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Polyomavirus BK (BKV) infection has been lately recognized as a major cause of renal allograft dysfunction. BKV-related interstitial nephropathy (PVAN) may affect 1-10% of renal allograft recipients, occurring more frequently in the first 6 months after transplantation. Progression to irreversible allograft failure has been observed in up to 45% of all cases; thanks to increased PVAN awareness and improved diagnostic techniques, the rate of graft loss has lowered, more consistently in centres with active screening and intervention programs. PVAN pathogenesis is characterized by multiple synergizing factors, among which immunodepression plays a key role. PVAN diagnosis requires the evaluation of a renal biopsy showing polyomavirus cytopathic changes and confirming BKV through an ancillary technique such as immunohistochemistry. Given the focal nature of the disease, early diagnosis may be difficult to obtain. Thus, quantification of BKV-DNA in plasma has been suggested as surrogate marker for PVAN. To date, given the lack of controlled trials, there is no consensus on a 'standard' management of PVAN. However, evidence based on reported observations suggests that a step-wise reduction of immunosuppression, preceded by pulsed steroids in case of coexistent acute rejection, may improve outcomes. Additional options may be represented by drugs with antiviral activity, such as cidofovir, leflunomide or quinolones. Application of a preventive treatment based on viremia monitoring has been recently proposed.

Our study reports pleural malignant mesothelioma (PMM) in seven female patients. All patients were resident in Catania area (Sicily), the median age was 69.2 years and ranged from 59 to 81 years. They were housewife. Their anamnesis was negative for both direct and indirect previous exposure to asbestos; the partners of all patients were also not exposed to asbestos. The exposure to X-rays was also excluded for these patients. Different pathogenetic mechanisms for the appearance of PMM in these patients can be hypothesized, for example, SV40 infection and genetic susceptibility; a minimal domestic exposure to asbestos can be not excluded. Therefore, further studies in a more large number of subjects are necessary to determine whether one or all of these hypothetic pathogenetic mechanisms are more significant for the develop of PMM.

Background: The etiopathogenic role of asbestos in causing malignant mesothelioma of the pleura is clearly supported by an impressive amount of data. Despite the frequent association with previous exposure to asbestos, only a relatively small fraction of those exposed develop malignant mesothelioma. The long latency period between initial exposure and onset of the tumor suggests that human mesothelioma, like many other tumors, has a multi-stage evolution with the occurrence of many mutating events involving various tumorigenic agents, probably in part initiating and in part promoting development. Recently this has raised great interest in the scientific world, in an attempt to identify possible factors which together with asbestos may have a role in developing this rare malignant tumor. Ionizing radiations and genetic susceptibility have occasionally been identified as the culprits. A virus called SV40 has been gaining increasing scientific credibility since the mid 1990's as a potential co-carcinogen of asbestos., Objectives: The aim of this article was to examine the supposed interaction between asbestos and SV40 in the pathogenesis of mesothelioma and the way this simian virus has become a human virus., Methods: All biomolecular and epidemiological data available from medical literature along with the results of the experiments performed during the last 7 years in our department laboratories were reviewed and compared., Results: The first two pieces of experimental evidence of the presence of SV40-like DNA sequences in mesothelioma samples were obtained in 1994 in the United States, and one year later in our laboratories. After these two studies many research groups started carrying out similar experiments, obtaining comparable results in most cases. Moreover, beyond the mere detection of viral DNA sequences large amount of biomolecular data has recently been added in favour of its role in the pathogenesis of mesothelioma. Epidemiological studies published to date were unable to provide similar unanimous results. Data regarding the source of human infection are still debatable, even if the inadvertent administration of contaminated poliovaccines to millions of people in Europe and the United States between 1955 and 1963 remains one of the most reasonable hypotheses., Conclusions: On the basis of all the biomolecular data reviewed and partially on the basis of epidemiological studies, SV40 seems to be the best candidate as a cofactor with asbestos in the development of human mesothelioma.

The occurrence of infections in organ transplantation is one of the most significant determinants of transplant outcome, because it is the most common life-threatening complication of long-term immunosuppressive therapy. Recently, besides the well-known direct effect of infections, other relevant biochemical factors such as cytokines, chemokines and growth factors have been considered. Aim of this review is to deal with the infections by mainly considering the unusual consequences of several infectious diseases like malignancies, graft loss and atherosclerosis. The number of patients affected by malignancies is increasing in all registries. Viral pathogens play a pathophysiological role in the development of the most frequent malignancies after solid organ transplantation. In some cases viruses act by altering cell transformation. Moreover, some pathogens may contribute to global immunosuppression and work together to promote oncogenesis. The viral load surveillance is recommended in the prevention of malignancies. The BK virus nephropathy in renal transplant recipients is emerging as an unusual consequence of graft loss. In this paper we examine the risk factors, the clinical characteristics and especially the diagnostic tools and treatments actually available. The third unusual consequence is the transplant vascular sclerosis, a multifactorial late complication of solid organ transplantation. The transplant vascular sclerosis has emerged as an important limitation in long-term graft survival. Several epidemiological, clinical and therapeutic interventional studies have shown how several potential contributing etiologic factors, such as Chlamydia and CMV infection, have been identified as being definitely associated with the development of transplant vascular sclerosis.

The BK virus (BKV) belongs to the family of the polyoma group. Although up to 60% of AIDS patients excrete BKV in the urine, there have been few reports of infection of kidney, lung, retina, brain and peripheral blood mononuclear cells. We report the case of a 37 year-old male HIV positive patient with BKV encephalitis. This diagnosis should be considered in AIDS patients with signs of cerebral disease.

Background: Polyoma virus (PV) is a double-stranded DNA virus, member of the Papovaviridae family. BKV and JCV are the most studied in human pathology, whereas simian virus 40 (SV40) is pathogenic in the monkey and has been implicated in human carcinogenesis. PV is associated with renal and urinary tract pathology. The initial infection by PV occurs in childhood, probably by airways, and is usually asymptomatic. Subsequently, it remains latent in kidneys, tonsils and CNS and may reactivate in concomitance with significant T-cell dysfunction. Infection in immunocompromised patients can be clinically relevant. However, asymptomatic viruria may be detected in 0.3 % of individuals without a known history of immunodeficiency., Case Report: We describe the case of a male patient, aged 31, admitted to our Unit for arterial hypertension and urinary abnormalities. He had a history of hemorrhagic cystitis in 1996 and persistent microscopic hematuria thereafter. Renal function was normal, arterial pressure well controlled with an ACE-inhibitor; urine culture was negative and most of the immunologic and rheumatologic tests were normal, with the exception of slightly reduced levels of C3 and an inverted CD4/CD8 ratio. Serology for HCV, HBV, HIV and screening for tumor markers were negative. Renal ultrasonography displayed an increased reflectivity, as seen in medical nephropathies; no nephrolithiasis was found. Urinary cytology showed "decoy cells", as typically found in PV infection, whose presence was confirmed by n-PCR. Diagnosis at discharge from the hospital was primary arterial hypertension and urinary JCV infection. Currently, no treatment of proven efficacy against PV is available., Conclusions: We think that there is an increasing amount of evidence to include screening for PV in the diagnosis of urinary tract abnormalities of unknown origin, even in apparently immunocompetent patients. Urinary cytology, in experienced hands, may be a useful and relatively inexpensive first step diagnostic tool.