title: Trichodysplasia spinulosa-associated polyomavirus (TSV) and Merkel cell polyomavirus: correlation between humoral and cellular immunity stronger with TSV.
abstract: Merkel Cell Polyomavirus (MCV) is a common infectious agent likely to be involved in the pathogenesis of most Merkel cell carcinomas (MCC). Trichodysplasia spinulosa-associated polyomavirus (TSV), which exhibit high seroprevalence in general population, has been detected in trichodysplasia spinulosa (TS) skin lesions suggesting an etiological role for this disease. Previous studies have shown strong MCV-specific T-cell responses, while no data exist on T-cell immunity against TSV. In order to characterize Th-cell immunity against TSV, and to allow comparisons with the MCV-specific Th-cell immunity, we studied TSV-specific proliferation, IFN-γ, IL-10 and IL-13, and MCV-specific IFN-γ and IL-10 responses in 51 healthy volunteers, and in one MCC patient. Recombinant TSV and MCV VP1 virus-like particles (VLPs) were used as antigens. A significant correlation was found between virus-specific Th-cell and antibody responses with TSV; with MCV it proved weaker. Despite significant homology in amino acid sequences, Th-cell crossreactivity was not evident between these viruses. Some subjects seronegative to both TSV and MCV exhibited Th-cell responses to both viruses. The agent initially priming these Th-cells remains an enigma. As CD8(+) cells specific to MCV T-Ag oncoprotein clearly provide an important defense against established MCC, the MCV VP1-specific Th-cells may, by suppressing MCV replication with antiviral cytokines such as IFN-γ, significantly contribute to preventing the full process of oncogenesis.
authors.affiliation: Departments of Virology, Haartman Institute, University of Helsinki, Helsinki, Finland. arun.kumar@helsinki.fi
authors.forename: Arun
authors.initials: A
authors.lastname: Kumar
authors.forename: Anu
authors.initials: A
authors.lastname: Kantele
authors.forename: Tommi
authors.initials: T
authors.lastname: Järvinen
authors.forename: Tingting
authors.initials: T
authors.lastname: Chen
authors.forename: Heli
authors.initials: H
authors.lastname: Kavola
authors.forename: Mohammadreza
authors.initials: M
authors.lastname: Sadeghi
authors.forename: Klaus
authors.initials: K
authors.lastname: Hedman
authors.forename: Rauli
authors.initials: R
authors.lastname: Franssila
mesh_terms: D000328:Adult; D000946:Antigens, Fungal / Q000276:immunology; D000956:Antigens, Viral / Q000276:immunology; D002176:Candida albicans / Q000276:immunology; D036022:Capsid Proteins / Q000276:immunology; D015266:Carcinoma, Merkel Cell / Q000276:immunology / Q000821:virology; D049109:Cell Proliferation; D002478:Cells, Cultured; D005260:Female; D000949:Histocompatibility Antigens Class II / Q000378:metabolism / Q000502:physiology; D006801:Humans; D007111:Immunity, Cellular; D056724:Immunity, Humoral; D007074:Immunoglobulin G / Q000097:blood; D007371:Interferon-gamma / Q000378:metabolism; D016753:Interleukin-10 / Q000378:metabolism; D008297:Male; D059965:Merkel cell polyomavirus / Q000276:immunology* / Q000502:physiology; D008875:Middle Aged; D027601:Polyomavirus Infections / Q000097:blood / Q000276:immunology* / Q000821:virology; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology* / Q000378:metabolism / Q000502:physiology / Q000821:virology; D014412:Tumor Virus Infections / Q000097:blood / Q000276:immunology* / Q000821:virology; D014779:Virus Replication; D055815:Young Adult
chemical_list: D000946:Antigens, Fungal; D000956:Antigens, Viral; D036022:Capsid Proteins; D000949:Histocompatibility Antigens Class II; C508609:IL10 protein, human; D007074:Immunoglobulin G; C062481:VP1 protein, polyomavirus; D016753:Interleukin-10; D007371:Interferon-gamma