HSV-1 inhibits melanogenesis of PIG1 cells through downregulation of VN1R5/ERK pathway
- Arch Dermatol Res. 2025 Feb 6;317(1):347. doi: 10.1007/s00403-025-03844-5.
- 1. Department of Dermatology, The First Hospital of China Medical University, Shenyang, Liaoning, China.
- 2. Key Laboratory of Immunodermatology, Ministry of Education and NHC, National Joint Engineering Research Center for Theranostics of Immunological Skin Diseases, Shenyang, China.
- 3. Department of Dermatology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
- 4. Department of Thoracic Surgery, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Ji'nan, China.
- 5. Department of Dermatology, Beijing Friendship Hospital, Capital Medical University, Beijing, 100050, China.
- 6. Department of Dermatology, The First Hospital of China Medical University, Shenyang, Liaoning, China. [email protected].
- 7. Key Laboratory of Immunodermatology, Ministry of Education and NHC, National Joint Engineering Research Center for Theranostics of Immunological Skin Diseases, Shenyang, China. [email protected].
- 8. Key Laboratory of Immunodermatology, Ministry of Education and NHC, National Joint Engineering Research Center for Theranostics of Immunological Skin Diseases, Shenyang, China. [email protected].
- 9. Department of Dermatology, Shengjing Hospital of China Medical University, Shenyang, China. [email protected].
Herpes simplex virus type 1 (HSV-1) is an ubiquitous pathogen that can infect humans through skin or mucous regions. This study was to explore the effects and underlying mechanism of HSV-1 as examined within the human epidermal melanocyte cell line, PIG1. Our results showed that following HSV-1 Infection, PIG1 cells shrank and acquired a rounded shape, while the numbers and lengths of their dendrites decreased and melanogenesis was inhibited. Meanwhile, the HSV-1 receptors (nectin-1, herpes virus entry mediator, paired immunoglobulin-like type 2 receptor alpha) and phospho-extracellular signal-regulating kinase (p-ERK) were all substantially decreased, while vomeronasal type-1 receptor 5 (VN1R5) increased. Results of RNA interference and protein inhibitor assays revealed that knockdown of VN1R5 increased the expression of p-ERK and microphthalmia-associated transcription factor (MITF), while an inhibition of ERK decreased VN1R5 expression. Taken together, our study provides the first evidence that HSV-1 can infect human normal melanocytes and inhibit melanogenesis through VN1R5/ERK pathway.