Abstract
To date, 14 human polyomaviruses (HPyVs) have been identified using high-throughput technologies. Among them, MCPyV, HPyV6, HPyV7 and TSPyV present a skin tropism, but a causal role in skin diseases has been established only for MCPyV as a causative agent of Merkel cell carcinoma (MCC) and TSPyV as an etiological agent of Trichodysplasia Spinulosa (TS). In the search for a possible role for cutaneous HPyVs in the development of skin malignant lesions, we investigated the prevalence of MCPyV, HPyV6, HPyV7 and TSPyV in actinic keratosis (AK), a premalignant skin lesion that has the potential to progress towards a squamous cell carcinoma (SCC). One skin lesion and one non-lesion skin from nine affected individuals were analyzed by qualitative PCR. MCPyV was detected in 9 out of 9 lesion biopsies and 6 out of 8 non-lesion biopsies. HPyV6 was detected only in healthy skin, while HPyV7 and TSPyV were not detected in any skin sample. These findings argue against a possible role of cutaneous HPyVs in AK. However, considering the small sample size analyzed, a definitive conclusion cannot be drawn. Longitudinal studies on large cohorts are warranted.
Highlights
Introduction iationsHuman Polyomaviruses (HPyVs) are ubiquitous viruses with high seroprevalences in the general population [1,2]
The presence of Merkel cell polyomavirus (MCPyV), HPyV6, HPyV7, and Trichodysplasia Spinulosa-associated PyV (TSPyV) DNA in lesion and non-lesion skin sections was determined by qualitative PCR
This preliminary study speaks against a possible causal role of the four human polyomaviruses investigated in actinic keratosis (AK)
Summary
Human Polyomaviruses (HPyVs) are ubiquitous viruses with high seroprevalences in the general population [1,2]. They contain a circular double-stranded DNA genome of approximately 5.0 kbp [1,2] encoding regulatory proteins and structural proteins. The major regulatory proteins are the large tumor antigen (LT) and the small tumor antigen (sT), while at least two structural proteins (VP1 and VP2) form the capsid. The regulatory proteins are expressed early during infection and participate in viral replication and viral transcription, while the structural proteins are expressed later in the infection cycle [1]. HPyVs may encode additional regulatory and structural proteins (e.g., ALTO, VP3, VP4, agnoprotein) [1]. HPyVs can establish a latent infection in different organs and tissues such as the brain, urogenital tract, and skin [1,2].
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