Trichodysplasia spinulosa polyomavirus

A human-pathogenic, nonenveloped, double-stranded DNA virus of the Polyomaviridae family that is associated, in particular, with the rare follicular skin disorder trichodysplasia spinulosa in immunocompromised patients. The virus exhibits a pronounced tropism for follicular keratinocytes and, in the absence of adequate immune control, can cause a proliferative disorder of the hair follicle epithelium.

Virological Characteristics

• Family:Polyomaviridae 
• Genus: Alphapolyomavirus (see also Human Polyomaviruses)
• Genome: Circular, double-stranded DNA
• Genome size: Approx. 5.2 kbp
• Virion: Icosahedral, non-enveloped
• Diameter: Approx. 40–50 nm
• Structural proteins: VP1, VP2, VP3
• Early proteins: Large T antigen (LT), Small T antigen (sT)
• Primary target cells: Follicular keratinocytes
• Clinical association:Trichodysplasia spinulosa

TSPyV is widespread worldwide. Serological studies show that infection often occurs as early as childhood. In adults, seroprevalence rates of approximately 60–80% have been reported, depending on the population studied and the testing method used. Primary infection is predominantly asymptomatic in immunocompetent individuals.

Clinically manifest trichodysplasia spinulosa, on the other hand, is extremely rare and occurs almost exclusively in association with severe immunosuppression, particularly in:

• organ transplant recipients
• Patients with hematologic neoplasms
• Patients undergoing intensive immunosuppressive therapy
• Patients with severe congenital or acquired immunodeficiencies

In immunocompromised patients, TSPyV infection manifests as trichodysplasia spinulosa with the following key symptoms:

• Numerous skin-colored to erythematous, follicular papules with whitish, spiny keratin spicules.
• Prevalent involvement of the central face, particularly the nose, forehead, and cheeks.
• Loss of eyebrows and, occasionally, eyelashes.
• In severe cases, thickening of the facial skin with facies leonina.
• Occasional pruritus; the course is often largely asymptomatic.

TSPyV DNA detected by PCR from follicular horn spicules or skin biopsies. The detection of the virus alone does not prove the presence of clinically manifest disease. The decisive factor is the combination of a typical clinical presentation, histopathological changes, and detection of the virus.

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