Rosa Rubicondior: Malevolent Designer News - The Clever Way The Herpes Virus Gets Reactivated

UVA IDs Trigger for Those Annoying Cold Sore Flare-ups

The herpes viruses are ingenious designs of creationism's divine malevolence which are highly infectious and, once infected, you have them for life.

Of course, there is no point in designing a virus to just live inside its hosts cells doing nothing to increase the suffering in the world, so they come with a number of responses to various triggers which cause them to proliferate and start infecting other people.

Since these abilities are undoubtedly beneficial to the virus, there is no rational way that this can be presented as 'devolution' from some assumed created perfection - the forlorn attempt by Michael J. Behe to excuse the Christin god from culpability for parasites.

However, William A. Dembski, another Deception Institute Fellow, claims that anything which a gene produces must have been specified by an intelligent designer, so followers of the ID cult are obliged by dogma to give credit to their preferred creator deity for the herpes virus.

Now researchers at the University of Virginia have discovered a surprising way in which herpes can be reactivated, and, true to creationism's divine malevolence's form, it takes advantage of the hosts response to other infections and rides piggy-back on the hosts immune system - an immune system the same alleged designer designed to protect us from the viruses it designed to make us sick (if you believe that childish superstition).

The Herpes virus can respond to a protein produced by cells subject to stress which normally activates the immune system. However, the herpes virus is reactivated and starts producing lots of new virus particles, so the sufferer becomes infectious again and infects lots of other people. Then, job, jobbed, the herpes virus goes back into hiding to wait for the next chance to be reactivated and begin to replicate again, often many years later.

Tell me all about the herpes viruses and what triggers an outbreak of cold sores and genital herpes. Herpesviruses Overview

Herpesviruses are a family of large, double-stranded DNA viruses known as Herpesviridae. They are characterized by their ability to establish lifelong infections and persist in the host in a latent state, with the potential for reactivation. There are eight known herpesviruses that infect humans:

Herpes Simplex Virus Type 1 (HSV-1) - Primarily causes oral herpes (cold sores) but can also cause genital herpes.
Herpes Simplex Virus Type 2 (HSV-2) - Primarily causes genital herpes.
Varicella-Zoster Virus (VZV or HHV-3) - Causes chickenpox and can reactivate as shingles.
Epstein-Barr Virus (EBV or HHV-4) - Associated with mononucleosis and some cancers (e.g., Burkitt's lymphoma).
Cytomegalovirus (CMV or HHV-5) - Can cause serious disease in immunocompromised individuals.
Human Herpesvirus 6 (HHV-6) - Causes roseola in infants and may be linked to neurological conditions.
Human Herpesvirus 7 (HHV-7) - Similar to HHV-6, often asymptomatic.
Kaposi's Sarcoma-Associated Herpesvirus (KSHV or HHV-8) - Associated with Kaposi's sarcoma, particularly in immunocompromised individuals.
Cold Sores and Genital Herpes

Both cold sores and genital herpes are caused by the Herpes Simplex Virus (HSV), with HSV-1 being the primary cause of oral herpes (cold sores) and HSV-2 being the primary cause of genital herpes. However, due to oral-genital contact, HSV-1 can also cause genital herpes, and HSV-2 can sometimes be found in the oral region.

Cold Sores (Oral Herpes)

Caused primarily by HSV-1.
Appears as painful blisters around the lips, mouth, or nose.
Spread through direct contact with saliva or skin (e.g., kissing, sharing utensils).
Virus establishes latency in the trigeminal ganglion (a nerve cluster near the face).

Genital Herpes

Caused primarily by HSV-2, though HSV-1 can also be involved.
Appears as painful blisters or ulcers on the genitals, buttocks, or inner thighs.
Transmitted through sexual contact, including vaginal, anal, or oral sex.
Virus establishes latency in the sacral ganglion (a nerve cluster near the lower spine).

What Triggers an Outbreak?

Since herpes viruses establish lifelong latency, certain triggers can cause them to reactivate. Common triggers include:

Weakened Immune System

Illness (e.g., colds, flu)
HIV/AIDS or other immunosuppressive conditions
Chemotherapy or immunosuppressive drugs

Physical and Emotional Stress

Lack of sleep
Anxiety or depression
Major life changes (e.g., exams, job stress, loss of a loved one)

Hormonal Changes

Menstrual cycle (common trigger for women)
Pregnancy (can increase severity and risk of neonatal herpes)

UV Light and Sun Exposure

Sunburn can activate HSV-1, leading to cold sores.
UV radiation suppresses local immunity.

Physical Trauma or Injury

Dental work or lip injuries (for cold sores)
Friction from sexual activity (for genital herpes)

Fever or Other Infections

Any condition that stresses the immune system, such as the flu, can trigger an outbreak.

Certain Foods

Some people report outbreaks triggered by foods high in arginine, such as chocolate, nuts, and seeds.
A diet high in lysine (found in dairy, fish, and meat) may help suppress outbreaks.

Alcohol and Poor Diet

Excessive alcohol can weaken the immune system.
Poor nutrition can also contribute to immune suppression.

Managing and Preventing Outbreaks

Antiviral Medications

Acyclovir (Zovirax), Valacyclovir (Valtrex), Famciclovir (Famvir) - Reduce the severity and frequency of outbreaks.
Can be taken during an outbreak or daily as suppressive therapy to reduce recurrences.

Lifestyle and Immune Support

Get enough sleep and manage stress.
Maintain a healthy diet rich in vitamins and minerals.
Use sunscreen to prevent UV-triggered outbreaks.

Avoiding Triggers

Identify and avoid personal triggers (e.g., stress, certain foods, excessive sun exposure).
Use lip balm with SPF to protect against UV-induced cold sores.

Safe Practices to Prevent Spread

Avoid kissing or sharing utensils when a cold sore is present.
Use condoms or antiviral medication to reduce the risk of genital herpes transmission.
Wash hands after touching affected areas.

Conclusion

Herpes viruses are highly contagious and remain in the body for life. Cold sores and genital herpes can be triggered by a variety of factors, primarily immune system suppression, stress, hormonal changes, and UV exposure. While there is no cure, antiviral medications and lifestyle adjustments can help manage outbreaks and reduce transmission risks.

What they discovered is the subject of a paper in Proceeding of the National Academy of Science (PNAS). Their research is explained in a UVHealth press release:

UVA IDs Trigger for Those Annoying Cold Sore Flare-ups
School of Medicine researchers have discovered an unknown way the virus that causes cold sores (and many cases of genital herpes) reactivates in the body. This could pave the way for preventive treatments.
Scientists have a new target to prevent cold sores after School of Medicine researchers discovered an unexpected way the herpes virus re-activates in the body. The finding could also have important implications for genital herpes caused by the same virus.

The discovery from UVA’s Anna Cliffe, PhD, and colleagues seems to defy common sense. She and her team found that the slumbering herpes virus will make a protein to trigger the body’s immune response as part of its escape from dormancy. You’d think this would be bad for the virus – that activating the body’s antiviral defenses would be like poking a bear. But, instead, it’s the opposite: The virus highjacks the antiviral process in infected neurons (nerve cells) to make the type of comeback nobody wants.

Our findings identify the first viral protein required for herpes simplex virus to wake up from dormancy, and, surprisingly, this protein does so by triggering responses that should act against the virus. This is important because it gives us new ways to potentially prevent the virus from waking up and activating immune responses in the nervous system that could have negative consequences in the long term.

Dr. Anna R. Cliffe, lead author
Department of Microbiology
Immunology and Cancer Biology
University of Virginia, Charlottesville, VA. USA.
Herpes Simplex Virus-Associated Disease

Cold sores are caused primarily by herpes simplex virus 1 (HSV-1), one of two forms of the herpes virus. HSV-1 is very contagious, and more than 60% of people under 50 have been infected worldwide, the World Health Organization estimates. That’s more than 3.8 billion people.

In addition to causing cold sores, herpes simplex virus 1 can also cause genital herpes, a condition most often associated with HSV-1’s cousin, herpes simplex virus 2. Now, however, there are more new cases of genital herpes in the United States caused by HSV-1 than HSV-2. Notably, the UVA researchers found that herpes simplex virus 2 also makes this same protein and may use a similar mechanism to reactivate. So UVA’s new discovery may also lead to new treatments for genital herpes.

In addition to cold sores and genital herpes, HSV-1 can also cause viral encephalitis (brain inflammation) and has been linked to the development of Alzheimer’s disease.

Once HSV-1 makes its way into our bodies, it stays forever. Our immune systems can send it into hiding, allowing infected people to be symptom free. But stress, other infections and even sunburns are known to cause it to flare. UVA’s new discovery adds another, surprising way it can spring back into action.

The researchers found that while the virus can make a protein called UL12.5 to reactivate, the protein was not needed in the presence of another infection. The scientists believe this is because the infections trigger certain “sensing pathways” that act as the home security system for neurons. Detection of a pathogen alone may be sufficient to trigger the herpes virus to begin replicating, the scientists believe, even in instances of “abortive infections” – when the immune system contains the new pathogen before it can replicate.

We were surprised to find that HSV-1 doesn’t just passively wait for the right conditions to reactivate – it actively senses danger and takes control of the process. Our findings suggest that the virus may be using immune signals as a way to detect cellular stress – whether from neuron damage, infections or other threats – as a cue to escape its host and find a new one.

Patryk A. Krakowiak, first author.
Department of Microbiology
Immunology and Cancer Biology
University of Virginia, Charlottesville, VA. USA.

With the new understanding of how herpes flares can be triggered, scientists may be able to target the protein to prevent them, the researchers say.

We are now following up on this work to investigate how the virus is highjacking this response and testing inhibitors of UL12.5 function. Currently, there are no therapies that can prevent the virus from waking up from dormancy, and this stage was thought to only use host proteins. Developing therapies that specifically act on a viral protein is an attractive approach that will likely have fewer side effects than targeting a host protein.

Dr. Anna R. Cliffe.
Publication:
P.A. Krakowiak, M.E. Flores, S.R. Cuddy, A.L. Whitford, S.A. Dochnal, A. Babnis, T. Miyake, M. Tigano, D.A. Engel, & A.R. Cliffe
Co-option of mitochondrial nucleic acid–sensing pathways by HSV-1 UL12.5 for reactivation from latent infection.
Proc. Natl. Acad. Sci. U.S.A. 122 (4) e2413965122, https://doi.org/10.1073/pnas.2413965122 (2025).

Significance
Herpes simplex virus-1 (HSV-1) persists as a latent infection of neurons and reactivates to cause disease. Understanding host pathways required for reactivation is crucial to developing therapeutics. The HSV-1 protein, UL12.5, activates antiviral pathways, but its function in the viral infection was unknown. We found that UL12.5 is required for reactivation and acts at an early stage, previously thought to solely depend on host proteins, and therefore identifies UL12.5 as a potential therapeutic target to prevent reactivation. We show that a pathway associated with antiviral activities is proviral in the context of HSV-1 reactivation. The expression of UL12.5 and activation of antiviral pathways early during reactivation have important implications for the long-term impact of HSV-1 infection on the nervous system.

Abstract
Although viruses subvert innate immune pathways for their replication, there is evidence they can also co-opt antiviral responses for their benefit. The ubiquitous human pathogen, Herpes simplex virus-1 (HSV-1), encodes a protein (UL12.5) that induces the release of mitochondrial nucleic acid into the cytosol, which activates immune-sensing pathways and reduces productive replication in nonneuronal cells. HSV-1 establishes latency in neurons and can reactivate to cause disease. We found that UL12.5 is required for HSV-1 reactivation in neurons and acts to directly promote viral lytic gene expression during initial exit from latency. Further, the direct activation of innate immune-sensing pathways triggered HSV-1 reactivation and compensated for a lack of UL12.5. Finally, we found that the induction of HSV-1 lytic genes during reactivation required intact RNA- and DNA-sensing pathways, demonstrating that HSV-1 can respond to and active antiviral nucleic acid–sensing pathways to reactivate from a latent infection.

P.A. Krakowiak, M.E. Flores, S.R. Cuddy, A.L. Whitford, S.A. Dochnal, A. Babnis, T. Miyake, M. Tigano, D.A. Engel, & A.R. Cliffe
Co-option of mitochondrial nucleic acid–sensing pathways by HSV-1 UL12.5 for reactivation from latent infection.
Proc. Natl. Acad. Sci. U.S.A. 122 (4) e2413965122, https://doi.org/10.1073/pnas.2413965122 (2025).

© 2025 National Academy of Sciences.
Reprinted under the terms of s60 of the Copyright, Designs and Patents Act 1988.

Here we have yet another example of how William A. Dembski contradicts Michael J. Behe's valiant attempt to absolve his god of any culpability for pathogens and the harm they do, and, by misrepresenting both evolution and information theory, plonks the blame fairly and squarely back on the creator god he is too keen to credit for complex genetic information.

Meanwhile, the Deception Institute is sitting on the fence, unable to decide whether Dembski's 'complex specified information' is the result of the intervention of an intelligent designer as Dembski asserts, who is therefore also responsible for the 'complex specified information' that makes pathogenic parasites successful, or whether it isn't.

The best they are able to come up with to explain away parasites is Behe's biologically nonsensical notion of 'devolution' and 'genetic entropy' as the source of the 'complex specified information' in parasites, which also blows out of the water the claim that intelligent design has nothing to do with religion and Christian creationist mythology, by invoking the biblical myth of 'The Fall' as the cause of this alleged genetic entropy.

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