👄 Cold Sore Trigger Simulator

Ultraviolet Light and Lip HSV-1 Reactivation

Placeholder: UV radiation is a classic, well-documented cold sore trigger.

• ~48h: UV outbreak onset (Placeholder timing note)
• +20%: Risk contribution (Placeholder weight)
• High: Photoprotection benefit (Placeholder note)
• Summer: Common season (Placeholder note)

UV-triggered reactivation pathway

Placeholder: UV exposure damages skin and disrupts local immune control.

Stress Hormones and Latent Virus Reactivation

Placeholder: chronic and acute stress both raise outbreak frequency.

• Moderate: Stress correlation (Placeholder note)
• +18%: Risk contribution (Placeholder weight)
• Immunosuppressive: Cortisol effect (Placeholder note)
• Days: Onset delay (Placeholder note)

Stress-immune axis mechanism

Placeholder: cortisol suppresses local T-cell surveillance at nerve endings.

Febrile Illness as Classic Reactivation Trigger

Placeholder: fever blisters are named for this exact association.

• "Fever blister": Historic name (Placeholder note)
• +22%: Risk contribution (Placeholder weight)
• Cold/flu: Common cause (Placeholder note)
• 1-3 days: Onset window (Placeholder note)

Systemic fever and ganglion reactivation

Placeholder: fever cytokines destabilize latency in trigeminal ganglion neurons.

Cyclic Hormones and Perioral Outbreak Timing

Placeholder: some people notice outbreaks tied to menstrual timing.

• Cyclic: Reported association (Placeholder note)
• +15%: Risk contribution (Placeholder weight)
• Perimenstrual: Peak phase (Placeholder note)
• Hormonal: Mechanism (Placeholder note)

Hormone-linked immune fluctuation

Placeholder: estrogen and progesterone shifts modulate local immunity.

Immunosuppression and Loss of Latency Control

Placeholder: weakened immunity removes the brakes on reactivation.

• Transplant, HIV: High-risk groups (Placeholder note)
• +25%: Risk contribution (Placeholder weight)
• Higher: Outbreak severity (Placeholder note)
• Elevated: Recurrence rate (Placeholder note)

Immune surveillance and viral latency

Placeholder: CD8+ T-cells normally patrol ganglia to keep HSV-1 dormant.

Placeholder: combined triggers compound risk beyond any single factor.