One may postulate that after infecting the host, SV-40 may exert its tumourigenic potential when the immune system is impaired. while its mutagenic activities have been detected Anisomycin in different animal and human cell types [3,4]. In human tumours, SV-40 was identified for the first time in a patient affected by a cutaneous melanoma [5], that shares the onset model with UM. Altogether these data were the background that prompted us to investigate the association between UM and SV-40 by analysing the prevalence of SV-40 antibodies in serum samples from UM affected patients. This study was carried out, Anisomycin as reported before, by an indirect Enzyme-Linked Immunosorbent Assay (ELISA) with SV-40 specific synthetic peptides derived from its viral proteins, without cross-reactivity with the closely related BKV and JCV which are obiquitous polyomaviruses in humans [6]. In this investigation, serum samples Anisomycin from UM affected patients (n?=?48) and healthy subjects with ocular nevi (HSON; n?=?71) and without ocular nevi (HS; n?=?168), with the same median age (66?yrs), were analysed for presence of SV-40 antibodies. All patients and subjects were vaccinated against the poliomyelitis. The immunologic study was carried out by indirect ELISAs employing two specific mimotopes from SV-40 viral capsid proteins 1 and 2C3, named B and C peptides, respectively [6]. In our experiments, serum samples were considered SV-40 VP-positive upon reacting to both peptides B and C. Informed written consent was obtained from the patients and subjects. The study was approved by the County Ethical Committee, Ferrara, Italy. The overall prevalence, by combining SV-40-positive sera for both VP1 B and VP2/3 C peptides, in Anisomycin UM patients was 33%, higher than that detected in HSON or HS, 17% and 15% respectively. The difference between UM patients and HSON or HS is usually statistically significant (p?=?0.038 and p?=?0.004, respectively). Serologic profiles of serum antibody reactivity to SV40 mimotopes are reported in Physique?1. The difference of OD=optical density mean value of sera from UM and two control groups, is not statistically significant (p? ?0.05). Open in a separate window Physique 1 Serologic profile. Serologic profile of serum antibody reactivity to SV-40 mimotopes VP1 B (panel A) and VP2/3 C (panel B) and VPs B + C (panel C). Immunologic data are from patients affected by UM and from healthy individuals (HS) with and without ocular nevi. Data are OD values at 405?nm of serum samples diluted 1:20, detected in indirect ELISA. In scatter dot plotting, each plot represents the dispersion of OD values to a mean level indicated by the line inside the scatter with standard error mean (SEM) for each group of subjects analyzed (Mean OD SEM). Our immunologic data indicate that a subset (1/3) of UM is usually Anisomycin associated with SV-40, a small DNA tumour computer virus detected as a contaminant in early anti-polio vaccines [3,4,7]. At present, SV-40 infection seems to spread in humans by different ways, including the urine and the faecal-oral route [3,4,7]. UM onset, like other human cancers, is due to specific gene mutations. Since SV-40 Tbp is usually oncogenic, clastogenic, mutagenic and a transforming viral agent [3,7], may be a risk factor, together with other oncogenic brokers such as the U.V. irradiation, in the UM onset/progression [8]. One may postulate that after infecting the host, SV-40 may exert its tumourigenic potential when the immune system.
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