TY - JOUR
T1 - Serological Assessment of 18 Pathogens and Risk of AIDS-Associated Non-Hodgkin Lymphoma
AU - Halec, Gordana
AU - Waterboer, Tim
AU - Brenner, Nicole
AU - Butt, Julia
AU - Hardy, W. David
AU - D'Souza, Gypsyamber
AU - Wolinsky, Steven
AU - Macatangay, Bernard J.
AU - Pawlita, Michael
AU - Detels, Roger
AU - Martínez-Maza, Otoniel
AU - Hussain, Shehnaz K.
N1 - Funding Information:
From the *Department of Obstetrics and Gynecology, AIDS Institute, UCLA David Geffen School of Medicine, University of California Los Angeles (UCLA), Los Angeles, CA; †Infections and Cancer Epidemiology, Research Program Infection, Inflammation and Cancer, German Cancer Research Center (DKFZ), Heidelberg, Germany; ‡Division of Infectious Diseases, Johns Hopkins University School of Medicine, Baltimore, MD; §Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD; ║Division of Infectious Diseases, Depart-ment of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL; ¶Division of Infectious Diseases, Department of Medicine, University of Pittsburg School of Medicine, Pittsburgh, PA; #Department of Epidemiology, UCLA Fielding School of Public Health, Los Angeles, CA; and **Department of Medicine, Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center, Los Angeles, CA Supported in part by a supplement to U01-AI-035040, by R01-CA-168482, and by the Pendleton Charitable Trust and the McCarthy Family Foundation. The MACS is funded primarily by the National Institute of Allergy and Infectious Diseases (NIAID), with additional cofunding from the National Cancer Institute (NCI), the National Institute on Drug Abuse (NIDA), and the National Institute of Mental Health (NIMH). Targeted supplemental funding for specific projects was also provided by the National Heart, Lung, and Blood Institute (NHLBI), and the National Institute on Deafness and Communication Disorders (NIDCD). MACS data collection is also supported by UL1-TR001079 (JHU ICTR) from the National Center for Advancing Translational Sciences (NCATS), a com-ponent of the National Institutes of Health (NIH), and NIH Roadmap for Medical Research. The contents of this publication are solely the responsibility of the authors and do not represent the official views of the National Institutes of Health (NIH), Johns Hopkins ICTR, or NCATS. The MACS web site is located at http://aidscohortstudy.org/.
Funding Information:
The authors thank Larry Magpantay, Ute Koch, and Claudia Brandel for excellent technical assistance. Cancer incidence data were provided by the following state agencies: (1) Maryland Cancer Registry, Center for Cancer Prevention and Control, Department of Health and Mental Hygiene, Baltimore, MD 21201; (2) Illinois Department of Public Health, Illinois State Cancer Registry; (3) Bureau of Health Statistics & Research, Pennsylvania Department of Health, Harrisburg, Pennsylvania; (4) Ohio Cancer Incidence Surveillance System (OCISS), Ohio Department of Health (ODH), a cancer registry partially supported in the National Program of Cancer Registries at the Centers for Disease Control and Prevention (CDC) through Cooperative Agreement # 5U58DP000795-05; and (5) California Department of Public Health pursuant to California Health and Safety Code Section 103885; CDC’s National Program of Cancer Registries, under cooperative agreement 5NU58DP003862-04/ DP003862; the National Cancer Institute’s Surveillance, Epidemiology and End Results Program under contract HHSN261201000140C awarded to the Cancer Prevention Institute of California, contract HHSN261201000035C awarded to the University of Southern California, and contract HHSN261201000034C awarded to the Public Health Institute. We acknowledge the State of Maryland, the Maryland Cigarette Restitution Fund, and the National Program of Cancer Registries of the CDC for the funds that support the collection and availability of the cancer registry data. The analyses, findings, interpretations, and conclusions of this report are those of the authors. No endorsement by any of the states providing data, the National Cancer Institute, the CDC or their Contractors and Subcontractors is intended nor should be inferred.
Publisher Copyright:
© 2018 Wolters Kluwer Health, Inc.
PY - 2019/3/1
Y1 - 2019/3/1
N2 - Background:HIV infection is associated with increased susceptibility to common pathogens, which may trigger chronic antigenic stimulation and hyperactivation of B cells, events known to precede the development of AIDS-associated non-Hodgkin lymphoma (AIDS-NHL).Methods:To explore whether cumulative exposure to infectious agents contributes to AIDS-NHL risk, we tested sera from 199 AIDS-NHL patients (pre-NHL, average lead time 3.9 years) and 199 matched HIV-infected controls from the Multicenter AIDS Cohort Study, for anti-IgG responses to 18 pathogens using multiplex serology. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using conditional logistic regression models.Results:We found no association between cumulative exposure to infectious agents and AIDS-NHL risk (OR 1.01, 95% CI: 0.91 to 1.12). However, seropositivity for trichodysplasia spinulosa polyomavirus (TSPyV), defined as presence of antibodies to TSPyV capsid protein VP1, was significantly associated with a 1.6-fold increase in AIDS-NHL risk (OR 1.62, 95% CI: 1.02 to 2.57). High Epstein-Barr virus (EBV) anti-VCA p18 antibody levels closer to the time of AIDS-NHL diagnosis (<4 years) were associated with a 2.6-fold increase in AIDS-NHL risk (OR 2.59, 95% CI: 1.17 to 5.74). In addition, high EBV anti-EBNA-1 and anti-ZEBRA antibody levels were associated with 2.1-fold (OR 0.47, 95% CI: 0.26 to 0.85) and 1.6-fold (OR 0.57, 95% CI: 0.35 to 0.93) decreased risk of AIDS-NHL, respectively.Conclusions:Our results do not support the hypothesis that cumulative exposure to infectious agents contributes to AIDS-NHL development. However, the observed associations with respect to TSPyV seropositivity and EBV antigen antibody levels offer additional insights into the pathogenesis of AIDS-NHL.
AB - Background:HIV infection is associated with increased susceptibility to common pathogens, which may trigger chronic antigenic stimulation and hyperactivation of B cells, events known to precede the development of AIDS-associated non-Hodgkin lymphoma (AIDS-NHL).Methods:To explore whether cumulative exposure to infectious agents contributes to AIDS-NHL risk, we tested sera from 199 AIDS-NHL patients (pre-NHL, average lead time 3.9 years) and 199 matched HIV-infected controls from the Multicenter AIDS Cohort Study, for anti-IgG responses to 18 pathogens using multiplex serology. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using conditional logistic regression models.Results:We found no association between cumulative exposure to infectious agents and AIDS-NHL risk (OR 1.01, 95% CI: 0.91 to 1.12). However, seropositivity for trichodysplasia spinulosa polyomavirus (TSPyV), defined as presence of antibodies to TSPyV capsid protein VP1, was significantly associated with a 1.6-fold increase in AIDS-NHL risk (OR 1.62, 95% CI: 1.02 to 2.57). High Epstein-Barr virus (EBV) anti-VCA p18 antibody levels closer to the time of AIDS-NHL diagnosis (<4 years) were associated with a 2.6-fold increase in AIDS-NHL risk (OR 2.59, 95% CI: 1.17 to 5.74). In addition, high EBV anti-EBNA-1 and anti-ZEBRA antibody levels were associated with 2.1-fold (OR 0.47, 95% CI: 0.26 to 0.85) and 1.6-fold (OR 0.57, 95% CI: 0.35 to 0.93) decreased risk of AIDS-NHL, respectively.Conclusions:Our results do not support the hypothesis that cumulative exposure to infectious agents contributes to AIDS-NHL development. However, the observed associations with respect to TSPyV seropositivity and EBV antigen antibody levels offer additional insights into the pathogenesis of AIDS-NHL.
KW - AIDS-NHL
KW - HIV
KW - antibodies
KW - infections
KW - multiplex serology
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U2 - 10.1097/QAI.0000000000001916
DO - 10.1097/QAI.0000000000001916
M3 - Article
C2 - 30531297
AN - SCOPUS:85061494488
SN - 1525-4135
VL - 80
SP - E53-E63
JO - Journal of Acquired Immune Deficiency Syndromes
JF - Journal of Acquired Immune Deficiency Syndromes
IS - 3
ER -