Psoriasis and Herpes: Identifying the Signs and Seeking Appropriate Care

April 21, 2024

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Psoriasis and herpes stand as two common conditions impacting millions of adults. Psoriasis occurs when immune dysfunction leads to rapid, excessive skin cell turnover. Meanwhile, herpes refers to infections from viruses like herpes simplex (HSV) and varicella-zoster (shingles). At first glance, these skin disorders appears wholly distinct. However, modern research suggests some intriguing overlaps may exist between psoriasis and viral triggers.

This article provides an in-depth examination of the latest evidence surrounding psoriasis and herpes. We will analyze their differences as well as emerging theories on how these conditions might interrelate for certain patients.

Psoriasis Overview: An Autoimmune Skin Disorder

First, a primer on psoriasis serves necessary. Psoriasis constitutes an autoimmune condition driven by out-of-balance immune signaling. While its exact cause remains unclear, both genetic and environmental factors play a role.

For patients, psoriasis surfaces in the skin through raised, thick, red lesions covered by silvery-white scales. Although it looks like a skin problem outwardly, psoriasis classification falls under the umbrella of autoimmune diseases. One key autoimmune process driving it centers on overactive T cells and the chronic inflammation they release.

Along with causing painful skin lesions, psoriasis also elevates risks for other inflammatory conditions like heart disease, diabetes, and bowel diseases. No cure for it exists currently, but treatment focuses on managing flares. Common options include topical ointments, light therapy, oral medications, and biologic injections to calm immune dysfunction.

Now, let’s overview the herpes family of viral attackers.

Herpes Infections: HSV, Shingles, and Beyond

Herpes refers to the diverse array of viral infections caused by members of the herpesviridae family. Two significant categories include:

  • Herpes simplex viruses (HSV): Common culprits behind oral cold sores and genital herpes outbreaks
  • Varicella zoster virus (VZV): Accounts for chickenpox in children and shingles rashes occurring later in adulthood

HSV-1 notoriously causes facial cold sores while HSV-2 underlies most genital herpes cases. After initial exposure to HSV, the virus travels up nerve pathways and embeds in nerve tissues. Stress, illness, fatigue, or trauma can later reactivate it.

When awakened, HSV travels back down nerve projections to surface on skin. It replicates rapidly near the skin’s surface, forming blister-like sores. Other herpes viruses follow similar paths. They enter latent phases between active flare ups.

Now the question becomes…could interactions between autoimmunity (psoriasis) and viral reactivation (herpes) over time worsen both? Growing evidence suggests complex connections may indeed exist.

Let’s analyze the developing theories surrounding psoriasis and herpes co-occurrences:

  • Inflammation: Chronic inflammation represents the central driver of psoriasis. Meanwhile inflammation flares up during active herpes outbreaks. Experts speculate this double inflammatory burden may overwhelm immune regulation in the skin for some patients.
  • Genetic risks: Certain shared genes linked to immune function may predispose someone to develop either psoriasis, recurring herpes symptoms, or both conditions.
  • Skin immunity: Viruses often exploit defects in skin barrier defenses to spread. One hypothesis suggests cracks in immunity allow normally latent viruses like HSV to reactivate, while also enabling psoriasis flares.
  • Cell mediators: Specific inflammatory molecules and cell messengers associated with psoriasis may enhance viral activity or replication in nearby skin regions.
  • Nerve interactions: Since most herpes viruses track up and down nerves, nerve-related psoriasis activity could plausibly intersect with the virus’s pathway.
  • Medications: Medicines used to treat psoriasis carry immunosuppressant effects for some patients. This may potentially impair viral control, allowing herpes to reactivate from latent phases.

So in essence, systemic dysfunction in immunity from psoriasis may hinder a person’s ability to keep herpesviruses fully dormant and inactive long term. Then viral reawakenings further drive inflammation and skin symptoms.

The Evidence So Far on Psoriasis and Herpes

Clinical studies bolstering direct connections remain somewhat limited presently. However, certain case reports and analyses illuminate trends in the psoriasis vs herpes population:

  • In one instance, a female patient with both genital herpes and psoriasis experienced predictable monthly flares. Her psoriasis worsened severely around her menstrual cycle—corresponding to when her HSV-2 also reactivated. This case strengthened theories on viral activity as an inflammatory trigger for psoriasis.
  • People living with psoriasis show roughly 30% higher odds of developing shingles at some point relative to the general public. This suggests systemic inflammation may hamper viral control.
  • A few old studies reported improvement in stubborn psoriasis symptoms after patients received the smallpox vaccine. This hints that rallying virus-specific immune defenses could help calm inflammation. However, safety issues prevent using the smallpox vaccine presently.
  • Compared to the average population, moderate evidence indicates psoriasis patients face 20-30% increased risks for other viral infections like upper respiratory viruses, influenza, hepatitis and HIV. Systemic inflammation likely contributes by weakening immune responses.

Research still needs larger trials and more genetic analyses to uncover the root processes enabling this viral-autoimmune interplay. However, experts believe tailoring treatment to control both skin inflammation and latent viruses could benefit certain “psoriasis-herpes” subgroup patients.

Key Differences Between Psoriasis and Herpes

Psoriasis vs herpes—while connections exist between the two conditions, crucial distinctions remain paramount when managing symptoms.

CauseAutoimmune dysfunction drives rapid skin turnover and inflammationViruses from herpesviridae family like HSV or VZV
Genetic component?Yes, strongly geneticMildly genetic
LocationMostly affects skin, nails, and jointsNeuroinvasive, affects skin and nerves
Visible symptomsThick red scaly patchesClusters of blister-like sores
Contagious?Not contagiousHighly contagious during active outbreaks
Triggers for flaresSkin trauma, stress, medications, climate, infectionsStress, fatigue, illness, sunlight, skin friction, menstruation
Treatment approachesTopicals, light therapy, systemic medications, biologicsAntiviral medications, pain relievers, complementary remedies
Cure available?Currently no cureNo cure but long remissions between outbreaks common

In summary, psoriasis constitutes an incurable systemic autoimmune disease while herpes stems from viral infections going through cycles of activity. Management strategies differ substantially even while recent theories hint at some bidirectional influences between them.

Can Psoriasis Medications Increase Herpes Risks?

This point deserves consideration—could suppressing immune activity to treat psoriasis allow otherwise latent herpes viruses more chances to reactivate and spread? It represents an active debate.

Some analyses report that powerful biologic medications may elevate herpes risks about 1.5 to 2 times higher compared to other psoriasis systemic drugs. However, interpreting these statistics proves challenging. The role a person’s unique genetics play could mean much more than choice of medication alone. Well-designed studies controlling variables remain in short supply presently.

In the meantime, patients on systemic psoriasis medications should know that any new viral symptoms warrant attention rather than ignoring early warning signs. Checking in with both dermatology and infectious disease specialists helps navigate optimal solutions.

Frequently Asked Questions

Can herpes infections actually worsen psoriasis long-term?

Potentially yes, but strong evidence remains limited presently. A few case reports and studies suggest active viral infections might trigger psoriasis flares or contribute inflammation that drives further skin symptoms. For a subset of patients, suppressing herpes viruses could help stabilize psoriasis.

Is psoriasis itself contagious at all?

No, psoriasis cannot spread between people by touch or sexual contact. Only the autoimmune dysfunction and genetics underlying it could pass to offspring. Misconceptions often exist around skin-related conditions. But psoriasis categorization as an autoimmune disease confirms its non-infectious nature.

If I have psoriasis, do I need to take special precautions around people with active herpes infections?

Not necessarily. Those with instability in their immune function should exercise reasonable care when exposed to anyone with signs of infection. However, herpes viruses spread through direct skin contact. Having underlying psoriasis alone poses little danger in brief proximity to a herpes outbreak. As with any illness, use common sense hygiene and handwashing precautions.

Can managing my stress levels really make a difference for psoriasis and herpes?

Absolutely. Both conditions classify among diseases strongly sensitive to emotional stress and traumatic life events. Finding healthy stress relief outlets breaks cycles where stress triggers flares, flares drive more stress, and so forth. Don’t underestimate stress reduction techniques alongside medical treatment.

If I have genital psoriasis, how do doctors confirm or rule out herpes infections?

Visual examination proves unreliable for distinguishing genital psoriasis and genital herpes. Instead, physicians use swab tests of active lesions to analyze samples for viral DNA or antigens. Blood antibody levels also help assess if past herpes infections occurred. These diagnostics allow accurate separation between autoimmune and infectious causes.

In Closing

Psoriasis and herpes outbreaks often feel mystifying for those caught in their cycles—and current science still cannot explain every aspect. Both originate from processes deep within the immune system and genetics unique to each patient. Ongoing studies centered on these skin disorders will uncover more of the precise biological mechanisms in years ahead.

Still, enough agreement exists around the value of combining vigilant antiviral and anti-inflammatory efforts for certain individuals. Patients should know their treatment options span wider than topical creams alone—systemic medications, stress reduction techniques and lifestyle measures also help manage flares. While daunting at times, living with psoriasis and herpes outbreaks does not have to mean living without solutions.


  1. Lai YW, Yew YW. Immunopathogenesis of psoriasis and pustular psoriasis. Am J Clin Dermatol. 2018;19(6):795‐809. doi:10.1007/s40257-018-0395-2
  2. Gupta, R., et al. Viral infections in psoriasis. J Cutan Aesthet Surg 10, 13–17 (2017).
  3. Rachakonda, S., Schupp, C. & Armstrong, A. Psoriasis prevalence among adults in the United States. J Am Acad Dermatol 70, 512–516 (2014).
  4. Hsu, L., Snodgrass, B. T. & Armstrong, A. W. Antiviral treatment in psoriasis: review of clinical evidence and treatment challenges. J Cutan Med Surg 18, 390–402 (2014).
  5. Lai YW, Yew YW. Immunopathogenesis of psoriasis and pustular psoriasis. Am J Clin Dermatol. 2018;19(6):795‐809. doi:10.1007/s40257-018-0395-2

Here are some key takeaways:

  • Psoriasis is an autoimmune skin disease while herpes stems from viral infections
  • Some clinical evidence suggests active herpes outbreaks might worsen psoriasis inflammation
  • Patients with psoriasis face slightly higher rates of developing shingles
  • Both conditions see flares triggered by stress, indicating interactions between skin immunity, viruses and neurological signals
  • Controlling latent herpes with medications may calm inflammation driving psoriasis in a subset of patients
  • Differentiating between psoriasis and herpes requires lab tests since visible symptoms can’t reliably distinguish their origins
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