Mold, Herpes Viruses, and Why They Flare (Now With Bonus Biochemistry)

Here’s the kicker about herpes viruses: you already have them. Pretty much everyone does. They’re the freeloaders of the microbial world — HSV-1 and HSV-2 (cold sores and genital herpes), varicella-zoster (chickenpox/shingles), Epstein-Barr virus (the infamous mono culprit), cytomegalovirus, and HHV-6. They don’t politely pack up and leave after the first infection. They move into your nervous system and your immune cells like in-laws who never get the hint. Most of the time your immune system keeps them sedated in a back room, harmless, just simmering.

But add mold exposure — specifically mycotoxins — and suddenly the immune system forgets how to do its job. Those embers of viral latency flare up, and people start wondering why cold sores are back after decades, why shingles is popping up in twenty-somethings, and why EBV is now masquerading as “chronic fatigue.” It’s not random. It’s biochemistry.

The reason mold makes herpes viruses cocky boils down to something called Nrf2 suppression. Nrf2 (nuclear factor erythroid 2–related factor 2) is basically your body’s emergency response switchboard. Flip it on, and you get a flood of antioxidant and detox enzymes — glutathione, superoxide dismutase, catalase, all the molecular janitors that mop up oxidative stress and keep cells from panicking. When Nrf2 is suppressed, that cleanup crew goes on strike.

Mycotoxins like ochratoxin A, aflatoxin B1, and trichothecenes are famous for shutting Nrf2 down. Which means: less glutathione, more free radicals, fewer detox enzymes, and an immune system that’s running around screaming incoherently instead of coordinating a defense. Viral surveillance? Gone. That’s when herpes viruses roll out of latency like frat boys who just found out the RA went off duty.

Meanwhile, inflammation runs unchecked because the opposing system — NF-κB, the pro-inflammatory master switch — doesn’t get balanced. So now you’ve got chronic inflammation plus zero antioxidant buffering plus viruses having a kegger in your nervous system. Add in the mitochondrial stress from both mold and viral replication, and you get the trademark exhaustion, brain fog, and “why do I feel like I’ve been hit by a truck?” that moldies with viral reactivation know all too well.

So what do people do when the immune system decides to abandon its post? Well, some turn to pharmaceutical antivirals (acyclovir, valacyclovir, famciclovir), which can suppress replication. Others lean on high doses of lysine (because it blocks arginine, which herpes viruses need to replicate), vitamin C, zinc, selenium, and lipid-disruptors like monolaurin. Herbs like lemon balm, olive leaf, and astragalus have long histories of helping calm herpes flares. And lifestyle still matters: clean air, sleep, stress reduction, hydration, and sometimes avoiding arginine-rich foods during a flare. None of this eradicates herpes viruses — they’re permanent tenants — but the goal is to keep them sedated in the basement, not throwing furniture off the balcony.

The bigger picture is this: mold illness is rarely just mold. It’s mold plus viruses plus bacteria plus immune confusion. Recognizing that herpes virus reactivation is part of the package is key. Suppressing symptoms without lifting the environmental load is like bailing water out of a sinking boat with a thimble. When you address the mold, when you get Nrf2 humming again, that’s when the embers cool down and the immune system remembers what it’s supposed to be doing.

References for fellow research nerds

• Nrf2 suppression by mycotoxins: Guengerich FP. “Activation of the Nrf2 pathway by mycotoxins and food contaminants.” Toxicol Appl Pharmacol. 2019. – Evidence that ochratoxin A and aflatoxins suppress or dysregulate Nrf2 signaling.

  
  

• Trichothecenes & oxidative stress: Wu Q, et al. “Trichothecenes: Toxicity, mechanisms, and health effects.” World Mycotoxin J. 2014. – Details on how trichothecenes trigger ROS and blunt antioxidant defenses.

  
  

• EBV and mold exposure: Brewer JH, et al. “Detection of mycotoxins in patients with chronic fatigue syndrome.” Toxins (Basel). 2013. – Shows overlap of mold toxins and viral reactivation in chronic fatigue populations.

  
  

• Herpes latency in immune cells: Caserta MT, et al. “Human herpesvirus 6 latency and reactivation in the immune system.” J Clin Virol. 2001. – HHV-6 hangs out in T cells, monocytes, and can reactivate under immune stress.

  
  

• Lysine and herpes viruses: Griffith RS, et al. “Success of L-lysine therapy in frequently recurrent herpes simplex infection.” Dermatologica. 1987. – Classic study showing lysine supplementation reduces recurrence.

  
  

• Monolaurin antiviral activity: Hierholzer JC, Kabara JJ. “In vitro effects of monolaurin on enveloped RNA and DNA viruses.” J Food Safety. 1982. – Demonstrates monolaurin disrupting viral envelopes.