Abstract
The Polyomaviridae constitute a family of small DNA viruses infecting a variety of hosts. In humans, polyomaviruses can cause infections of the central nervous system, urinary tract, skin, and possibly the respiratory tract. Here we report the identification of a new human polyomavirus in plucked facial spines of a heart transplant patient with trichodysplasia spinulosa, a rare skin disease exclusively seen in immunocompromized patients. The trichodysplasia spinulosa-associated polyomavirus (TSV) genome was amplified through rolling-circle amplification and consists of a 5232-nucleotide circular DNA organized similarly to known polyomaviruses. Two putative “early” (small and large T antigen) and three putative “late” (VP1, VP2, VP3) genes were identified. The TSV large T antigen contains several domains (e.g. J-domain) and motifs (e.g. HPDKGG, pRb family-binding, zinc finger) described for other polyomaviruses and potentially involved in cellular transformation. Phylogenetic analysis revealed a close relationship of TSV with the Bornean orangutan polyomavirus and, more distantly, the Merkel cell polyomavirus that is found integrated in Merkel cell carcinomas of the skin. The presence of TSV in the affected patient's skin was confirmed by newly designed quantitative TSV-specific PCR, indicative of a viral load of 105 copies per cell. After topical cidofovir treatment, the lesions largely resolved coinciding with a reduction in TSV load. PCR screening demonstrated a 4% prevalence of TSV in an unrelated group of immunosuppressed transplant recipients without apparent disease. In conclusion, a new human polyomavirus was discovered and identified as the possible cause of trichodysplasia spinulosa in immunocompromized patients. The presence of TSV also in clinically unaffected individuals suggests frequent virus transmission causing subclinical, probably latent infections. Further studies have to reveal the impact of TSV infection in relation to other populations and diseases.
Highlights
Members of the polyomavirus family (Polyomaviridae) infect mammals and birds, and can affect various organs
In 2007, two additional human polyomaviruses were described, KI-polyomavirus (KIPyV or KIV) and WU-polyomavirus (WUPyV or WUV) [1,2], which were isolated from the respiratory tract and whose pathogenicity is still unclear
We describe the identification of a new human polyomavirus that combines specific properties of other human polyomaviruses, as it infects the skin and seems to cause disease only in immunocompromized patients probably as the result of unrestricted virus and host cell proliferation, possibly the inner root sheath cells of hair follicles
Summary
Members of the polyomavirus family (Polyomaviridae) infect mammals (rodents, bovines, primates) and birds (fowl, psittacines), and can affect various organs. JC-polyomavirus (JCPyV or JCV) and BK-polyomavirus (BKPyV or BKV), are established pathogens in immunocompromized hosts causing progressive multifocal leukoencephalopathy in AIDS patients and nephropathy in renal transplant recipients, respectively. In 2007, two additional human polyomaviruses were described, KI-polyomavirus (KIPyV or KIV) and WU-polyomavirus (WUPyV or WUV) [1,2], which were isolated from the respiratory tract and whose pathogenicity is still unclear. We describe the identification of a new human polyomavirus that combines specific properties of other human polyomaviruses, as it infects the skin and seems to cause disease only in immunocompromized patients probably as the result of unrestricted virus and host cell proliferation, possibly the inner root sheath cells of hair follicles
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