Rosa Rubicondior: Malevolent Designer News - How Cold Sores Are Cleverly Designed To Maximise Suffering.

(Top) Cropped representative STORM-PAINT images of EdC-AF647 labeled hDNA (magenta), immunolabeled H3 (green), and their merge in mock and HSV-1 infected A549 cells. Scale bar: 2 µm. (Bottom) Zoomed-in regions are shown inside yellow boxes. Scale bar: 200 nm.

González-Almela, E., Castells-Garcia, A., Le Dily, F. et al. (2025)

Centre for Genomic Regulation Website

One of the many problems with Intelligent Design (ID) creationism is its complete failure to account for evolutionary arms races.

According to leading ID proponents like William A. Dembski and Michael J. Behe, living organisms and their parasites — including viruses — must have been intelligently designed because they are supposedly “irreducibly complex” and exhibit “complex specified information”. But if that were true, it would mean the same designer is deliberately crafting both parasites and the defence mechanisms their hosts use to fend them off — hardly the mark of a supremely intelligent creator.

A further problem, and one that creationists prefer to ignore, is theological: designing pathogens like viruses is fundamentally incompatible with the notion of a benevolent creator. In fact, it suggests a malevolent intelligence — one more concerned with maximising suffering than promoting life and maximising happiness. So, when science uncovers yet another example of a virus behaving with surgical precision and apparent ingenuity, ID creationists find themselves in a bind. Is irreducible complexity and complex specified genetic information not evidence of intelligent design after all? Or must they admit that the designer is, at best, morally indifferent — or worse, actively malevolent?

The latest headache for the ID camp comes courtesy of the Herpes simplex virus — the one responsible for cold sores. Researchers at the Centre for Genomic Regulation (CRG) in Barcelona, Catalunya, Spain, with colleagues in Guangdong Provincial People’s Hospital, Guangdong, China, have discovered that the virus can radically reorganise a host cell’s genetic architecture — and it does so using the host's own cellular machinery. Their findings have just been published open access in Nature Communications.

What is known of the origins and evolutionary history of the Herpes simplex virus? The Herpes simplex virus (HSV), like other herpesviruses, has a long and complex evolutionary history that stretches back hundreds of millions of years. Here's a summary of what is currently known or hypothesised about its origins and evolutionary trajectory:

Family and Classification

HSV belongs to the Herpesviridae family, a large group of double-stranded DNA viruses. HSV specifically is part of the Alphaherpesvirinae subfamily, which is characterised by:

Rapid replication cycles
Latency in sensory neurons
A broad host range (though HSV is largely restricted to humans)

There are two main HSV types in humans:

HSV-1: Typically causes oral herpes (cold sores)
HSV-2: More often associated with genital herpes

Ancient Origins: Deep Evolutionary Roots

Herpesviruses are ancient and have co-evolved with their vertebrate hosts. The divergence between the major herpesvirus subfamilies (Alpha-, Beta-, and Gammaherpesvirinae) likely occurred over 400–500 million years ago, during the early evolution of vertebrates.

This means that herpesviruses were infecting early fish and continued to evolve alongside their hosts through the rise of amphibians, reptiles, mammals, including primates and humans.

o-speciation and Host-Switching

The evolution of herpesviruses is generally consistent with co-speciation — the virus and its host evolving together. However, there are also instances of host-switching, especially among closely related species.

In the case of HSV-1 and HSV-2:

HSV-1 appears to have co-evolved with early hominins, possibly arising as humans split from other great apes.
HSV-2 has a more intriguing origin: genetic studies indicate that it likely jumped from ancestral chimpanzees to early humans, possibly through hunting, scavenging, or close contact around 1.6 to 3 million years ago.

This makes HSV-2 a case of zoonotic transfer — a virus crossing from one species to another — long before the agricultural revolution or modern human civilisation.

Genomic Studies and Viral Evolution

Comparative genomics reveals:

High conservation among herpesviruses due to the stability of double-stranded DNA.
Slow mutation rates compared to RNA viruses like influenza or coronaviruses.
Distinct viral genes involved in immune evasion, latency, and neurotropism (ability to infect nerve cells) have likely undergone positive selection due to host immune pressures.

Phylogenetic analyses show clear divergence between HSV-1 and HSV-2, estimated to have split from a common ancestor around 6 million years ago, coinciding roughly with the human-chimpanzee split.

Latency and Adaptation

One of the hallmark features of HSV evolution is its ability to establish lifelong latency in host neurons. This is an extremely successful evolutionary strategy, allowing:

Persistent infection without killing the host
Periodic reactivation and transmission without overwhelming immune detection

This trait likely evolved early in the Alphaherpesvirinae lineage and was strongly selected for in host species with longer lifespans and complex immune systems — such as primates.

Summary Points

Herpesviruses date back over 400 million years.
HSV-1 co-evolved with early hominins.
HSV-2 likely jumped from chimpanzees to humans \~1.6–3 million years ago.
The virus mutates slowly but has evolved sophisticated mechanisms of latency and immune evasion.
Evolutionary strategies include neurotropism, latency, and episodic reactivation for transmission.

The CRG has also provided a lay explanation in a press release.

Herpes virus plays interior designer with human DNA
Viruses are entirely dependent on their hosts to reproduce. They ransack living cells for parts and energy and hijack the host’s cellular machinery to make new copies of themselves. Herpes simplex virus-1 (HSV-1), it turns out, also redecorates, according to a new study in Nature Communications.
Researchers at the Centre for Genomic Regulation (CRG) in Barcelona have discovered the cold sore virus reshapes the human genome’s architecture, rearranging its shape in three-dimensional space so that HSV-1 can access host genes most useful for its ability to reproduce.

HSV-1 is an opportunistic interior designer, reshaping the human genome with great precision and choosing which bits it comes into contact with. It’s a novel mechanism of manipulation we didn’t know the virus had to exploit host resources.

Dr. Esther González Almela, co-first author.
Medical Research Institute
Guangdong Provincial People’s Hospital (Guangdong Academy of Medical Sciences)
Southern Medical University
Guangzhou, China.

While other herpes viruses have been seen compacting and reshaping host chromosomes, it was unclear whether it was a side effect of the virus invading and setting up its own viral replication factories. The study is the first proof that HSV-1 reshapes the human genome deliberately and within hours of infection.

Crucially, the researchers found that blocking a single host enzyme, topoisomerase I, completely blocked HSV-1’s ability to rearrange the human genome during infection, bringing the hostile takeover to a halt. The discovery represents a new potential strategy to control a virus which infects nearly four billion people worldwide.

In cell culture, inhibiting this enzyme stopped the infection before the virus could make a single new particle. That gives us a potential new therapeutic target to stop infection.

Professor Maria Pia Cosma, corresponding author
Medical Research Institute
Guangdong Provincial People’s Hospital (Guangdong Academy of Medical Sciences)
Southern Medical University
Guangzhou, China. And Centre for Genomic Regulation (CRG)
The Barcelona Institute of Science and Technology,
Barcelona, Catalunya, Spain.

The researchers made the findings by combining super-resolution microscopy, an imaging technique which can see structures 20 nanometres wide, around 3,500 times thinner than a strand of hair, with Hi-C, a technique that reveals which bits of DNA are touching inside the nucleus. They used both techniques to gain new mechanistic insights into how HSV-1 hijacks human cells.

They found the hostile takeover begins within the first hour, with the virus hijacking the human RNA-polymerase II enzyme to help synthesise its own proteins. Topoisomerase I, an enzyme that snips DNA to release torsional stress, and cohesin, a structural protein, followed human RNA-polymerase II into the newly forming viral replication compartments.

Three hours after infection, most polymerase and a sizeable fraction of the other two factors had abandoned human genes. The wholesale theft causes transcription to collapse across the host genome, which in turn caused chromatin, the human genome’s natural state inside cells, to be crushed into a dense shell just 30% of its original volume.

This was an unexpected finding, as the structure of chromatin is thought to dictate transcription.

We always thought dense chromatin shut genes down but here we see the opposite: stop enough transcription first and the DNA compacts afterwards. The relationship between activity and structure might be a two-way street.

Dr. Álvaro Castells García, co-first author.
Medical Research Institute
Guangdong Provincial People’s Hospital (Guangdong Academy of Medical Sciences)
Southern Medical University
Guangzhou, China.

Two in every three people under age 50 live with HSV-1. Once infected, people have the virus for life, though most cases are asymptomatic or manifest as recurrent cold sores. Rarely, the virus can cause blindness or life-threatening disease in newborns and immunocompromised people.

The findings of the study can help address the public health burden of HSV-1, which is considered a global health challenge because of its prevalence and ability to cause recurrent outbreaks. Though treatments are available to manage symptoms, drug-resistant strains are on the rise, and there is no cure.

Abstract
Herpes simplex virus type 1 (HSV-1) remodels the host chromatin structure and induces a host-to-virus transcriptional switch during lytic infection. We combine super-resolution imaging and chromosome-capture technologies to identify the mechanism of remodeling. We show that the host chromatin undergoes massive condensation caused by the hijacking of RNA polymerase II (RNAP II) and topoisomerase I (TOP1). In addition, HSV-1 infection results in the rearrangement of topologically associating domains and loops, although the A/B compartments are maintained in the host. The position of viral genomes and their association with RNAP II and cohesin is determined nanometrically. We reveal specific host–HSV-1 genome interactions and enrichment of upregulated human genes in the most contacting regions. Finally, TOP1 inhibition fully blocks HSV-1 infection, suggesting possible antiviral strategies. This viral mechanism of host chromatin rewiring sheds light on the role of transcription in chromatin architecture.

González-Almela, E., Castells-Garcia, A., Le Dily, F. et al.
Herpes simplex virus type 1 reshapes host chromatin architecture via transcription machinery hijacking. Nat Commun 16, 5313 (2025). https://doi.org/10.1038/s41467-025-60534-6

Copyright: © 2025 The authors.
Published by Springer Nature Ltd. Open access.
Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)

This discovery poses a serious challenge to proponents of Intelligent Design, who insist that complex biological features exhibiting "irreducible complexity" and "complex specified information" must be the product of an intelligent mind. Herpes simplex type 1 (HSV-1) is a masterclass in both. It has evolved the ability to manipulate the host cell’s internal architecture with precision, using the host’s own molecular tools to establish a lifelong infection. It remains latent for years, reactivating opportunistically — all while avoiding immune detection with remarkable efficiency. If this isn’t an example of what ID theorists call "specified complexity", then the term has no coherent meaning.

So, what are we to make of this? If HSV-1 is intelligently designed, who — or what — is the intelligence behind it? The virus causes recurrent painful sores, and in rare cases, life-threatening encephalitis. It exploits the nervous system and offers no benefit to its host. It is not symbiotic, not neutral — it is purely parasitic. To attribute such a design to a benevolent creator is theologically and morally problematic.

ID advocates are therefore faced with a dilemma: either admit that this exquisitely adapted virus is not the product of intelligent design — thereby undermining their criteria for recognising design — or accept that the designer is capable of creating agents of harm and suffering. In doing so, they edge away from a benevolent deity and toward a capricious or even malevolent designer. Which is it? Either way, the ID framework fails to provide a coherent or satisfying answer.

Until Intelligent Design theorists can offer a consistent explanation for why parasitic, pathogenic entities like HSV-1 qualify as "designed" yet do not reflect the intent or morality of their supposed designer, their argument remains hollow. They cannot have it both ways — attributing biological marvels to divine intelligence while dismissing biological malevolence as merely "a consequence of the Fall" or some other theological patch. The Herpes virus is not just a scientific puzzle; it is a theological one — and ID is woefully ill-equipped to solve it.

So, is there an ID advocate out there who feels up to offering some coherent answers to this conundrum, rather than the traditional threats of divine retribution for having the temerity to ask such awkward questions?

Advertisement

Amazon