WUPyV Research Articles

Antibody responses to common viruses according to COVID-19 severity and postacute sequelae of COVID-19.

Limited research suggests that certain viruses reactivate in severe-acute-respiratory-syndrome-coronavirus 2 infection, contributing to the development of postacute sequelae of COVID-19 (PASC). We examined 1083 infected individuals from a population-based cohort, and assessed differences in plasma immunoglobulin (Ig)G and immunoglobulin A levels against Epstein-Barr virus (EBV), cytomegalovirus, varicella zoster virus (VZV), BK polyomavirus, KI polyomavirus, WU polyomavirus (WUPyV), respiratory syncytial virus, and Adv-36 according to the severity of previous COVID-19 and PASC history. Individuals who had experienced severe COVID-19 had higher antibody responses to latent viruses. Ever PASC, active persistent PASC, and PASC with neuropsychiatric symptoms were associated with higher immnoglobulin G to EBV early antigen-diffuse, VZV, and WUPyV even among individuals without previous severe COVID-19.

WU and KI polyomaviruses

WU and KI polyomaviruses

WU and KI polyomaviruses

WU and KI polyomaviruses

Metagenomic Next-Generation Sequencing Reveals the Profile of Viral Infections in Kidney Transplant Recipients During the COVID-19 Pandemic.

BackgroundTo study the clinical application of metagenomic next-generation sequencing (mNGS) in the detection of viral infections in kidney transplant recipients (KTRs) during the COVID-19 pandemic.MethodsUsing mNGS technology, 50 human fluid samples of KTRs were detected, including 20 bronchoalveolar lavage fluid (BALF) samples, 21 urine samples and 9 blood samples. The detected nucleic acid sequences were compared and analyzed with the existing viral nucleic acid sequences in the database, and the virus infection spectrum of KTRs was drawn.ResultsThe viral nucleic acids of 15 types of viruses were detected in 96.00% (48/50) of the samples, of which 11 types of viruses were in BALF (95.00%, 19/20), and the dominant viruses were torque teno virus (TTV) (65.00%; 13/20), cytomegalovirus (CMV) (45.00%; 9/20) and human alphaherpesvirus 1 (25.00%; 5/20). 12 viruses (95.24%, 20/21) were detected in the urine, and the dominant viruses were TTV (52.38%; 11/21), JC polyomavirus (52.38%; 11/21), BK polyomavirus (42.86%; 9/21), CMV (33.33%; 7/21) and human betaherpesvirus 6B (28.57%; 6/21). 7 viruses were detected in the blood (100.00%, 9/9), and the dominant virus was TTV (100.00%; 9/9). Four rare viruses were detected in BALF and urine, including WU polyomavirus, primate bocaparvovirus 1, simian virus 12, and volepox virus. Further analysis showed that TTV infection with high reads indicated a higher risk of acute rejection (P < 0.05).ConclusionsmNGS detection reveals the rich virus spectrum of infected KTRs, and improves the detection rate of rare viruses. TTV may be a new biomarker for predicting rejection.

KI and WU Polyomaviruses: Seroprevalence Study and DNA Prevalence in SARS-CoV-2 RNA Positive and Negative Respiratory Samples.

The aim of this work was to study the possible co-infection of KI and WU polyomavirus (KIPyV and WUPyV, respectively) and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in respiratory samples and to detect the seroprevalence of KIPyV and WUPyV. A total of 1030 nasopharyngeal samples were analyzed from SARS-CoV-2 RNA positive (n = 680) and negative (n = 350) adults and children (age: 1 day to 94.2 years) collected from August 2020 to October 2021. KIPyV DNA was detected in two SARS-CoV-2-positive samples (2/680, 0.29%) and in three SARS-CoV-2-negative samples (3/350, 0.86%). WUPyV DNA was observed in one-one samples from both groups (1/680, 0.15% vs. 1/350, 0.29%). We did not find an association between SARS-CoV-2 and KIPyV or WUPyV infection, and we found low DNA prevalence of polyomaviruses studied after a long-term lockdown in Hungary. To exclude a geographically different distribution of these polyomaviruses, we studied the seroprevalence of KIPyV and WUPyV by enzyme-linked immunosorbent assay among children and adults (n = 692 for KIPyV and n = 705 for WUPyV). Our data confirmed that primary infections by KIPyV and WUPyV occur mainly during childhood; the overall seropositivity of adults was 93.7% and 89.2% for KIPyV and WUPyV, respectively. Based on our data, we suggest that the spread of KIPyV and WUPyV might have been restricted in Hungary by the lockdown.

A STUDY OF THE NOVEL WU AND KI POLYOMAVIRUSES, BOCAVIRUS ADENOVIRUS IN CHILDREN WITH UPPER RESPIRATORY TRACT INFECTIONS.

The aim: To find out the frequency of WU and KI polyomaviruses, and Human Boca and Adenoviruses infections among children with different types of acute upper respiratory tract infections and to compare the frequency of these viruses among immune-competent and immune compromised patients. Materials and methods: A case-control study conducted in children aged 3-18 years with acute upper respiratory tract infections. The samples were taken from: Group 1: 100 immuno competent children with acute upper respiratory tract infections. Group 2: 100 immuno compromised children (Leukemic, cancer, Nephrotic syndrome, chronic renal failure and children with renal transplant) with acute upper respiratory tract infections. Group 3: 100 apparently healthy children without respiratory infections as control group. Nasal swap samples were collected from children and then viral DNA extracted from these samples. Then detection of WU, KI polyomaviruses HBoV and HAdv was done by using real time PCR. Results: All of 300 samples were negative for WU and KI polyomaviruses. However, human Bocavirus was detected in the three groups (immunocompromised, immunocompetent and control group) and the positivity rates were 61.61%, 37.37% and 18.18%, respectively. While human adenovirus was found only in 2% of immunocompromised patients and 1.1% of immunocompetent patients also there were cases positive for both HBoV and HAdv in 5.5% of immunocompromised patients, and 8.8% of immunocompetent patients. Conclusions: High frequency of HBoV especially in immunocompromised patients while low number of positive cases for HAdv by using nasal swab samples, WU and KI polyomaviruses could not be detected in samples.

Complete Genome Sequences of Two WU Polyomaviruses Detected in Pediatric Patients with Fatal Respiratory Infection.

ABSTRACTHere, we report the complete genome sequences of two WU polyomavirus (WUPyV) strains, both obtained in 2020 from pediatric patients with fatal respiratory infection in Beijing, China. The double-stranded DNA (dsDNA) genome sequences of BCH2008-1 and BCH2020_1 are 5,229 bp and 5,228 bp long, respectively.

Molecular Screening of KI and WU Polyomaviruses among Patients with Chronic Kidney Disease and Urinary Tract Infections

KIPyV and WUPyV were recognized based on commercial standard and PCR techniques. To occurrenceof KIPyV and WUPyV DNA among chronic kidney disease (CKD) and UTI patients using VP2 gene fordetection of KIPyV and VP1 gene for WUPyV. Molecular assay results of this study revealed the presenceof KIPyV in 6 (5.3%) of CKD patients and 3 (2.7%) of UTI patients while the presence of WUPyV was1 (0.88%) in CKD patients and negative result in UTI patients. WUPyV DNA and KIPyV DNA was notdetected in plasma of healthy persons. The distribution of KIPyV and WUPyV according to gender amongCKD showed a no significance difference among both sexes in which (P value = 0.27) and (P value =0.36) respectively while the distribution of KIPyV and WUPyV among urinary tract infections showed a nosignificance difference among both sexes in which (P value = 0.13) and (P value = 0.79) respectively .Thecurrent study survey about both viruses show that female was higher than male in KIPyV in which 2 (3.22%)of KIPyV DNA were detected in male and 4 (7.84%) in female out of 113 (100%) among chronic kidneydisease patients while in urinary tract infection, patients revealed a higher percentage rate of KIPyV infemale than male in which 0 (0%) of KIPyV DNA were in male and 3 (4.54%) in female out of 111 (100%)while doesn’t detect any isolate of WUPyV in both sexes.

Human genomics of the humoral immune response against polyomaviruses.

Human polyomaviruses are widespread in humans and can cause severe disease in immunocompromised individuals. To identify human genetic determinants of the humoral immune response against polyomaviruses, we performed genome-wide association studies and meta-analyses of qualitative and quantitative immunoglobulin G responses against BK polyomavirus (BKPyV), JC polyomavirus (JCPyV), Merkel cellpolyomavirus (MCPyV), WU polyomavirus (WUPyV), and human polyomavirus 6 (HPyV6) in 15,660 individuals of European ancestry from three independent studies. We observed significant associations for all tested viruses: JCPyV, HPyV6, and MCPyV associated with human leukocyte antigen class II variation, BKPyV and JCPyV with variants in FUT2, responsible for secretor status, MCPyV with variants in STING1, involved in interferon induction, and WUPyV with a functional variant in MUC1, previously associated with risk for gastric cancer. These results provide insights into the genetic control of a family of very prevalent human viruses, highlighting genes and pathways that play a modulating role in human humoral immunity.

KI and WU Polyomavirus in Respiratory Samples of SARS-CoV-2 Infected Patients.

Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) has been declared a global pandemic. Our goal was to determine whether co-infections with respiratory polyomaviruses, such as Karolinska Institutet polyomavirus (KIPyV) and Washington University polyomavirus (WUPyV) occur in SARS-CoV-2 infected patients. Oropharyngeal swabs from 150 individuals, 112 symptomatic COVID-19 patients and 38 healthcare workers not infected by SARS-CoV-2, were collected from March 2020 through May 2020 and tested for KIPyV and WUPyV DNA presence. Of the 112 SARS-CoV-2 positive patients, 27 (24.1%) were co-infected with KIPyV, 5 (4.5%) were positive for WUPyV, and 3 (2.7%) were infected simultaneously by KIPyV and WUPyV. Neither KIPyV nor WUPyV DNA was detected in samples of healthcare workers. Significant correlations were found in patients co-infected with SARS-CoV-2 and KIPyV (p < 0.05) and between SARS-CoV-2 cycle threshold values and KIPyV, WUPyV and KIPyV and WUPyV concurrently detected (p < 0.05). These results suggest that KIPyV and WUPyV may behave as opportunistic respiratory pathogens. Additional investigations are needed to understand the epidemiology and the prevalence of respiratory polyomavirus in COVID-19 patients and whether KIPyV and WUPyV could potentially drive viral interference or influence disease outcomes by upregulating SARS-CoV-2 replicative potential.

Heterogeneous associations of polyomaviruses and herpesviruses with allergy-related phenotypes in childhood

BackgroundEvidence suggests a complex interplay between infections and allergic diseases. ObjectiveTo explore the association of 14 common viruses with eczema, asthma, and rhinoconjunctivitis in childhood. MethodsWe used cross-sectional (n = 686) and prospective (n = 440) data from children participating in the Rhea birth cohort. Immunoglobulin G to polyomaviruses (BK polyomavirus, JC polyomavirus, KI polyomavirus [KIPyV], WU polyomavirus [WUPyV], human polyomavirus 6, human polyomavirus 7, Trichodysplasia spinulosa polyomavirus, Merkel cell polyomavirus, human polyomavirus 9, and human polyomavirus 10) and herpesviruses (Epstein-Barr virus, Cytomegalovirus, Herpes simplex virus-1, Herpes simplex virus-2) were measured at age 4 years by fluorescent bead-based multiplex serology. Definitions of eczema, asthma, and rhinoconjunctivitis at ages 4 and 6 years were based on questionnaires. Mediation of the associations by immune biomarkers was tested. ResultsLess likely to have eczema at age 4 years were KIPyV-seropositive (odds ratio [OR], 0.47; 95% confidence interval [CI], 0.27-0.82) and human polyomavirus 6 (OR, 0.44; 95% CI, 0.26-0.73) compared with their seronegative counterparts. Seropositivity to Epstein-Barr virus was negatively associated with eczema at age 4 years (OR, 0.39; 95% CI, 0.22-0.67) and 6 years (OR, 0.50; 95% CI, 0.25-0.99). Children with a higher burden of herpesviruses or of skin polyomaviruses had the lowest odds of eczema at age 4 years. Higher odds for asthma at age 4 years were found for WUPyV-seropositive children (OR, 3.98; 95% CI, 1.38-11.51), and for children seropositive to both respiratory polyomaviruses (KIPyV and WUPyV) (OR, 7.35; 95% CI, 1.66-32.59) compared with children seronegative to both. No associations were observed for rhinoconjunctivitis. There was no evidence of mediation by immune biomarkers. ConclusionA heterogeneous pattern of infections and allergic diseases was observed with common infections associated with a decreased eczema risk and an increased asthma risk in children.

Survey of WU and KI polyomaviruses, coronaviruses, respiratory syncytial virus and parechovirus in children under 5 years of age in Tehran, Iran

Severe acute respiratory infections (SARI) remain an important cause for childhood morbidity worldwide. We designed a research with the objective of finding the frequency of respiratory viruses, particularly WU and KI polyomaviruses (WUPyV & KIPyV), human coronaviruses (HCoVs), human respiratory syncytial virus (HRSV) and human parechovirus (HPeV) in hospitalized children who were influenza negative. Throat swabs were collected from children younger than 5 years who have been hospitalized for SARI and screened for WUPyV, KIPyV, HCoVs, HRSV and HPeV using Real time PCR. A viral pathogen was identified in 23 (11.16%) of 206 hospitalized children with SARI. The rate of virus detection was considerably greater in infants <12 months (78.2%) than in older children (21.8%). The most frequently detected viruses were HCoVs with 7.76% of positive cases followed by KIPyV (2%) and WUPyV (1.5%). No HPeV and HRSV were detected in this study. This research shown respiratory viruses as causes of childhood acute respiratory infections, while as most of mentioned viruses usually causes mild respiratory diseases, their frequency might be higher in outpatient children. Meanwhile as HRSV is really sensitive to inactivation due to environmental situations and its genome maybe degraded, then for future studies, we need to use fresh samples for HRSV detection. These findings addressed a need for more studies on viral respiratory tract infections to help public health.

Investigation of simian virus 40 (SV40) and human JC, BK, MC, KI, and WU polyomaviruses in glioma.

The gliomagenesis remains not fully established and their etiological factors still remain obscure. Polyomaviruses were detected and involved in several human tumors. Their potential implication in gliomas has been not yet surveyed in Africa and Arab World. Herein, we investigated the prevalence of six polyomaviruses (SV40, JCPyV, BKPyV, MCPyV, KIPyV, and WUPyV) in 112 gliomas from Tunisian patients. The DNA sequences of polyomaviruses were examined by PCR assays. Viral infection was confirmed by DNA in situ hybridization (ISH) and/or immunohistochemistry (IHC). The relationships between polyomavirus infection and tumor features were evaluated. Specific SV40 Tag, viral regulatory, and VP1 regions were identified in 12 GBM (10.7%). DNA ISH targeting the whole SV40 genome and SV40 Tag IHC confirmed the PCR findings. Five gliomas yielded JCPyV positivity by PCR and DNA ISH (2.7%). However, no BKPyV, KIPyV, and WUPyV DNA sequences were identified in all samples. MCPyV DNA was identified in 30 gliomas (26.8%). For GBM samples, MCPyV was significantly related to patient age (p = 0.037), tumor recurrence (p = 0.024), and SV40 (p = 0.045) infection. No further significant association was identified with the remaining tumor features (p > 0.05) and patient survival (Log Rank, p > 0.05). Our study indicates the presence of SV40, JCPyV, and MCPyV DNA in Tunisian gliomas. Further investigations are required to more elucidate the potential involvement of polyomaviruses in these destructive malignancies.

Associations of Viral Seroreactivity with AIDS-Related Non-Hodgkin Lymphoma.

Infection with human immunodeficiency virus (HIV) is associated with substantially increased incidence of non-Hodgkin lymphoma (NHL). This risk may be driven, in part, by reduced immune control over viral infections in the setting of acquired immunodeficiency syndrome (AIDS), although the lymphomagenic mechanisms are not yet established. We used bead-based multiplex assays to measure antibody seroreactivity to 32 viral antigens representing 22 different viral infections (human herpesviruses 1-8, hepatitis B and C virus, human T-lymphotropic virus type-1, and human polyomaviruses) in two prospective HIV cohorts. Incident (n = 28) and prevalent (n = 38) AIDS-related NHL cases were matched by age, sex, race, and CD4 count to 67 HIV-positive control individuals without AIDS-NHL. Logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for associations of AIDS-NHL with the number of different viruses to which an individual was seropositive and seroreactivity to individual antigens. Seropositivity to an increasing number of viruses was inversely associated with AIDS-NHL (OR per virus = 0.84, 95% CI = 0.72-0.98). Seroreactivity to herpes simplex virus 2 2mgG unique antigen (OR = 0.47; 95% CI = 0.23-0.97) and to WU polyomavirus viral capsid protein (OR = 0.26, 95% CI = 0.10-0.65) was significantly lower in AIDS-NHL cases compared to controls. In this evaluation of antibodies to multiple viruses, we observed an inverse association between seropositivity to a larger number of viruses and AIDS-NHL. While in need of further evaluation, our data raise the novel hypothesis that insufficient exposures or impaired humoral immune responses to viral infections may be associated with AIDS-related lymphomagenesis.

Vira-Ome: A Tool to Detect DNA Viruses in the Cell-Free DNA

Introduction Viral infections are commonly reported in immunocompromised patients such as hematopoietic stem cell transplant recipients. While there are several reports on the effect of individual viruses, such as CMV, there is increasing evidence that the composition of the blood-virome may reflect the immune status of patients. High resolution virome analysis may provide an accurate measure of a patient's immune status as well as provide pathogen surveillance. Next generation sequencing (NGS) of cell-free DNA (cfDNA) purified from plasma is being investigated for assessment of diseases such as graft vs host disease, making unbiased sequence data readily available for analyses of a patient's virome. Here we present a computational tool (Vira-ome) which probes the presence of a targeted panel of DNA viruses following NGS sequencing of cfDNA. Method We developed a pipeline which initially removes host DNA reads, then performs a reference-assisted assembly operation. The resulting assemblies were then passed to a K-mer profile based taxonomic classifier for annotation to the species level. We trained the K-mer based classifier for 3 different K-mer values using ∼14,000 DNA-virus genomes representing 36 prevalent and pathogenic species. Predictions of three different K-mer classifiers were used to make final predictions, applying a majority-wins rule. We tested our method on 30 simulated (1, 2, or 3 species mix with 50,100 or 500 NGS reads each) and 29 clinical samples obtained from a biorepository. Results The Vira-ome tool utilized cfDNA NGS data to screen for the presence of a targeted set of nine pathogenic viruses (human adenovirus, human herpesvirus 1, 2, 6, 7 and 8, BK polyomavirus, human parvovirus B19, JC polyomavirus, KI polyomavirus, WU polyomavirus, torque teno virus, Epstein Barr virus, human cytomegalovirus, and varicella-zoster virus). On the simulated set of viral sample mixes, our protocol had 100% accuracy with no false-positive predictions. For 29 clinical samples, our pipeline predicted: (A) Torque teno virus in 13/29 samples, (B) pathogenic viruses in 11/15 cases were predominated by BK polyomavirus (7/15 samples) and (C) at least one viral species in 10/14 cases. Selected samples were then analyzed by qPCR, which confirmed the presence of BKV, JCV, HHV7 and EBV in 8/9, 3/4, 1/1, 2/2 samples, respectively. Viral loads ranged from 6 – 106 copies/mL. Five samples predicted positive for the adenovirus, were not confirmed by qPCR, emphasizing the need of in vitro validation for in silico predictions. Conclusions The Vira-ome tool, designed to detect pathogenic viruses using cfDNA data, performed well both on simulated and clinical samples with a majority of results confirmed by qPCR. Our results emphasize how computational predictions can complement clinical diagnostic approaches.

Prevalence of DNA of fourteen human polyomaviruses determined in blood donors.

BACKGROUNDHuman polyomaviruses (HPyVs), like herpesviruses, cause persistent infection in a large part of the population. In immunocompromised and elderly patients, PyVs cause severe diseases such as nephropathy (BK polyomavirus [BKPyV]), progressive multifocal leukoencephalopathy (JC polyomavirus [JCPyV]), and skin cancer (Merkel cell polyomavirus [MCPyV]). Like cytomegalovirus, donor‐derived PyV can cause disease in kidney transplant recipients. Possibly blood components transmit PyVs as well. To study this possibility, as a first step we determined the presence of PyV DNA in Dutch blood donations.STUDY DESIGN AND METHODSBlood donor serum samples (n = 1016) were analyzed for the presence of DNA of 14 HPyVs using HPyV species‐specific quantitative polymerase chain reaction (PCR) procedures. PCR‐positive samples were subjected to confirmation by sequencing. Individual PCR findings were compared with the previously reported PyV serostatus.RESULTSMC polyomavirus DNA was detected in 39 donors (3.8%), JCPyV and TS polyomavirus (TSPyV) DNA in five donors (both 0.5%), and HPyV9 DNA in four donors (0.4%). BKPyV, WU polyomavirus (WUPyV), HPyV6, MW polyomavirus (MWPyV), and LI polyomavirus (LIPyV) DNA was detected in one or two donors. Amplicon sequencing confirmed the expected product for BKPyV, JCPyV, WUPyV, MCPyV, HPyV6, TSPyV, MWPyV, HPyV9, and LIPyV. For JCPyV a significant association was observed between detection of viral DNA and the level of specific IgG antibodies.CONCLUSIONIn 5.4% of Dutch blood donors PyV DNA was detected, including DNA from pathogenic PyVs such as JCPyV. As a next step, the infectivity of PyV in donor blood and transmission via blood components to immunocompromised recipients should be investigated.

Viruses in Vietnamese Patients Presenting with Community-Acquired Sepsis of Unknown Cause.

Community-acquired (CA) sepsis is a major public health problem worldwide, yet the etiology remains unknown for >50% of the patients. Here we applied metagenomic next-generation sequencing (mNGS) to characterize the human virome in 492 clinical samples (384 sera, 92 pooled nasal and throat swabs, 10 stools, and 6 cerebrospinal fluid samples) from 386 patients (213 adults and 173 children) presenting with CA sepsis who were recruited from 6 hospitals across Vietnam between 2013 and 2015. Specific monoplex PCRs were used subsequently to confirm the presence of viral sequences detected by mNGS. We found sequences related to 47 viral species belonging to 21 families in 358 of 386 (93%) patients, including viruses known to cause human infections. After PCR confirmation, human viruses were found in 52 of 386 patients (13.4%); picornavirus (enteroviruses [n = 14], rhinovirus [n = 5], and parechovirus [n = 2]), hepatitis B virus (n = 10), cytomegalovirus (n = 9), Epstein-Barr virus (n = 5), and rotavirus A (n = 3) were the most common viruses detected. Recently discovered viruses were also found (gemycircularvirus [n = 5] and WU polyomavirus, Saffold virus, salivirus, cyclovirus-VN, and human pegivirus 2 [HPgV2] [n, 1 each]), adding to the growing literature about the geographic distribution of these novel viruses. Notably, sequences related to numerous viruses not previously reported in human tissues were also detected. To summarize, we identified 21 viral species known to be infectious to humans in 52 of 386 (13.4%) patients presenting with CA sepsis of unknown cause. The study, however, cannot directly impute sepsis causation to the viruses identified. The results highlight the fact that it remains a challenge to establish the causative agents in CA sepsis patients, especially in tropical settings such as Vietnam.

Prevalence of Respiratory Polyomaviruses Among Pediatric Patients With Respiratory Symptoms in Singapore.

Background: Although WU polyomavirus (WU) and KI polyomavirus (KI) have been demonstrated to infect the human respiratory tract, it remains unclear if WU or KI cause human disease. We sought to further investigate the relationship between WU and KI infection and respiratory disease in a pediatric population with respiratory symptoms in Singapore.Methods: We conducted a cross-sectional study of pediatric patients with respiratory symptoms in a Singaporean pediatrics hospital. Upon consent, residual respiratory samples from pediatric inpatients, previously screened for common respiratory viruses, were collected and further screened for WU and KI using qPCR. The amplicons of positive samples were sequenced for confirmation. The severity of a patient's illness was assessed by chart review post-discharge looking for clinical markers of respiratory status such as presenting symptoms, diagnoses, and interventions.Results: From December 2016 to April 2017, 201 patients with residual respiratory samples were enrolled in the study. The average age of all participants recruited was 45 months. WU and KI were detected in 13% (26/201) and 3% (6/201) of patients, respectively. Conducting bivariate and multivariate modeling, patients with WU or KI positivity were not at increased risk of SARI, need for additional oxygen, intravenous fluids, and did not receive additional oral antibiotics or bronchodilators during admission. In contrast, patients with RSV detections were at increased risk of requiring supplemental oxygen during hospital admission.Conclusion: While limited in sample size, our pilot study data do not support the hypothesis that molecular evidence of WU or KI was associated with increased morbidity among a sample of general, pediatric patients with respiratory illness in Singapore.

WU polyomavirus detected in children with severe respiratory failure

BackgroundWU polyomavirus (WUPyV) is a relatively new virus associated with respiratory infections. However, its role is unclear in children with severe respiratory failure. ObjectivesWe aimed to evaluate the characteristics of severe respiratory failure associated with WUPyV infection in children. Study designWe retrospectively reviewed cases of respiratory tract infection at a tertiary children's hospital in Japan and performed real-time polymerase chain reaction (PCR) for WUPyV using residual extracted nucleic acid samples taken from respiratory tract samples of pediatric patients primarily with respiratory failure. We investigated the clinical characteristics of patients positive for WUPyV and assessed samples positive for WUPyV for other respiratory pathogens using multiplex PCR. ResultsWUPyV was detected in 14 of 318 specimens of respiratory tract infections. The median age was 34 months and males were predominant (n = 11, 64%). An underlying disease was found in 11 (79%) patients including five preterm and three immunocompromised patients. The most common clinical diagnosis was pneumonia (n = 13, 93%). The majority of the samples were endotracheal tube aspirates (n = 11, 79%). Other viruses were co-detected in nine (64%) patients, while WUPyV was the only pathogen detected in five patients with a history of admission to the neonatal intensive care unit. These five patients presented with fever and cough, and perihilar infiltrates were detected on chest radiograph in several days. ConclusionsWUPyV was detected in children with severe respiratory failure independently or concurrently with other pathogens. WUPyV can be a pathogen for children with a history of preterm birth or an underlying disease.

Abstract 3243: Associations of polyomavirus seroreactivity with AIDS-related non-Hodgkin's lymphoma

Abstract Background: Human polyomaviruses have a suspected role in carcinogenesis. In the setting of human immunodeficiency virus (HIV) infection, coinfection with MCV polyomavirus is associated with high risk of Merkel cell carcinoma. A role in lymphomagenesis has also been suggested by studies in the general population, but there are no prior studies in individuals with the acquired immunodeficiency syndrome (AIDS). Methods: We measured antibodies against 11 common polyomaviruses in archived serum and plasma samples from two prospective cohort studies of HIV infection. Patients with incident (n=28) and prevalent (n=38) AIDS-related non-Hodgkin lymphoma (NHL) were matched by age, sex, and CD4 count to 67 HIV-positive AIDS-free controls. Seroreactivity was measured by fluorescent bead-based multiplex serology, quantified as median fluorescence intensity (MFI). Logistic regression models were used to estimate adjusted odds ratios (ORs) and 95% confidence intervals (95% CIs) for NHL risk. Multinomial logistic regression compared incident and prevalent NHL cases to lymphoma-free controls and heterogeneity between case groups was evaluated by Wald tests. Differences in MFI were assessed by Kruskal-Wallis tests. Based on log-transformed MFI values for 15 masked duplicate samples, estimated coefficients of variation (CV) were &amp;lt;20% and intraclass correlation coefficients (ICC) were &amp;gt;90% for all antibodies except LPV (CV 29%, ICC 67%). Results: Cases had significantly lower prevalence of antibodies to WU polyomavirus than lymphoma-free controls (64% vs. 85%), with OR 0.28 (95% CI 0.12-0.68). Cases had non-significantly lower prevalence of antibodies to JC, TSV, MCV and KI polyomaviruses (ORs 0.42-0.71); similar prevalence of antibodies to BK, HPyV6 and HPyV7 polyomaviruses (ORs 0.98-1.18); and non-significantly higher prevalence of antibodies to HPyV10, LPV and HPyV9 polyomaviruses (ORs 1.35-1.77). MFIs for anti-WU antibodies were also lower for cases (median 552.6, interquartile range [IQR] 140.3-1298.3) than controls (median 1096.3, IQR 410.3-2044.3; p-value 0.047). The association of anti-WU antibody with NHL was stronger in samples obtained post-diagnosis (OR 0.18, 95% CI 0.07-0.48) than pre-diagnosis (OR 0.66, 95% CI 0.19-2.31; p-heterogeneity=0.037). Conclusion: Our data do not directly implicate known polyomaviruses as lymphomagenic in the setting of HIV-associated immunodeficiency. Nevertheless, impaired antibody response to WU may be a harbinger of AIDS-related lymphoma. Citation Format: Minkyo Song, Noemi Bender, James J. Goedert, Cheryl A. Winkler, Nicole Brenner, Tim Waterboer, Charles S. Rabkin. Associations of polyomavirus seroreactivity with AIDS-related non-Hodgkin's lymphoma [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 3243.