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Publication Record


Rhinovirus Viremia in Patients Hospitalized With Community-Acquired Pneumonia.
Lu X, Schneider E, Jain S, Bramley AM, Hymas W, Stockmann C, Ampofo K, Arnold SR, Williams DJ, Self WH, Patel A, Chappell JD, Grijalva CG, Anderson EJ, Wunderink RG, McCullers JA, Edwards KM, Pavia AT, Erdman DD
(2017) J Infect Dis 216: 1104-1111
MeSH Terms: Adolescent, Adult, Aged, Aged, 80 and over, Child, Child, Preschool, Community-Acquired Infections, Female, Humans, Male, Middle Aged, Pneumonia, Viral, Real-Time Polymerase Chain Reaction, Rhinovirus, Viremia
Show Abstract · Added July 27, 2018
Background - Rhinoviruses (RVs) are ubiquitous respiratory pathogens that often cause mild or subclinical infections. Molecular detection of RVs from the upper respiratory tract can be prolonged, complicating etiologic association in persons with severe lower respiratory tract infections. Little is known about RV viremia and its value as a diagnostic indicator in persons hospitalized with community-acquired pneumonia (CAP).
Methods - Sera from RV-positive children and adults hospitalized with CAP were tested for RV by real-time reverse-transcription polymerase chain reaction. Rhinovirus species and type were determined by partial genome sequencing.
Results - Overall, 57 of 570 (10%) RV-positive patients were viremic, and all were children aged <10 years (n = 57/375; 15.2%). Although RV-A was the most common RV species detected from respiratory specimens (48.8%), almost all viremias were RV-C (98.2%). Viremic patients had fewer codetected pathogens and were more likely to have chest retractions, wheezing, and a history of underlying asthma/reactive airway disease than patients without viremia.
Conclusions - More than 1 out of 7 RV-infected children aged <10 years hospitalized with CAP were viremic. In contrast with other RV species, RV-C infections were highly associated with viremia and were usually the only respiratory pathogen identified, suggesting that RV-C viremia may be an important diagnostic indicator in pediatric pneumonia.
Published by Oxford University Press for the Infectious Diseases Society of America 2017. This work is written by (a) US Government employee(s) and is in the public domain in the US.
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Endothelial JAM-A promotes reovirus viremia and bloodstream dissemination.
Lai CM, Boehme KW, Pruijssers AJ, Parekh VV, Van Kaer L, Parkos CA, Dermody TS
(2015) J Infect Dis 211: 383-93
MeSH Terms: Animals, Cell Adhesion Molecules, Cells, Cultured, Endothelial Cells, Fibroblasts, Male, Mice, Mice, Inbred C57BL, Receptors, Cell Surface, Receptors, Virus, Reoviridae, Tight Junctions, Viremia
Show Abstract · Added January 20, 2015
Viruses that cause systemic disease often spread through the bloodstream to infect target tissues. Although viremia is an important step in the pathogenesis of many viruses, how viremia is established is not well understood. Reovirus has been used to dissect mechanisms of viral pathogenesis and is being evaluated in clinical trials as an oncolytic agent. After peroral entry into mice, reovirus replicates within the gastrointestinal tract and disseminates systemically via hematogenous or neural routes. Junctional adhesion molecule-A (JAM-A) is a tight junction protein that serves as a receptor for reovirus. JAM-A is required for establishment of viremia and viral spread to sites of secondary replication. JAM-A also is expressed on the surface of circulating hematopoietic cells. To determine contributions of endothelial and hematopoietic JAM-A to reovirus dissemination and pathogenesis, we generated strains of mice with altered JAM-A expression in these cell types and assessed bloodstream spread of reovirus strain type 1 Lang (T1L), which disseminates solely by hematogenous routes. We found that endothelial JAM-A but not hematopoietic JAM-A facilitates reovirus T1L bloodstream entry and egress. Understanding how viruses establish viremia may aid in development of inhibitors of this critical step in viral pathogenesis and foster engineering of improved oncolytic viral vectors.
© The Author 2014. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.
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13 MeSH Terms
Dengue virus envelope protein domain I/II hinge determines long-lived serotype-specific dengue immunity.
Messer WB, de Alwis R, Yount BL, Royal SR, Huynh JP, Smith SA, Crowe JE, Doranz BJ, Kahle KM, Pfaff JM, White LJ, Sariol CA, de Silva AM, Baric RS
(2014) Proc Natl Acad Sci U S A 111: 1939-44
MeSH Terms: Amino Acid Sequence, Animals, Antibodies, Neutralizing, Antibodies, Viral, Dengue, Dengue Virus, HEK293 Cells, Humans, Immunity, K562 Cells, Macaca mulatta, Molecular Sequence Data, Neutralization Tests, Protein Multimerization, Protein Structure, Tertiary, Recombinant Proteins, Serotyping, Species Specificity, Structure-Activity Relationship, Time Factors, Viral Envelope Proteins, Viremia
Show Abstract · Added January 26, 2016
The four dengue virus (DENV) serotypes, DENV-1, -2, -3, and -4, are endemic throughout tropical and subtropical regions of the world, with an estimated 390 million acute infections annually. Infection confers long-term protective immunity against the infecting serotype, but secondary infection with a different serotype carries a greater risk of potentially fatal severe dengue disease, including dengue hemorrhagic fever and dengue shock syndrome. The single most effective measure to control this threat to global health is a tetravalent DENV vaccine. To date, attempts to develop a protective vaccine have progressed slowly, partly because the targets of type-specific human neutralizing antibodies (NAbs), which are critical for long-term protection, remain poorly defined, impeding our understanding of natural immunity and hindering effective vaccine development. Here, we show that the envelope glycoprotein domain I/II hinge of DENV-3 and DENV-4 is the primary target of the long-term type-specific NAb response in humans. Transplantation of a DENV-4 hinge into a recombinant DENV-3 virus showed that the hinge determines the serotype-specific neutralizing potency of primary human and nonhuman primate DENV immune sera and that the hinge region both induces NAbs and is targeted by protective NAbs in rhesus macaques. These results suggest that the success of live dengue vaccines may depend on their ability to stimulate NAbs that target the envelope glycoprotein domain I/II hinge region. More broadly, this study shows that complex conformational antibody epitopes can be transplanted between live viruses, opening up similar possibilities for improving the breadth and specificity of vaccines for influenza, HIV, hepatitis C virus, and other clinically important viral pathogens.
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Hepatitis C viremia and the risk of chronic kidney disease in HIV-infected individuals.
Lucas GM, Jing Y, Sulkowski M, Abraham AG, Estrella MM, Atta MG, Fine DM, Klein MB, Silverberg MJ, Gill MJ, Moore RD, Gebo KA, Sterling TR, Butt AA, NA-ACCORD of the IeDEA
(2013) J Infect Dis 208: 1240-9
MeSH Terms: Adult, Canada, Chi-Square Distribution, Cohort Studies, Female, Glomerular Filtration Rate, HIV Infections, Hepacivirus, Hepatitis C, Humans, Incidence, Male, Middle Aged, Proportional Hazards Models, RNA, Viral, Renal Insufficiency, Chronic, Risk Factors, Substance Abuse, Intravenous, United States, Viremia
Show Abstract · Added May 29, 2014
BACKGROUND -  The role of active hepatitis C virus (HCV) replication in chronic kidney disease (CKD) risk has not been clarified.
METHODS -  We compared CKD incidence in a large cohort of HIV-infected subjects who were HCV seronegative, HCV viremic (detectable HCV RNA), or HCV aviremic (HCV seropositive, undetectable HCV RNA). Stages 3 and 5 CKD were defined according to standard criteria. Progressive CKD was defined as a sustained 25% glomerular filtration rate (GFR) decrease from baseline to a GFR < 60 mL/min/1.73 m2. We used Cox models to calculate adjusted hazard ratios (HRs) and 95% confidence intervals (CIs).
RESULTS -  A total of 52 602 HCV seronegative, 9508 HCV viremic, and 913 HCV aviremic subjects were included. Compared with HCV seronegative subjects, HCV viremic subjects were at increased risk for stage 3 CKD (adjusted HR 1.36 [95% CI, 1.26, 1.46]), stage 5 CKD (1.95 [1.64, 2.31]), and progressive CKD (1.31 [1.19, 1.44]), while HCV aviremic subjects were also at increased risk for stage 3 CKD (1.19 [0.98, 1.45]), stage 5 CKD (1.69 [1.07, 2.65]), and progressive CKD (1.31 [1.02, 1.68]).
CONCLUSIONS -  Compared with HIV-infected subjects who were HCV seronegative, both HCV viremic and HCV aviremic individuals were at increased risk for moderate and advanced CKD.
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Mechanisms of reovirus bloodstream dissemination.
Boehme KW, Lai CM, Dermody TS
(2013) Adv Virus Res 87: 1-35
MeSH Terms: Animals, Apoptosis, Capsid Proteins, Cell Adhesion Molecules, Cell Cycle Checkpoints, Humans, Intestinal Mucosa, Intestines, Lung, Mice, Receptors, Cell Surface, Receptors, Virus, Reoviridae, Reoviridae Infections, Respiratory Mucosa, Viremia, Virus Replication
Show Abstract · Added December 10, 2013
Many viruses cause disease within an infected host after spread from an initial portal of entry to sites of secondary replication. Viruses can disseminate via the bloodstream or through nerves. Mammalian orthoreoviruses (reoviruses) are neurotropic viruses that use both bloodborne and neural pathways to spread systemically within their hosts to cause disease. Using a robust mouse model and a dynamic reverse genetics system, we have identified a viral receptor and a viral nonstructural protein that are essential for hematogenous reovirus dissemination. Junctional adhesion molecule-A (JAM-A) is a member of the immunoglobulin superfamily expressed in tight junctions and on hematopoietic cells that serves as a receptor for all reovirus serotypes. Expression of JAM-A is required for infection of endothelial cells and development of viremia in mice, suggesting that release of virus into the bloodstream from infected endothelial cells requires JAM-A. Nonstructural protein σ1s is implicated in cell cycle arrest and apoptosis in reovirus-infected cells but is completely dispensable for reovirus replication in cultured cells. Surprisingly, a recombinant σ1s-null reovirus strain fails to spread hematogenously in infected mice, suggesting that σ1s facilitates apoptosis of reovirus-infected intestinal epithelial cells. It is possible that apoptotic bodies formed as a consequence of σ1s expression lead to reovirus uptake by dendritic cells for subsequent delivery to the mesenteric lymph node and the blood. Thus, both host and viral factors are required for efficient hematogenous dissemination of reovirus. Understanding mechanisms of reovirus bloodborne spread may shed light on how microbial pathogens invade the bloodstream to disseminate and cause disease in infected hosts.
Copyright © 2013 Elsevier Inc. All rights reserved.
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Reovirus nonstructural protein sigma1s is required for establishment of viremia and systemic dissemination.
Boehme KW, Guglielmi KM, Dermody TS
(2009) Proc Natl Acad Sci U S A 106: 19986-91
MeSH Terms: Animals, Animals, Newborn, Brain, Cells, Cultured, Mammalian orthoreovirus 3, Mice, Mice, Inbred C57BL, Orthoreovirus, Mammalian, Reoviridae Infections, Viral Nonstructural Proteins, Viremia, Virus Replication
Show Abstract · Added December 10, 2013
Serotype-specific patterns of reovirus disease in the CNS of newborn mice segregate with the viral S1 gene segment, which encodes attachment protein sigma1 and nonstructural protein sigma1s. The importance of receptor recognition in target cell selection by reovirus implicates the sigma1 protein as the primary effector of disease outcome. However, the contribution of sigma1s to reovirus disease is unknown. To define the function of sigma1s in reovirus pathogenesis, we generated a sigma1s-deficient virus by altering a single nucleotide to disrupt the sigma1s translational start site. Viruses were recovered that contain nine gene segments from strain type 3 Dearing and either the wild-type or sigma1s-null S1 gene segment from strain type 1 Lang. Following peroral inoculation of newborn mice, both viruses replicated in the intestine, although the wild-type virus achieved higher yields than the sigma1s-null virus. However, unlike the wild-type virus, the sigma1s-deficient virus failed to disseminate to sites of secondary viral replication, including the brain, heart, and liver. Within the small intestine, both viruses were detected in Peyer's patches, but only the wild-type virus reached the mesenteric lymph node. Concordantly, wild-type virus, but not sigma1s-deficient virus, was detected in the blood of infected animals. Wild-type and sigma1s-null viruses produced equivalent titers following intracranial inoculation, indicating that sigma1s is dispensable for viral growth in the murine CNS. These results suggest a key role for sigma1s in virus spread from intestinal lymphatics to the bloodstream, thereby allowing the establishment of viremia and dissemination to sites of secondary replication within the infected host.
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A randomized study of antiviral medication switch at lower- versus higher-switch thresholds: AIDS Clinical Trials Group Study A5115.
Riddler SA, Jiang H, Tenorio A, Huang H, Kuritzkes DR, Acosta EP, Landay A, Bastow B, Haas DW, Tashima KT, Jain MK, Deeks SG, Bartlett JA
(2007) Antivir Ther 12: 531-41
MeSH Terms: ADP-ribosyl Cyclase 1, Adult, Anti-HIV Agents, CD4 Lymphocyte Count, CD8-Positive T-Lymphocytes, Drug Administration Schedule, Drug Resistance, Viral, Drug Therapy, Combination, Female, HIV Infections, HIV-1, Humans, Male, Pilot Projects, RNA, Viral, Reverse Transcriptase Inhibitors, Treatment Outcome, Viremia
Show Abstract · Added March 13, 2015
BACKGROUND - Clinical stability has been observed with continued antiretroviral therapy (ART) in the setting of partial virological suppression. The optimal time to switch treatment in patients with low but detectable HIV-1 RNA is not known.
METHODS - Subjects on stable ART with HIV-1 RNA 200-10,000 copies/ml were randomized to an immediate treatment switch, or to a delayed switch when HIV-1 RNA increased to > or = 10,000 copies/ml or CD4+ T-cell count decreased by 20%. The primary outcome measures were immune activation (proportion of CD8+ T-cells expressing CD38 at week 48) and evolution of genotypic drug resistance.
RESULTS - The study failed to fully accrue the originally planned 108 subjects. Only 47 subjects were randomized to immediate- or delayed-switch arms. Of the subjects in the delayed-switch arm, 10/23 (43%) met the criteria for ART switch during the study (median follow-up 82 weeks). After 48 weeks of observation, the level of immune activation was comparable in the two arms. New resistance mutations were observed in 3/17 and 8/19 subjects in the immediate- and delayed-switch groups, respectively. The loss of future treatment options, however, was comparable in the delayed- and immediate-switch groups.
CONCLUSIONS - Individuals with partial viral suppression tend to remain immunologically stable, however, the accumulation of drug resistance mutations is an ongoing risk. Delayed switch in ART may be a reasonable short-term strategy for individuals with very limited treatment options.
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18 MeSH Terms
Efficient replication, and evolution of Sindbis virus genomes with non-canonical 3'A/U-rich elements (NC3ARE) in neonatal mice.
James FD, Hietala KA, Eldar D, Guess TE, Cone C, Mundell NA, Mundall N, Barnett JV, Raju R
(2007) Virus Genes 35: 651-62
MeSH Terms: 3' Untranslated Regions, Alphavirus Infections, Animals, Animals, Newborn, Cell Line, Chlorocebus aethiops, Cricetinae, Evolution, Molecular, Female, Mice, Pregnancy, RNA, Viral, Sindbis Virus, Viral Plaque Assay, Viremia, Virus Replication
Show Abstract · Added July 9, 2010
Sindbis virus (SIN) is a mosquito-transmitted animal RNA virus. We previously reported that SIN genomes lacking a canonical 19 nt 3'CSE undergo novel repair processes in BHK cells to generate a library of stable atypical SIN genomes with non-canonical 3'A/U-rich elements (NC3AREs) adjacent to the 3' poly(A) tail [1]. To determine the stability and evolutionary pressures on the SIN genomes with NC3AREs to regain a 3'CSE, five representative SIN isolates and a wild type SIN were tested in newborn mice. The key findings of this study are: (a) all six SIN isolates, including those that have extensive NC3AREs in the 3'NTRs, replicate well and produce high titer viremia in newborn mice; (b) 7-9 successive passages of these isolates in newborn mice produced comparable levels of viremia; (c) while all isolates produced only small-sized plaques during primary infection in animals, both small- and large-sized plaques were generated in all other passages; (d) polymerase stuttering occurs on select 3' oligo(U) motifs to add more U residues within the NC3AREs; (e) the S3-8 isolate with an internal UAUUU motif in the 3'poly(A) tail maintains this element even after 9 passages in animals; (f) despite differences in 3'NTRs and variable tissue distribution, all SIN isolates appear to produce similar tissue pathology in infected animals. Competition experiments with wt SIN and atypical SIN isolates in BHK cells show dominance of wt SIN. As shown for BHK cells in culture, the 3'CSE of the SIN genome is not required for virus replication and genome stability in live animals. Since the NC3AREs of atypical SIN genomes are not specific to SIN replicases, alternate RNA motifs of alphavirus genome must confer specificity in template selection. These studies fulfill the need to confirm the long-term viability of atypical SIN genomes in newborn mice and offer a basis for exploring the use of atypical SIN genomes in biotechnology.
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Cytomegalovirus viremia associated with death or retransplantation in pediatric lung-transplant recipients.
Danziger-Isakov LA, DelaMorena M, Hayashi RJ, Sweet S, Mendeloff E, Schootman M, Huddleston CB, DeBaun MR
(2003) Transplantation 75: 1538-43
MeSH Terms: Adolescent, Adult, Case-Control Studies, Child, Child, Preschool, Cohort Studies, Cytomegalovirus Infections, Female, Ganciclovir, Graft Rejection, Humans, Infant, Infant, Newborn, Lung Transplantation, Male, Reoperation, Time Factors, Tissue Donors, Viremia
Show Abstract · Added November 27, 2013
BACKGROUND - Cytomegalovirus (CMV) infection is a frequent complication of lung transplantation. However, there is limited information regarding the incidence and sequelae of CMV infections in pediatric lung-transplant recipients. On the basis of case series suggesting that CMV infection was associated with excess morbidity and mortality in lung-transplant recipients, we hypothesize that CMV viremia increases the risk of bronchiolitis obliterans (BOS) or death and retransplantation in the first year following transplantation.
METHODS - A case-cohort study of pediatric primary lung-transplant recipients was performed. Univariate analysis was used to assess whether CMV viremia was associated with BOS or death and retransplantation within 1 year after transplantation. Patients at high risk for CMV infection received ganciclovir prophylaxis for 42 days posttransplantation.
RESULTS - From July 1990 to November 2000, 194 pediatric patients received primary lung transplants. Twenty-three percent of patients developed CMV viremia. Eighty percent of CMV viremia episodes occurred before 120 days posttransplant. A first episode of CMV viremia was associated with retransplantation or death between days 90 and 365 (RR=4.1, 95% confidence interval [CI] 1.1-14.5) and was not associated with BOS (RR=1.3, 95% CI 0.5-3.3).
CONCLUSIONS - CMV viremia in the first year after pediatric primary lung transplantation is associated with increased risk of death or retransplantation between 90 and 365 days posttransplant, when CMV prophylaxis has stopped. A phase II pilot trial is warranted to assess safety and short-term efficacy of increasing the duration of CMV prophylaxis from 42 to 120 days.
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Host genetic profiles predict virological and immunological control of HIV-1 infection in adolescents.
Tang J, Wilson CM, Meleth S, Myracle A, Lobashevsky E, Mulligan MJ, Douglas SD, Korber B, Vermund SH, Kaslow RA, REACH Study Group. Reaching for Excellence in Adolescent Care and Health
(2002) AIDS 16: 2275-84
MeSH Terms: Adolescent, Algorithms, Alleles, CD4 Lymphocyte Count, Female, Follow-Up Studies, Genes, MHC Class II, Genetic Markers, Genetic Predisposition to Disease, HIV Infections, HIV-1, Haplotypes, Histocompatibility Testing, Humans, Male, Prognosis, Receptors, CCR2, Receptors, Chemokine, Viral Load, Viremia
Show Abstract · Added March 5, 2014
OBJECTIVE - To evaluate the correlation between host genetic profiles and virological and immunological outcomes among HIV-1-seropositive participants from the Reaching for Excellence in Adolescent Care and Health (REACH) cohort.
METHODS - HLA class I and chemokine coreceptor (CCR) alleles and haplotypes were resolved in 227 HIV-1-seropositive adolescents (ages 13-18 years; 75% females; 71% African-Americans) and 183 HIV-seronegative individuals, with quarterly follow-up visits between 1996 and 2000. Each HLA and CCR variant with consistent risk and protective effect on HIV-1 pathogenesis was assigned a score of -1 and +1, respectively. All individual markers and genetic scores were analyzed in relation to plasma viral load (VL) and CD4 T lymphocytes during a 6-12-month interval when no antiretroviral therapy was taken.
RESULTS - HLA-B*57 alone was a strong predictor of VL (P < 0.0001), but composite genetic profiles found in over 50% of patients consistently outperformed the individual component markers in multivariable analyses with or without adjustment for gender, race, age, and membership of clinical patient groups. Adolescents (n = 37) with a favorable combination of VL (< 1000 copies/ml) and CD4 T cell counts (> 450 x 10(6) cells/l) consistently had more positive (+1 to +2) than negative (-1 to -4) HLA and CCR scores compared with those (n = 56) with an unfavorable combination (VL > 16,000 copies/ml and CD4 cells < 450 x 10(6) cells/l) or the remainder (n = 134) of the cohort (overall P < 0.0001).
CONCLUSION - A generalizable genetic scoring algorithm based on seven HLA class I and CCR markers is highly predictive of viremia and immunodeficiency in HIV-1-infected adolescents.
Copyright 2002 Lippincott Williams & Wilkins
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