WUPyV Research Articles

Is it the Lower Respiratory Tract a Real Replication Site for KI Polyomavirus?

Is it the Lower Respiratory Tract a Real Replication Site for KI Polyomavirus? Recently two novel KI and WU polyomaviruses have been identified from human respiratory specimens. The spectrum of clinical manifestations and their role in respiratory tract are currently unknown. Here, to determine the prevalence and codetection of KIPyV and WUPyV polyomaviruses in the lower respiratory tract specimens of immunocompromised patients eighty-seven bronchoalveolar lavages or bronchoaspirates from 73 immunocompromised patients with acute respiratory symptoms were screened by quantitative real-time PCR.

KI, WU, and Merkel Cell Polyomavirus DNA was not Detected in Guthrie Cards of Children who Later Developed Acute Lymphoblastic Leukemia

Neonatal dried blood spots (Guthrie cards) have been used to demonstrate a prenatal origin of clonal leukemia-specific genetic aberrations in several subgroups of childhood acute lymphoblastic leukemia (ALL). One hypothesis suggests that an infectious agent could initiate genetic transformation already in utero. In search for a possible viral agent, Guthrie cards were analyzed for the presence of 3 newly discovered polyomavirus Karolinska Institutet polymavirus (KIPyV), Washington University polyomavirus (WUPyV), and Merkel cell polyomavirus (MCPyV). Guthrie cards from 50 children who later developed ALL and 100 matched controls were collected and analyzed by standard or real-time polymerase chain reaction for the presence of the VP1 region of KIPyV, WUPyV, and MCPyV, and the LT region for MCPyV. DNA from KIPyV, WUPyV, and MCPyV was not detected in neonatal blood samples from children with ALL or controls. Prenatal infections with these viruses are not likely to be etiological drivers for childhood leukemogenesis.

WU Polyomavirus Infections in Children in Fuzhou, China

In this study, we tested for the presence of WUV in children with respiratory tract infection in Fuzhou, Fujian, China. Nasopharyngeal aspirates (NPA) were collected from children with respiratory tract infection from Nov. 2007 to Oct. 2008. A total of 58 clinical respiratory tract samples were tested for WUV by using PCR method. The positive products were sequenced and compared with those in Genbank. 4 of 58 were positive (WUV was 6.9%). All of children who were positive for WUV had respiratory manifestations. WUV was tested positive in the sputum and vomited specimen, and in the fecal specimen of one outpatient child who also had acute gastroenteritis. Co-infections with other respiratory viruses were found in 3 (75.0%) of WUV positive NPA samples. Polyomavirus WUV infection may be associated with upper and lower respiratory infection. WUV might also be transmitted through the gastrointestinal tract.

Seroepidemiology of WU polyomavirus among children exposed perinatally to HIV‐1

WU polyomavirus (WUPyV), a new member of the genus wukipolyomavirus in the family Polyomaviridae, has been detected in serum and tissues of individuals infected with HIV. However, the epidemiology of WUPyV among children exposed perinatally to HIV-1 is unknown. To investigate the epidemiology of WUPyV in children exposed to and infected perinatally with HIV, serum samples from 150 children exposed to HIV and 114 children infected with HIV were screened for IgG antibodies to WUPyV. A subset was screened for IgM antibodies to WUPyV. Both antibody detection assays were performed using a recombinant WUPyV VP1-based ELISA. The overall seroprevalence of WUPyV IgG was 76.3% in children infected with HIV and 62% in children exposed perinatally to HIV. In the group of children infected with HIV, the prevalence of WUPyV IgG antibody reached its peak in 2-3 year olds (90.9%). In children 0-5 months of age, IgG seroprevalence was lower in those children exposed to HIV compared to children infected with HIV (43.1% vs.75%, P = 0.047). However, the seroprevalence of WUPyV IgM antibody was higher in children exposed to HIV compared to infants infected with HIV (27.4% vs. 8.3%, P = 0.044). WUPyV infection is acquired in early childhood in the majority of children born to mothers infected with HIV. The implication of this infection and the specific clinical syndrome that it produces, if any, remain to be defined.

Efficient propagation of archetype BK and JC polyomaviruses

BKPyV and JCPyV are closely related, ubiquitous human pathogens that cause disease in immunocompromised patients. The DNA sequence of the regulatory regions distinguishes two forms of these viruses, designated archetype and rearranged. Although cell culture systems exist for rearranged BKPyV and JCPyV, currently there is no robust cell culture system to study the archetype viruses. Large T antigen (TAg) is a virally encoded protein required to initiate viral DNA synthesis. Because archetype virus produces undetectable levels of TAg, we hypothesized that TAg overexpression would stimulate archetype virus replication. Efficient propagation of the archetype forms of BKPyV and JCPyV was observed in 293TT cells, human embryonic kidney cells overexpressing SV40 TAg. Importantly, the archetypal structure of the regulatory region was maintained during viral growth. Significant replication was not observed for Merkel cell, KI, or WU polyomaviruses. 293TT cells provide a means of propagating archetype BKPyV and JCPyV for detailed study.

WU Polyomavirus Infection Confirmed by Genetic and Serologic Tests in an Infant With Bronchitis

To the Editors: A 9-month-old previously healthy girl was admitted to the KKR Sapporo Medical Center with 1-day history of nasal discharge and high fever. A chest roentgenogram showed lung hyperinflation with increased vascular markings. She was diagnosed with bronchitis and was treated with hydration and inhalation therapy with a β2-stimulant. She was discharged from the hospital after 3 days. The nasopharyngeal (NP) sample was subjected to reverse transcription-polymerase chain reaction (RT-PCR) screening for 14 viral pathogens (respiratory syncytial virus (RSV), human metapneumovirus, human rhinovirus, human bocavirus, parainfluenza viruses 1–3, influenza A virus, influenza B virus, human enterovirus, human coronaviruses, adenovirus, KI polyomavirus, and WU polyomavirus [WUPyV]) as previously described.1 RSV and WUPyV were detected. Serum samples were studied for WUPyV DNA using a real-time PCR assay in the acute phase (4 days after onset) and the convalescent phase (13 days after onset), and IgG antibody titers to virus protein 1 (VP1; a capsid protein of WUPyV) were measured using an immunofluorescence assay as previously described.1,2 WUPyV DNA was detected in the acute phase (9.6 × 102 copies/mL) but not in the convalescent phase (<5.0 × 10 copies/mL). The titers of the IgG antibody against WUPyV VP1 increased from <1:10 (acute phase) to 1:40 (convalescent phase). In 2007, a novel virus, WUPyV, was cloned from respiratory tract samples in the United States.3 Although the WUPyV genome was detected in 1.2% to 16.4% of NP samples in patients with respiratory tract infections,1,3 it was not clear whether WUPyV caused infection or was an innocent bystander.4 Other viruses (RSV, human metapneumovirus, human rhinovirus, human bocavirus, and parainfluenza virus 1) were simultaneously detected in 44.7% of the WUPyV-positive NP samples, which complicated understanding the role of WUPyV in respiratory tract infections.1 Clinical findings of our case were indistinguishable from those for patients with RSV-positive bronchitis, but the present study demonstrated infection with WUPyV in a patient with bronchitis by genetic and serologic testing. Both detection of the WUPyV genome in serum samples by real-time PCR and measurement of antibody titers against WUPyV VP1 by an immunofluorescence assay are useful for analysis of the pathogenesis of WUPyV infection. Shinobu Teramoto, MD Department of Pediatrics Hokkaido University Graduate School of Medicine Naoko Koseki, MD Mikio Yoshioka, MD, PhD Yukiko Matsunami, MD Noriko Yanazume, MD Mitsuru Nawate, MD Takaaki Shikano, MD, PhD Yutaka Takahashi, MD, PhD Department of Pediatrics KKR Sapporo Medical Center Sapporo, Japan Hideaki Kikuta, MD, PhD Pediatric Clinic Touei Hospital Sapporo, Japan Nobuhisa Ishiguro, MD, PhD Department of Pediatrics Hokkaido University Graduate School of Medicine Sapporo, Japan

New respiratory viruses and the elderly.

The diagnostics of respiratory viral infections has improved markedly during the last 15 years with the development of PCR techniques. Since 1997, several new respiratory viruses and their subgroups have been discovered: influenza A viruses H5N1 and H1N1, human metapneumovirus, coronaviruses SARS, NL63 and HKU1, human bocavirus, human rhinoviruses C and D and potential respiratory pathogens, the KI and WU polyomaviruses and the torque teno virus. The detection of previously known viruses has also improved. Currently, a viral cause of respiratory illness is almost exclusively identifiable in children, but in the elderly, the detection rates of a viral etiology are below 40%, and this holds also true for exacerbations of chronic respiratory illnesses. The new viruses cause respiratory symptoms like the common cold, cough, bronchitis, bronchiolitis, exacerbations of asthma and chronic obstructive pulmonary disease and pneumonia. Acute respiratory failure may occur. These viruses are distributed throughout the globe and affect people of all ages. Data regarding these viruses and the elderly are scarce. This review introduces these new viruses and reviews their clinical significance, especially with regard to the elderly population.

Prokaryotic expression and pilot application of capsid proteins of WU polyomavirus

Objective To express the capsid proteins of WU polyomavirus(WUPyV) for research and find antigen for diagnostic value. Methods Coding sequences of capsid proteins of WU polyomavirus by PCR were cloned in prokaryotic expression vector PGEX-20T. Recombinant plasmids were transformed into E. coli BL21(DE3) and induced by IPTG for proteins expression. Recombinant proteins were identified by Western blot. Results SDS-PAGE proved that recombinant proteins showed three bands with molecular relative mass of 69×103, 63×103 and 56×103. The recombinant proteins were recognized by anti-GST McAb. The antigenicity was tested by Western blot using 16 WU polyomavirus positive and 70 negative sera. Conclusion Recombinant VP1, VP2 and VP3 expressed in E. coli can combine with WUPyV-Ab and have good antigenicity. They can be used for further research. Key words: WU polyomavirus; Capsid protein; Prokaryotic expression

Detection of KI polyomavirus and WU polyomavirus DNA by real-time polymerase chain reaction in nasopharyngeal swabs and in normal lung and lung adenocarcinoma tissues

ABSTRACTPolyomaviruses KI (KIPyV) and WU (WUPyV) were detected from 7 (3.0%) and 38 (16.4%) of 232 children with respiratory tract infections by real‐time PCR. The rates of infection by KIPyV and WUPyV alone were 3 of 7 (42.9%) and 20 of 38 (52.6%), respectively. In the other samples, various viruses (human respiratory syncytial virus, human metapneumovirus, human rhinovirus, parainfluenza virus 1 and human bocavirus) were detected simultaneously. One case was positive for KIPyV, WUPyV and hMPV. There was no obvious difference in clinical symptoms between KIPyV‐positive and WUPyV‐positive patients with or without coinfection. KIPyV was detected in one of 30 specimens of lung tissue (3.3%). Neither of the viruses was detected in 30 samples of lung adenocarcinoma tissue.

WU and KI polyomavirus infections in pediatric hematology/oncology patients with acute respiratory tract illness

Background WU and KI polyomaviruses (PyV) were discovered in 2007 in respiratory tract samples in adults and children. Other polyomaviruses (BKPyV and JCPyV) have been associated with illness in immunocompromised patients, and some studies suggest a higher prevalence of WUPyV and KIPyV in this population. Objective To determine whether a higher prevalence or viral load for WUPyV and KIPyV exists in immunocompromised children compared with immunocompetent children. Study design We measured the prevalence and viral load of WU and KI PyV by quantitative real-time PCR of viral DNA in respiratory tract specimens from pediatric hematology/oncology patients and immunocompetent controls with acute respiratory illnesses. Results The prevalence of WUPyV in the immunocompromised population was 5/161 (3%) versus 14/295 (5%) in the control population ( P = 0.5), and 9/161 (5.6%) versus 7/295 (2.3%) respectively for KIPyV ( P = 0.13). The mean viral load (in copies per cell or mL of sample) for KIPyV, was higher in the immunocompromised group compared to the control group ( P = 0.019), but was not statistically different for WUPyV. A higher prevalence was seen in the hematopoietic stem cell transplant recipients compared with other immunocompromised patients (6/26 versus 3/43, P = 0.054). Viral persistence was demonstrated only in 1/25 (4%) of sequential samples for KIPyV, and no persistence was seen for WUPyV. Conclusions A higher prevalence of WUPyV or KIPyV in the immunocompromised population compared with the immunocompetent group was not demonstrated. Higher viral loads for KIPyV in the immunocompromised group may suggest an increased pathogenic potential in this population.

WU polyomavirus infection among children in South China

This study aimed at investigating the prevalence and clinical characteristics of children with respiratory infection by WU polyomavirus (WUPyV) in Southern China. Nasopharyngeal aspirate samples were collected from 771 children with acute respiratory tract infection admitted to hospital and 82 samples from healthy subjects for routine examination at the outpatient service at the Second Affiliated Hospital of Shantou University, Medical College from July 2008 to June 2009. WUPyV was detected by the polymerase chain reaction (PCR) and DNA sequencing. All WUPyV-positive specimens were characterized further for nine viruses causing common respiratory infections, including influenza A and B, respiratory syncytial virus (RSV), parainfluenza virus (PIV) 1 and 3, human metapneumovirus, human bocavirus, adenovirus, and rhinovirus by PCR or real time (RT)-PCR. Fifteen out of 771 specimens from patients with acute respiratory tract infection, but none from healthy subjects, were positive for WUPyV and the positivity rate was 2%. Patients with WUPyV infection were between 2 and 48 months of age, and nine of the patients were male while six female. Four out of 15 patients were co-infected with RSV, one with adenovirus or rhinovirus, respectively. Patients with WUPyV infection displayed predominantly cough, moderate fever, and wheezing, and were diagnosed with pneumonia (n = 8), bronchiolitis (n = 4), upper respiratory tract infections (n = 2) and bronchitis (n = 1). One patient developed encephalitis. Therefore, WUPyV infection can cause acute respiratory tract infection with atypical symptoms, including severe complications, in children.

Secondary lymphoid tissue as an important site for WU polyomavirus infection in immunocompetent children

The polyomaviruses KI and WU (KIPyV and WUPyV) have been identified in respiratory specimens from children with acute respiratory infections, which suggests the respiratory tract as a possible site of infection. However, the persistence of infection in the lymphoid system is unknown. Fresh samples (n = 211) of tonsils, adenoids, and peripheral blood mononuclear cells (PBMCs) from 83 immunocompetent children (mean age 4.8 years) were tested for amplification of the KIPyV VP1 and WUPyV VP2 genes. The known BK and JC polyomaviruses and the lymphotropic human herpesvirus (HHV)-6 were also investigated by quantitative real-time PCR and direct sequencing. In addition, 98 nasopharyngeal swabs collected from children (mean age 6.2 years) affected by seasonal influenza-like illness were tested. Of the lymphoid tissues, 34.9% were positive for WUPyV, 4.8% for BK virus, and 33.8% for HHV-6. KIPyV and JC virus were not detected in these specimens. None of the polyomaviruses were detected in PBMCs. Among the nasopharyngeal samples, the prevalence of WUPyV was 27.5%, although 70% of the positive samples were co-infected with at least one of the following respiratory viruses: influenza virus, adenovirus, and respiratory syncytial virus. Phylogenetic analysis revealed high sequence homology (99%) between lymphoid- and nasopharynx-derived WUPyV strains. These results suggest that the tonsils and adenoids of immunocompetent children are a reservoir for WUPyV infection; probably due to the respiratory route of transmission. In addition, the prevalence of WUPyV was high among the children, and the virus was identified more frequently in older children than during the first years of life.

Contribution of common and recently described respiratory viruses to annual hospitalizations in children in South Africa

The contribution of viruses to lower respiratory tract disease in sub‐Saharan Africa where human immunodeficiency virus may exacerbate respiratory infections is not well defined. No data exist on some of these viruses for Southern Africa. Comprehensive molecular screening may define the role of these viruses as single and co‐infections in a population with a high HIV‐AIDS burden. To address this, children less than 5 years of age with respiratory infections from 3 public sector hospitals, Pretoria South Africa were screened for 14 respiratory viruses, by PCR over 2 years. Healthy control children from the same region were included. Rhinovirus was identified in 33% of patients, RSV (30.1%), PIV‐3 (7.8%), hBoV (6.1%), adenovirus (5.7%), hMPV (4.8%), influenza A (3.4%), coronavirus NL63 (2.1%), and OC43 (1.8%). PIV‐1, PIV‐2, CoV‐229E, ‐HKU1, and influenza B occurred in <1.5% of patients. Most cases with adenovirus, influenza A, hMPV, hBoV, coronaviruses, and WU virus occurred as co‐infections while RSV, PIV‐3, and rhinovirus were identified most frequently as the only respiratory pathogen. Rhinovirus but not RSV or PIV‐3 was also frequently identified in healthy controls. A higher HIV sero‐prevalence was noticed in patients with co‐infections although co‐infections were not associated with more severe disease. RSV, hPMV, PIV‐3, and influenza viruses had defined seasons while rhinovirus, adenovirus, and coronavirus infections occurred year round in this temporal region of sub‐Saharan Africa. J. Med. Virol. 83:1458–1468, 2011. © 2011 Wiley‐Liss, Inc.

Prevalence of WU and KI polyomaviruses in plasma, urine, and respiratory samples from renal transplant patients

WU and KI polyomaviruses (WUPyV, KIPyV) have been detected in respiratory, blood, stool, and lymphoid tissue, but not in urine samples. PCR based detection revealed higher frequency in immunocompromised individuals. In this study the prevalence of WUPyV and KIPyV was analyzed in respiratory, urine, and blood samples from renal transplant patients compared with healthy individuals. WUPyV and KIPyV were detected by nested PCR. The PCR products were sequenced and viral DNA loads were determined by quantitative real-time PCR. WUPyV and KIPyV were found in plasma (3.6%; 7/195), urine (14%; 7/50), and respiratory samples (10%; 9/90) of renal transplant patients, but not in plasma (0/200) and urine (0/36) specimens from healthy blood donors. WUPyV and KIPyV were detected mainly early after renal transplantation and the viral loads were low. A higher prevalence of WUPyV was found in plasma and urine samples, KIPyV was found more frequently in respiratory samples from renal transplant patients. It is hypothesized that immunosuppression due to the transplantation may result in reactivation of these viruses or may establish greater susceptibility to infection with KIPyV and WUPyV.

Abstract 950: Merkel cell polyomavirus infection in cutaneous squamous cell carcinomas

Abstract Objective: Merkel cell polyomavirus (MCV) DNA has been reported previously in 0-25% of squamous cell carcinomas (SCC) occurring in immunocompetent individuals. No studies have investigated MCV seroreactivity in individuals with SCC. We conducted a clinic-based case-control study to investigate the association between MCV seroreactivity and SCC, overall and stratified by MCV DNA status of the SCC tumor tissue. Methods: Patients with histologically-confirmed cutaneous SCC (n=173) were recruited from a university dermatology clinic. Controls were patients undergoing skin cancer screening exams who screened negative for and had no history of skin or other cancers (n=300). Levels of antibodies against capsid antigens for MCV and other polyomavirus controls (JC virus (JCV) and KI virus (KIV)) were determined by fluorescent bead-based multiplex serology. Fresh-frozen tumor tissues were obtained from 145 SCC cases, and DNA from six polyomaviruses (MCV, JCV, KIV, WU virus (WUV), BK virus (BKV) and simian virus 40 (SV40)) was measured using multiplexed PCR. Polyomavirus seropositivity, based on binary cutpoints, and quartiles of seroreactivity, based on the control distribution, were compared between SCC cases and controls, overall and stratified by the presence or absence of MCV DNA in SCC tumor tissues. Associations were estimated by calculating odds ratios (OR) and 95% confidence intervals (CI) using logistic regression to adjust for age, sex, and skin reaction to the sun. Results: MCV seropositivity was associated with a statistically significant increased risk of SCC (OR=1.80, 95% CI=1.03-3.12), whereas no association was observed for JCV (OR=1.17, 95% CI=0.72-1.92) or KIV (OR=0.88, 95% CI=0.37-2.09) seropositivity. MCV DNA was detected in 55 (38%) of SCC tumor tissues, whereas all tissues were negative for DNA from the other five polyomaviruses. Using controls as the reference group, MCV DNA-positive SCC cases were three times as likely to be MCV seropositive (OR=3.15, 95% CI=1.11-8.92) and almost six times as likely to have MCV antibody levels in the fourth versus first quartile (OR=5.94, 95% CI=1.79-19.74, ptrend=0.001). No associations were observed between MCV seropositivity and MCV DNA-negative SCC (OR=1.40, 95% CI=0.78-2.77) or between JCV or KIV seropositivity and MCV DNA-negative or DNA-positive SCC. Conclusion: SCC patients were significantly more likely than controls to exhibit MCV seroreactivity, particularly if they had MCV DNA in their SCC tumor tissue. This association was specific to MCV, with no associations observed for the other polyomaviruses studied. These results suggest that past exposure to MCV may be a risk factor for SCC in immunocompetent individuals. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 950. doi:10.1158/1538-7445.AM2011-950

Infrequent Detection of KI, WU and MC Polyomaviruses in Immunosuppressed Individuals with or without Progressive Multifocal Leukoencephalopathy

Conflicting prevalence of newly identified KI(KIPyV), WU(WUPyV) and Merkel Cell Carcinoma(MCPyV) polyomaviruses have been reported in progressive multifocal leukoencephalopathy(PML) patient samples, ranging from 0 to 14.3%. We analyzed the prevalence of these polyomaviruses in cerebrospinal fluid(CSF), peripheral blood mononuclear cells(PBMC), and bone marrow samples from PML patients, immunosuppressed individuals with or without HIV, and multiple sclerosis(MS) patients. Distinct PCR tests for KIPyV, WUPyV and MCPyV DNA performed in two independent laboratories detected low levels of MCPyV DNA only in 1/269 samples. The infrequent detections of these viruses in multiple samples from immunosuppressed individuals including those with PML suggest that their reactivation mechanisms may be different from that of JC polyomavirus (JCPyV) and that they do not play a role in the pathogenesis of PML.

Newly discovered KI, WU, and Merkel cell polyomaviruses: No evidence of mother-to-fetus transmission

BackgroundThree* human polyomaviruses have been discovered recently, KIPyV, WUPyV and MCPyV. These viruses appear to circulate ubiquitously; however, their clinical significance beyond Merkel cell carcinoma is almost completely unknown. In particular, nothing is known about their preponderance in vertical transmission. The aim of this study was to investigate the frequency of fetal infections by these viruses. We sought the three by PCR, and MCPyV also by real-time quantitative PCR (qPCR), from 535 fetal autopsy samples (heart, liver, placenta) from intrauterine fetal deaths (IUFDs) (N = 169), miscarriages (120) or induced abortions (246). We also measured the MCPyV IgG antibodies in the corresponding maternal sera (N = 462) mostly from the first trimester.ResultsNo sample showed KIPyV or WUPyV DNA. Interestingly, one placenta was reproducibly PCR positive for MCPyV. Among the 462 corresponding pregnant women, 212 (45.9%) were MCPyV IgG seropositive.ConclusionsOur data suggest that none of the three emerging polyomaviruses often cause miscarriages or IUFDs, nor are they transmitted to fetuses. Yet, more than half the expectant mothers were susceptible to infection by the MCPyV.

KI and WU Polyomaviruses and CD4+ Cell Counts in HIV-1–infected Patients, Italy

To investigate an association between KI and WU polyomavirus (KIPyV and WUPyV) infections and CD4+ cell counts, we tested HIV-1–positive patients and blood donors. No association was found between cell counts and virus infections in HIV-1–positive patients. Frequency of KIPyV infection was similar for both groups. WUPyV was more frequent in HIV-1–positive patients.

High prevalence of antibodies against polyomavirus WU, polyomavirus KI, and human bocavirus in German blood donors

BackgroundDNA of the polyomaviruses WU (WUPyV) and KI (KIPyV) and of human bocavirus (HBoV) has been detected with varying frequency in respiratory tract samples of children. However, only little is known about the humoral immune response against these viruses. Our aim was to establish virus-specific serological assays and to determine the prevalence of immunoglobulin G (IgG) against these three viruses in the general population.MethodsThe capsid proteins VP1 of WUPyV and KIPyV and VP2 of HBoV were cloned into baculovirus vectors and expressed in Sf9 insect cells. IgG antibodies against WUPyV VP1, KIPyV VP1, and HBoV VP2 were determined by immunofluorescence assays in 100 plasma samples of blood donors.ResultsThe median age of the blood donors was 31 years (range 20 - 66 yrs), 52% were male. 89% of the samples were positive for WUPyV IgG (median age 31 yrs, 49.4% male), 67% were positive for KIPyV IgG (median age 32 yrs, 46.3% male), and 76% were positive for HBoV IgG (median age 32 yrs, 51.3% male). For WUPyV and HBoV, there were no significant differences of the seropositivity rates with respect to age groups or gender. For KIPyV, the seropositivity rate increased significantly from 59% in the age group 20 - 29 years to 100% in the age group > 50 years.ConclusionsHigh prevalences of antibodies against WUPyV, KIPyV, and HBoV were found in plasma samples of healthy adults. The results indicate that primary infection with these viruses occurs during childhood or youth. For KIPyV, the seropositivity appears to increase further during adulthood.

Detection of respiratory viruses and the associated chemokine responses in serious acute respiratory illness

BackgroundA specific diagnosis of a lower respiratory viral infection is often difficult despite frequent clinical suspicion. This low diagnostic yield may be improved by use of sensitive detection methods and...