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Normally,

the bio-relationships that affect skin pigmentation can be summarized as follows:

Melanocytes & Melanin Synthesis Pathway

• Melanocytes are specialized pigment-producing cells derived from the neural crest, located primarily in the basal layer of the epidermis, hair follicles, uveal tract of the eye, inner ear, leptomeninges, and some mucous membranes.

• They produce melanin inside specialized organelles called melanosomes.

• Melanin synthesis (melanogenesis) follows the tyrosinase-dependent pathway:
• Tyrosine (amino acid) → (via tyrosinase) → DOPA (dihydroxyphenylalanine)

• DOPA → (via tyrosinase) → Dopaquinone

• Dopaquinone is then converted through several steps into eumelanin (brown/black) or pheomelanin (yellow/red), depending on enzyme activity and cellular environment.

Location of UV-B Photon Receptors & Role of the Sun

• UV-B radiation (280–315 nm) from sunlight is a key environmental stimulus for melanogenesis.

• DNA itself in keratinocytes and melanocytes acts as a primary UV-B photon receptor, triggering cellular responses.

• UV-B exposure induces DNA damage (cyclobutane pyrimidine dimers) in keratinocytes, leading to release of α-MSH (alpha-melanocyte-stimulating hormone), which binds to MC1R receptors on melanocytes — this stimulates melanogenesis.

• UV-B also stimulates melanocytes directly via p53 pathway activation and production of melanogenic factors.

• Melanin is then transferred from melanocytes to keratinocytes, forming a "supranuclear cap" over nuclei to protect against UV-induced DNA damage — this is the skin's photoprotective response.

Summary Role of the Sun:

• The sun is both a trigger and a target in this system: it provides UV-B photons that stimulate melanin production and is also the source of potentially damaging radiation from which melanin protects cells.

From "Normal" to "Post-COVID."

Where do viruses, like the SARS-CoV-2 virus, potentially interface with this system?

Viruses like SARS-CoV-2 primarily target epithelial cells, especially in the respiratory tract, but they can also affect skin cells in some cases. Here's how they might interface with the melanocyte-melanin system shown in the above ("normal") diagram:

Keratinocytes (Main SARS-CoV-2 Target in Skin):

Keratinocytes express ACE2 receptors, the entry point for SARS-CoV-2.

Infection may alter skin immune responses and pigmentation pathways indirectly.

This could potentially influence melanocyte activity by inflammatory signaling (e.g., cytokines like IL-6).

Melanocytes (Possible Indirect Target):

While melanocytes express low or variable ACE2, they are highly sensitive to inflammatory environments.

Viral infection might not directly infect melanocytes but could disrupt melanin synthesis via inflammatory mediators.

UV Exposure & Immune Modulation:

UV-B impacts melanocytes directly but also modulates immune responses in skin.

During viral infection, immune dysregulation could alter melanogenesis indirectly.

Post-viral Pigmentation Changes:

Reports of post-COVID skin changes (hyperpigmentation, vitiligo-like effects) suggest a complex interplay between viral infection, inflammation, and melanocyte function.

In summary, SARS-CoV-2 would most likely interface indirectly through keratinocyte infection and immune-mediated pathways, not by directly altering the melanocyte-melanin synthesis pathway itself.

"Who says?"

Here are several peer‑reviewed sources detailing post‑COVID dermatological changes, with a focus on keratinocyte infection, inflammation, and pigmentary disturbances:

   Keratinocyte Infection & ACE2 in Skin

High ACE2 expression in keratinocytes suggests SARS‑CoV‑2 can directly invade skin cells, potentially triggering inflammation and disrupting pigmentation. (PMC, PMC)

Immunohistochemical studies confirmed ACE2 presence in the epidermis and eccrine glands, indicating possible direct viral access to keratinocytes. (MDPI, ResearchGate)

喙 Post‑COVID Inflammation and Skin Changes

A systematic review found ~20% of post‑COVID patients experience skin issues including rashes, dermatitis, pigmentation changes, and autoimmune components—pointing to immune‑mediated pathways (e.g., IL‑6, CD8 T cell dysregulation). (Spandidos Publications)

Versions of these lesions have been linked to post‑inflammatory hyperpigmentation (PIH), commonly emerging after skin inflammation triggered by COVID. (The Open Dermatology Journal)

 Pigment Alterations: Hyperpigmentation & Pigment Loss

Reports from Wuhan indicate that a subset of COVID‑19 patients developed hyperpigmentation, possibly linked to PIH following the inflammatory “mask.” (The Open Dermatology Journal)

A case series highlighted 15.3% of recovered patients displaying notable skin pigmentation changes. (The Open Dermatology Journal)

Although less common, there are documented cases of vitiligo or vitiligo‑like lesions emerging after COVID‑19 or vaccination, reinforcing the autoimmune / melanocyte‑targeting hypothesis. (MDPI)

Summary: How This Affects the Melanocyte–Melanin System

Viral entry via keratinocytes → triggers local inflammation.

Immune response (inflammatory cytokines, T‑cells) influences melanocyte function.

Post‑inflammatory pigmentation or hypopigmentation reflects melanocyte reaction to inflammatory signals.

Autoimmune melanocyte targeting, in rare cases, leads to pigment loss (e.g., vitiligo-like).

For Further Reading

These studies establish that SARS-CoV-2 can infect keratinocytes—via ACE2 expression—triggering immune responses that secondarily affect melanocytes, leading to pigmentation changes (hyperpigmentation, hypopigmentation, vitiligo-like lesions) in a notable subset of patients post-COVID.

"Not a tanning problem for me... More like an eczema-like dermatitis."

Here are several peer-reviewed sources that specifically address eczema-like or eczematous dermatitis appearing in the context of COVID‑19 infection, vaccination, or pandemic-related measures:

🧴 Allergic & Irritant Contact Dermatitis (Eczema-like)

Impact in Contact Dermatitis during and after SARS‑CoV‑2 Pandemic
A comprehensive review highlights a marked rise in irritant and allergic contact dermatitis—commonly referred to as eczema—during the pandemic. The study links these increases to frequent hand hygiene practices and extended use of PPE among both healthcare workers and the general public (SpringerLink).

Can COVID‑19 Infection or Vaccination Trigger Allergic Contact Dermatitis?
A retrospective chart review reported onset of allergic contact dermatitis (ACD) in a small subset of patients post-infection or vaccination. Although the cohort was small (~0.5% post-infection, ~1.1% post-vaccination), it included cases presenting with erythematous eczematous lesions on the face, eyelids, and body (Dermatology Advisor).

📈 Atopic Dermatitis & Eczema Flares

Large Cohort Study: Risk of Atopic Dermatitis After COVID‑19
This January 2024 study in Allergy found a statistically significant increase in new-onset atopic dermatitis—an eczema variant—among patients after COVID-19 infection (PubMed).

Impact of Pandemic on Atopic Dermatitis Patients
A systematic review involving 159 studies revealed mixed effects; while some patients saw no change, others—especially infants and the elderly—experienced worsened atopic eczema during the pandemic. Contributors included heightened stress, disrupted care routines, and increased immunologic triggers (PMC).

Aggravation of Pre‑Existing Eczema
An analysis of COVID-19–infected individuals documented exacerbation of existing skin conditions such as eczema, atopic dermatitis, and neurodermatitis during or after the acute phase of infection (The Open Dermatology Journal).

📋 Summary Table

🔍 What This Means for the Melanocyte System

Eczema-like inflammation—whether induced by allergies, infection, or irritant exposure—can trigger immune-mediated disruption of keratinocyte barrier function, engage cytokine cascades (e.g., IL‑13, IL‑4), and disturb epidermal homeostasis. Though not directly targeting melanocytes, such changes can secondarily affect melanin distribution and pigment integrity through persistent inflammation.

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