in the United States, the implication is that this virus too is the product of intentional design by the same creator that ID proponents insist is responsible for all life.

Within the framework of Intelligent Design creationism, the conclusion is inescapable: their designer deity—typically equated with the omniscient, omnibenevolent god of the Christian Bible—knowingly and deliberately created a pathogen that causes immense suffering. If ID logic is followed consistently, their deity is not a benevolent creator but a malevolent force that engineers disease and deformity with full foreknowledge of the consequences.

The only escape from this theological and philosophical bind is for ID creationists to refute their own criteria—to claim that irreducible complexity and complex specified information are compelling proof of design when found in beneficial biological systems, but somehow irrelevant or invalid when found in destructive pathogens. In doing so, they are forced to hold two mutually exclusive beliefs simultaneously.

In reality, these hallmarks of design touted by ID advocates are common outcomes of natural evolutionary processes — especially arms races between host defences and parasitic invaders. These processes are inherently unguided and wasteful, which in itself refutes the idea of intelligent planning.

Another striking example of this evolutionary struggle has just been published in Nature Microbiology by researchers from the University of Pittsburgh School of Medicine and the La Jolla Institute for Immunology. Their study sheds light on how the herpesvirus has evolved sophisticated strategies to evade the immune system — a feature that ID logic would classify as evidence of "design."

Background^ Cytomegalovirus and the Herpesvirus Family. Cytomegalovirus (CMV) is a member of the Herpesviridae family, a large group of DNA viruses that share several key characteristics. Like all herpesviruses, CMV can establish lifelong latency in the host after initial infection and may reactivate under certain conditions, particularly when the immune system is compromised.

CMV in Humans

CMV is widespread: by adulthood, between 50% and 80% of people have been infected.
Transmission occurs via bodily fluids — saliva, blood, urine, semen, and breast milk.
In healthy individuals, CMV is usually asymptomatic or causes mild flu-like illness.
However, CMV poses serious risks in:

Pregnancy – it can cross the placenta, infecting the developing foetus.
Immunocompromised patients – including transplant recipients and those with HIV/AIDS.

CMV and Birth Defects

CMV is the leading infectious cause of congenital birth defects in developed countries.
Congenital CMV can cause:

Hearing loss
Vision impairment
Intellectual disabilities
Seizures

The virus is able to evade the maternal immune system, enabling infection of the foetus despite the body’s natural defences.

The Herpesvirus Family

CMV is one of nine known herpesviruses that infect humans. Others include:

Herpes Simplex Virus Type 1 (HSV-1) – causes oral herpes (cold sores).
Herpes Simplex Virus Type 2 (HSV-2) – causes genital herpes.
Varicella-Zoster Virus (VZV) – causes chickenpox and shingles.
Epstein–Barr Virus (EBV) – linked to mononucleosis and some cancers.
Human Herpesvirus 6 and 7 (HHV-6, HHV-7) – associated with roseola in infants.
Human Herpesvirus 8 (HHV-8) – associated with Kaposi’s sarcoma.

All herpesviruses share the ability to persist in the body indefinitely, and many have evolved sophisticated immune evasion strategies, making them highly successful pathogens.

The University of Pittsburgh’s news release outlines the findings and their implications in detail:

Scientists Uncover How a Common Herpes Virus Outsmarts the Immune System
New research from the University of Pittsburgh School of Medicine and La Jolla Institute for Immunology (LJI), published June 30 in Nature Microbiology, reveals an opportunity for developing a therapy against cytomegalovirus (CMV), the leading infectious cause of birth defects in the United States.
Researchers discovered a previously unappreciated mechanism by which CMV, a herpes virus that infects the majority of the world’s adult population, enters cells that line the blood vessels and contributes to vascular disease. In addition to using molecular machinery that is shared by all herpes viruses, CMV employs another molecular “key” that allows the virus to sneak through a side door and evade the body’s natural immune defenses.

The finding might explain why efforts to develop prophylactic treatments against CMV have, so far, been unsuccessful. This research also highlights a new potential avenue for the development of future antiviral drugs and suggests that other viruses of the herpes family, such as Epstein-Barr and chickenpox, could use similar molecular structures to spread from one infected cell to the next while avoiding immune detection.

If we don’t know what weapons the enemy is using, it is hard to protect against it. We found a missing puzzle piece that represents one possible reason why immunization efforts against CMV have been unsuccessful.

Associate Professor Jeremy P. Kamil, co-senior author.
Department of Microbiology and Molecular Genetics
University of Pittsburgh School of Medicine
Pittsburgh, PA, USA.

In the United States, approximately one in every 200 babies is born with congenital CMV infection. Of the babies infected, one in five will have birth defects, such as hearing loss, or go on to have long-term health challenges. For most adults, CMV infections are asymptomatic. But a CMV infection during pregnancy presents significant health risks to the unborn child and could be deadly for people who are immunosuppressed, including organ transplant recipients.

Because of the large size of its genome and its complicated molecular machinery, CMV long evaded attempts to develop prophylactic treatments. Similar to other herpes viruses, CMV relies on a protein called gH to enter cells of the vessel lining. But unlike other herpes viruses, which use a protein partner called gL to facilitate infection, the new study found that CMV replaces gL with another partner called UL116 and recruits a protein called UL141. The resulting complex of gH-UL116-UL141, called GATE by the authors, then becomes an alternative tool for breaking into cells lining the blood vessels and causing internal damage while simultaneously preventing the body’s own immune system from recognizing the signs of infection.

The newly discovered GATE could become a potential vaccine target for CMV and other herpes viruses.

Previous attempts to generate a CMV vaccine have failed, but that was before we identified the GATE complex. We hope that new strategies targeting GATE will improve our chances to combat CMV infection, and also perhaps cleanse our bodies of this lifelong infection. If we can develop antiviral drugs or vaccines that inhibit CMV entry, this will allow us to combat the many diseases this virus causes in developing babies and immune-compromised people.

Associate Professor Chris A. Benedict, co-senior author
Center for Vaccine Innovation
La Jolla Institute for Immunology
La Jolla, CA, USA.

Other authors of this research are Michael Norris of the University of Toronto; Lauren Henderson and Mohammed Siddiquey, both of Louisiana State University Health Shreveport; and Jieyun Yin, Kwangsun Yoo, Simon Brunel, Michael Mor and Erica Ollmann Saphire, all of La Jolla Institute for Immunology.

Publication:
Norris, M.J., Henderson, L.A., Siddiquey, M.N.A. et al.
The GATE glycoprotein complex enhances human cytomegalovirus entry in endothelial cells.
Nat Microbiol 10, 1605–1616 (2025). https://doi.org/10.1038/s41564-025-02025-4

Abstract
Human cytomegalovirus can cause severe birth defects upon infection in pregnant women and complications in immunocompromised patients. A major challenge for vaccine design is our incomplete understanding of the diverse protein complexes this virus uses to infect cells. In Herpesviridae, glycoproteins H and L (gH and gL) form complexes with other viral proteins that bind receptors to mediate cell-type-specific entry. Here we identify a distinct gH complex that is abundant on human cytomegalovirus virions and enhances infection of endothelial cells. In this complex, gH associates with UL116 and UL141 (an immunoevasin previously known to function intracellularly) but not with gL. We term this the gH-associated tropism and entry (GATE) complex and provide the cryo-electron microscopy structure at ~3.5 Å. The structure shows gH-only scaffolding, UL141-mediated dimerization and a heavily glycosylated UL116 cap. These findings identify a third virion surface complex that promotes cell entry and may represent a new target for vaccines or antiviral therapies.

Norris, M.J., Henderson, L.A., Siddiquey, M.N.A. et al.
The GATE glycoprotein complex enhances human cytomegalovirus entry in endothelial cells.
Nat Microbiol 10, 1605–1616 (2025). https://doi.org/10.1038/s41564-025-02025-4

© 2025 Springer Nature Ltd.
Reprinted under the terms of s60 of the Copyright, Designs and Patents Act 1988.

This latest research reveals yet another layer of evolutionary sophistication in a virus that causes immense suffering. Cytomegalovirus has evolved molecular mechanisms to hide from the immune system and persist undetected—sometimes with devastating consequences for unborn children. From a biological perspective, these immune evasion strategies are the result of a long-standing evolutionary arms race between host and pathogen, shaped by natural selection over millions of years.

But from the perspective of Intelligent Design creationism, these findings pose an inescapable dilemma. If the virus exhibits the kind of complex, specific, and irreducibly intricate systems that ID theorists claim are hallmarks of a designer, then they must accept that these systems—like the ones allowing CMV to bypass maternal defences and attack a foetus—are also deliberately designed. In doing so, they must attribute the calculated targeting of the unborn to the intentions of their creator, typically equated with a benevolent deity.

The paradox is unavoidable: either harmful pathogens are products of the same intelligent agency ID advocates credit with the beauty and complexity of life, or the presence of such malevolent systems undermines their criteria for design. They cannot claim that complexity is proof of divine engineering in butterflies, blood-clotting cascades, or bacterial flagella—but not when it appears in viruses that cause deafness, blindness, and brain damage in newborns.

Once again, the evidence points not to a wise and compassionate creator, but to the blind, unguided processes of evolution—brutal, indifferent, and astonishingly effective. It is a conclusion many find uncomfortable, but unlike Intelligent Design, it is consistent, testable, and supported by the data.

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