APOL1 variant alleles associate with reduced risk for opportunistic infections in HIV infection.
Ping An, Efe Sezgin, Gregory D Kirk, Priya Duggal, Elizabeth Binns-Roemer, George Nelson, Sophie Limou, Mark L Van Natta, Douglas A Jabs, Michelle Estrella and 2 more
Synthesis in Communications biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.9field-weighted citation impact, top 29% of its field
1 · What the graph read from it
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
2 · The registry
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
3 · Its place in the literature
Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what money
Authors and funding
12 authors at 7 institutions in 3 countries.
Ping AnBasic Research Laboratory, Molecular Genetic Epidemiology Section, Basic Science Program, Frederick National Laboratory for Cancer Research, Frederick, MD, USA. ping.an@nih.gov.ORCID 0000-0002-5322-3510
Efe SezginBasic Research Laboratory, Molecular Genetic Epidemiology Section, Basic Science Program, Frederick National Laboratory for Cancer Research, Frederick, MD, USA.ORCID 0000-0002-8000-7485
Gregory D KirkDepartment of Epidemiology, the Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA.
Priya DuggalDepartment of Epidemiology, the Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA.ORCID 0000-0001-5809-2081
Elizabeth Binns-RoemerBasic Research Laboratory, Molecular Genetic Epidemiology Section, Basic Science Program, Frederick National Laboratory for Cancer Research, Frederick, MD, USA.
George NelsonCenter for Cancer Research Informatics Core, Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research, Frederick, MD, USA.
Sophie LimouBasic Research Laboratory, Molecular Genetic Epidemiology Section, Basic Science Program, Frederick National Laboratory for Cancer Research, Frederick, MD, USA.
Mark L Van NattaDepartment of Epidemiology, the Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA.
Douglas A JabsDepartment of Epidemiology, the Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA.
Michelle EstrellaKidney Health Research Collaborative, Department of Medicine, University of California San Francisco, San Francisco, CA, USA.
Jeffrey B KoppKidney Disease Section, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, MD, USA.ORCID 0000-0001-9052-186X
Cheryl A WinklerBasic Research Laboratory, Molecular Genetic Epidemiology Section, Basic Science Program, Frederick National Laboratory for Cancer Research, Frederick, MD, USA. winklerc@mail.nih.gov.ORCID 0000-0001-5552-0917
Johns Hopkins University · USFrederick National Laboratory for Cancer Research · USÉcole Centrale de Nantes · FRIzmir Institute of Technology · TRLeidos (United States) · USNational Institute of Diabetes and Digestive and Kidney Diseases · USUniversity of California, San Francisco · US
Funding
Virology CoreP30AI027767 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Latesha Ellen Elopre · 1988 to 2026
$84.1M
Engaging University of California Stakeholders for Biorespository ResearchUL1TR000004 · NCATS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GRANDIS, JENNIFER RUBIN · 2012 to 2015
$78.0M
Studies of Ocular Complications of AIDS - Coordinating CenterU10EY008057 · NEI · JOHNS HOPKINS UNIVERSITY · PI VAN NATTA, MARK L · 1988 to 2012
$78.0M
Virology, Immunology, and Microbiology CoreP30AI050410 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DAVID M. MARGOLIS · 2001 to 2026
$76.9M
Virology and Molecular Biomarkers CoreP30AI050409 · NIAID · EMORY UNIVERSITY · PI Ann M Chahroudi, Colleen F Kelley · 2002 to 2026
$74.0M
SF Bay Area MACS/WIHS Combined Cohort StudyU01HL146242 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Bradley E Aouizerat, Jennifer Cohen Price · 2019 to 2026
$36.3M
Sex differences in the role of multi-omicsin HIV-associated carotid artery atherosclerosisU01HL146193 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI Stephen J Gange, Elizabeth Topper · 2019 to 2026
$35.8M
Clinical Research Sites for the MACS/WIHS Combined Cohort Study (MACS/WIHS-CCS) - Baltimore/Wash DC Center - Admin Supplement: Vision and dual sensory loss in HIV-infected older adultsU01HL146201 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI TODD T BROWN, Joseph B. Margolick · 2019 to 2026
$33.7M
Sex differences in the role of multi-omics in HIV-associated carotid artery atherosclerosisU01HL146204 · NHLBI · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI David B. Hanna, Anjali Sharma · 2019 to 2026
$33.2M
University of Pittsburgh MWCCS Clinical Research SiteU01HL146208 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Bernard Jonas C Macatangay, CHARLES R RINALDO · 2019 to 2026
$32.2M
Study of Hearing and Balance in Middle Aged and Aging Men and Women in the MACS-WIHS Combined Cohort StudyU01HL146333 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Roger Detels, Matthew James Mimiaga · 2019 to 2026
$32.2M
Northwestern CORE Clinical Research Site: Trans-omics for HIV/AIDS ResearchU01HL146240 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Frank J Palella, Valentina Stosor · 2019 to 2026
Apolipoprotein L1 (APOL1), an innate immune factor against African trypanosoma brucei, inhibits HIV-1 in vitro. The impact of APOL1 G1-G2 variants on HIV-1-associated opportunistic infections (OIs) is unknown. Here, we report findings from a metaanalysis of four HIV/AIDS prospective cohorts (ALIVE, LSOCA, MACS, and WIHS) including 2066 African American participants. Using a global test combining all four cohorts, carriage of two APOL1 variant alleles is associated with a 50% reduction in odds of OI (combined OR 0.50, 95% CI 0.33-0.76). Subgroup analysis of OI etiological categories (viral, parasitic, fungal and Mycobacterial) suggests the possibility of specific protection from fungal infections (OR 0.54. 95% CI 0.32-0.93; P
Indexed as
Genetic VariationAdultAIDS-Related Opportunistic InfectionsApolipoprotein L1Black or African AmericanFemaleGenetic Predisposition to DiseaseHIV-1HIV InfectionsHumansImmunity, InnateMaleMiddle AgedPhenotypeProtective FactorsRisk AssessmentAPOL1 protein, humanApolipoprotein L1
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.
APOL1 variant alleles associate with reduced risk for opportunistic infections in HIV infection. · full record | OpenQuestion