AI Article Synopsis
- The study explores how the HPV8 virus interacts with skin keratinocyte stem cells (KSCs), particularly how it influences KSC proliferation and viral transmission.
- HPV8's E6 gene specifically targets and activates certain KSCs, leading to their expansion and potential vulnerability to cancer caused by sun exposure.
- The findings suggest that HPV8 may play a critical role in the development of actinic keratosis, a skin condition linked to increased cancer risk, by manipulating KSCs without permanently integrating into their genetic material.
Article Abstract
Despite epidermal turnover, the skin is host to a complex array of microbes, including viruses, such as HPV, which must infect and manipulate skin keratinocyte stem cells (KSCs) to survive. This crosstalk between the virome and KSC populations remains largely unknown. Here, we investigated the effect of HPV8 on KSCs using various mouse models. We observed that the HPV8 early region gene E6 specifically caused Lrig1+ hair follicle junctional zone KSC proliferation and expansion, which would facilitate viral transmission. Within Lrig1+ KSCs specifically, HPV8 E6 bound intracellular p300 to phosphorylate the STAT3 transcriptional regulatory node. This induced ΔNp63 expression, resulting in KSC expansion into the overlying epidermis. HPV8 was associated with 70% of human actinic keratoses. Together, these results define the "hit-and-run" mechanism for HPV8 in human actinic keratosis as an expansion of KSCs, which lack melanosome protection and are thus susceptible to sun light-induced malignant transformation.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11383611 | PMC |
| http://dx.doi.org/10.1172/jci.insight.177898 | DOI Listing |
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