Evidence map›Paper›PMID 38215691›Full record

ArticleEBioMedicine2024

Replicative fitness and pathogenicity of primate lentiviruses in lymphoid tissue, primary human and chimpanzee cells: relation to possible jumps to humans.

Denis M Tebit, Gabrielle Nickel, Richard Gibson, Myriam Rodriguez, Nicolas J Hathaway, Katie Bain, Angel L Reyes-Rodriguez, Pascal Ondoa, Jonathan L Heeney, Yue Li and 5 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in EBioMedicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.9field-weighted citation impact, top 30% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
4 · The record

Corrections and comments

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

15 authors at 6 institutions in 5 countries.

Denis M TebitDivision of Infectious Diseases, Department of Medicine, Case Western Reserve University, Cleveland, OH, USA; Global Biomed Scientific, LLC, P.O. Box 2368, Forest, VA, USA.
Gabrielle NickelDivision of Infectious Diseases, Department of Medicine, Case Western Reserve University, Cleveland, OH, USA.
Richard GibsonDepartment of Microbiology and Immunology, Western University, Ontario, Canada.
Myriam RodriguezDivision of Infectious Diseases, Department of Medicine, Case Western Reserve University, Cleveland, OH, USA.
Nicolas J HathawayDepartment of Pathology and Laboratory Medicine, Warren Alpert Medical School, Brown University, Providence, RI, USA.
Katie BainDepartment of Microbiology and Immunology, Western University, Ontario, Canada.
Angel L Reyes-RodriguezDepartment of Molecular Biology and Microbiology, Case Western Reserve University School of Medicine, Cleveland, OH, USA.
Pascal OndoaAfrican Society for Laboratory Medicine, Addis Ababa, Ethiopia; Department of Global Health, Institute of Global Health and Development, University of Amsterdam, Amsterdam, the Netherlands.
Jonathan L HeeneyLaboratory of Viral Zoonotics, Department of Veterinary Medicine, University of Cambridge, Cambridge, UK.
Yue LiDepartment of Microbiology and Immunology, Western University, Ontario, Canada.
Jennifer BongornoDepartment of Molecular Biology and Microbiology, Case Western Reserve University School of Medicine, Cleveland, OH, USA.
David CanadayDivision of Infectious Diseases, Department of Medicine, Case Western Reserve University, Cleveland, OH, USA.
David McDonaldDepartment of Molecular Biology and Microbiology, Case Western Reserve University School of Medicine, Cleveland, OH, USA.
Jeffrey A BaileyDepartment of Pathology and Laboratory Medicine, Warren Alpert Medical School, Brown University, Providence, RI, USA.
Eric J ArtsDivision of Infectious Diseases, Department of Medicine, Case Western Reserve University, Cleveland, OH, USA; Department of Microbiology and Immunology, Western University, Ontario, Canada. Electronic address: earts@uwo.ca.
Case Western Reserve University · USWestern University · CAUniversity School · USBrown University · USAmsterdam Institute for Global Health and Development · NLUniversity of Cambridge · GB

Funding

WG3: HIV, Co-infections and Co-morbiditiesP30AI036219 · NIAID · CASE WESTERN RESERVE UNIVERSITY · PI Alan David Levine · 1994 to 2026
$50.0M
Impact of HIV-1 Fitness on Disease ProgressionR01AI049170 · NIAID · UNIVERSITY OF WESTERN ONTARIO · PI ARTS, ERIC J · 2002 to 2024
$6.8M
Human copy number polymorphism and severe malariaR01AI099473 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI BAILEY, JEFFREY A. · 2012 to 2015
$2.3M
Mechanisms of increased susceptibility to TB in HIV-Infected individualsR01AI080313 · NIAID · CASE WESTERN RESERVE UNIVERSITY · PI CANADAY, DAVID H · 2010 to 2013
$2.0M
NIAID NIH HHS P30 AI036219NIAID NIH HHS R01 AI049170NIAID NIH HHS R01 AI080313NIAID NIH HHS R01 AI099473
6 · The paper itself

Abstract

backgroundSimian immunodeficiency viruses (SIV) have been jumping between non-human primates in West/Central Africa for thousands of years and yet, the HIV-1 epidemic only originated from a primate lentivirus over 100 years ago.

methodsThis study examined the replicative fitness, transmission, restriction, and cytopathogenicity of 22 primate lentiviruses in primary human lymphoid tissue and both primary human and chimpanzee peripheral blood mononuclear cells.

findingsPairwise competitions revealed that SIV from chimpanzees (cpz) had the highest replicative fitness in human or chimpanzee peripheral blood mononuclear cells, even higher fitness than HIV-1 group M strains responsible for worldwide epidemic. The SIV strains belonging to the "HIV-2 lineage" (including SIVsmm, SIVmac, SIVagm) had the lowest replicative fitness. SIVcpz strains were less inhibited by human restriction factors than the "HIV-2 lineage" strains. SIVcpz efficiently replicated in human tonsillar tissue but did not deplete CD4+ T-cells, consistent with the slow or nonpathogenic disease observed in most chimpanzees. In contrast, HIV-1 isolates and SIV of the HIV-2 lineage were pathogenic to the human tonsillar tissue, almost independent of the level of virus replication.

interpretationOf all primate lentiviruses, SIV from chimpanzees appears most capable of infecting and replicating in humans, establishing HIV-1. SIV from other Old World monkeys, e.g. the progenitor of HIV-2, replicate slowly in humans due in part to restriction factors. Nonetheless, many of these SIV strains were more pathogenic than SIVcpz. Either SIVcpz evolved into a more pathogenic virus while in humans or a rare SIVcpz, possibly extinct in chimpanzees, was pathogenic immediately following the jump into human.

fundingSupport for this study to E.J.A. was provided by the NIH/NIAID R01 AI49170 and CIHR project grant 385787. Infrastructure support was provided by the NIH CFAR AI36219 and Canadian CFI/Ontario ORF 36287. Efforts of J.A.B. and N.J.H. was provided by NIH AI099473 and for D.H.C., by VA and NIH AI AI080313.

Indexed as

HIV-1Lentiviruses, PrimateSimian Acquired Immunodeficiency SyndromeSimian Immunodeficiency VirusAnimalsHumansLeukocytes, MononuclearLymphoid TissueOntarioPan troglodytesPrimatesVirulenceHIV-1PathogenesisPrimate lentivirusesZoonosis

Identifiers

PMID38215691
PMCPMC10827413
OpenAlexW4390821231

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.