Multiplication of poliomyelitis virus for vaccine production in 1955-1961 was realized in kidney cell culture from M. rhesus naturally infected with SV-40 simian virus. Hence, some lots of the vaccine were contaminated with this virus. It was found that SV-40 is oncogenic for laboratory rodents. Since 1963, in accordance with WHO recommendation, green monkey kidneys containing no SV-40 were used instead of M. rhesus kidneys. Overall vaccination of the population with poliomyelitis vaccine in 1955-1961 led to infection of many humans in Russia and many foreign countries with SV-40. The possibility of horizontal transmission of the virus was demonstrated. As a result, virus (its DNA sequences) was detected in individuals who were never vaccinated. Hundreds of reports, often contradictory, discuss this problem. Our study is based on the analyses of 460 blood specimens from subjects living in different regions of Russia (Krasnodar region, Moscow, Novosibirsk region, Krasnoyarsk territory). The percent of individuals infected with SV-40 varies from 16 to 49%.
We aimed to assess the connection between chronic inflammatory disorders (CIDs) and Merkel cell carcinoma (MCC).
Merkel cell carcinoma cases diagnosed in 1978-2009 were extracted from the Finnish Cancer Registry and controls from the Population Registry. Information on reimbursed CIDs was linked to clinicopathological data including Merkel cell polyomavirus (MCV) status by qPCR and immunohistochemistry for the large T antigen of MCV (LTA), Ki-67 and tumour-infiltrating lymphocytes.
Chronic inflammatory disorders increased the risk of MCC significantly (odds ratio (OR) 1.39, 95% confidence interval (CI) 1.03-1.88), specifically connective tissue/systemic diseases (OR 1.75, 95% CI 1.09-1.80) and diabetic conditions (OR 1.51, 95% CI 1.03-2.22). Chronic inflammatory disorders associated with larger tumour diameter (P=0.02) and higher Ki-67 expression (P=0.005). The expression of LTA was seen significantly more often in the absence of CIDs (P=0.05).
Patients with CID are at significantly higher risk for aggressive MCC. Merkel cell polyomavirus positivity is more common in MCC patients unafflicted by CID.
BACKGROUND: The importance of two recently identified polyomaviruses, WUV and KIV, as respiratory pathogens in populations with a high HIV prevalence needs to be defined, since human polyomaviruses can cause significant morbidity and mortality in patients with immunosuppression. Geographic distribution and disease association of WUV and KIV genotypes are not yet clearly defined. OBJECTIVES: To investigate the prevalence of WUV and KIV in HIV-positive and HIV-negative patients with respiratory infections in hospitals in South Africa and determine their genotypes. STUDY DESIGN: Specimens from patients with acute respiratory infections from hospitals serving Pretoria were screened for WUV and KIV. Positive specimens were sequenced and subjected to phylogenetic analysis. RESULTS: WUV was identified in (7%) and KIV in (1%) of mainly pediatric patients. Co-infections were common in WUV- and KIV-infected patients (71% and 66.6%, respectively); 57% of patients with WUV and 33% of patients with KIV were HIV-positive while the HIV prevalence in the respiratory virus patient group screened in this study was 33% WUV and KIV patients presented with moderate to severe lower respiratory tract disease. Four distinct and 2 unique WUV strains were identified clustering into 2 of 4 globally identified genotypes. KIV strains were identical to strains from Sweden. CONCLUSION: WUV is frequently detected in HIV-infected patients with respiratory disease, but its role as respiratory pathogen remains uncertain.
To test the hypothesis that Merkel cell polyomavirus (MCPyV) can infect cells of the lymphoid system, we analyzed 353 specimens, including 152 non-Hodgkin lymphomas, 44 Hodgkin lymphomas, 110 benign lymph nodes, 27 lymph nodes with metastasis, and 20 extranodal tissue samples. MCPyV DNA was detected by quantitative PCR in 13 (6.6%) of 196 lymphomas, including 5 (20.8%) of 24 chronic lymphocytic leukemia specimens, and in 11 (10%) of 110 benign lymph nodes, including 8 (13.1%) of 61 samples of reactive hyperplasia and 3 (10.3%) of 29 normal lymph nodes. Other samples were MCPyV negative. Sequence analysis of 9 virus-positive samples confirmed the identity of MCPyV; 3 viral strains were represented. Immunohistochemical testing showed that 1 T-cell lymphoma expressed MCPyV T-antigen. These findings suggest that the lymphoid system plays a role in MCPyV infection and may be a site for MCPyV persistence.
Viral infections remain the cause of key complications following haematopoietic stem cell transplantation (HSCT). The impact of multiple, concurrent viral reactivations/infections remains to be delineated.
The clinical correlates of single or multiple viremic infections following HSCT and especially the occurrence of respiratory viruses in the bloodstream were investigated. We retrospectively searched for 23 viruses in a total of 184 sera from 53 paediatric patients. The time-points of interest were pre-HSCT, one, two and three months post-HSCT, and at discharge or death. The viruses were analyzed by quantitative or qualitative PCR.
Of the 53 patients, 13 (25%) had viraemias by multiple viruses and 27 (51%) by a single virus. Thirteen patients (25%) had no viruses detected by PCR during the study period. In the children with viremic co-infections, polyomaviruses predominated over herpes viruses. Nearly half the patients, 24/53 (45%) had a polyomavirus in their serum at one or more time-points. At 12/15 time-points and in 11/13 patients with co-infections polyomaviruses were involved, compared with 6/15 time-points and 6/13 patients for cytomegalovirus. Acute graft-versus-host disease (GvHD) and steroid use were significant risk factors for the viraemias caused by more than one virus.
Viral co-detection is a common finding in children undergoing HSCT. With large-scale viral screening also viruses other than CMV could be found as potential pathogens. In this study, BKPyV predominated over CMV as a contributor in viraemias caused by multiple viruses in children receiving HSCT.
WU polyomavirus was detected in nasopharyngeal aspirates in 2 (2.5%) of 79 children with respiratory infections (both infected with respiratory syncytial virus) and in 5 (6.4%) of 78 asymptomatic children during the same winter season in Canada. The strains were closely related to Australian and American viruses based on analysis of large T antigen (TAg) and VP2 genes. The pathogenic role of WU virus is still uncertain.