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.