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Record W4416914617 · doi:10.1128/jvi.01548-25

Ancestral reconstruction supports that loss of Nef-mediated T cell modulation coincided with the emergence of pathogenic lentiviruses

2025· article· en· W4416914617 on OpenAlexafffund
Angelina M. Baldino, Mitchell J. Mumby, Cassandra R. Edgar, Abayomi S. Olabode, Art F. Y. Poon, Jimmy D. Dikeakos

Bibliographic record

VenueJournal of Virology · 2025
Typearticle
Languageen
FieldImmunology and Microbiology
TopicHIV Research and Treatment
Canadian institutionsWestern University
FundersCanadian Institutes of Health Research
KeywordsDownregulation and upregulationT cellCD28PathogenesisSimian immunodeficiency virusLineage (genetic)CellProtein subunitSignal transduction

Abstract

fetched live from OpenAlex

Human immunodeficiency virus type 1 (HIV-1) originated following cross-species transmission of simian immunodeficiency virus (SIV) infecting chimpanzees (SIVcpz). While SIV infection of its natural primate hosts is typically non-pathogenic, SIVcpz/HIV-1 is highly pathogenic. SIV/HIV pathogenesis is influenced by the viral accessory protein Nef, which manipulates several immune factors to facilitate disease progression. Specifically, Nef can modulate T cell activation by downregulating the T cell receptor subunit CD3ζ and the co-stimulatory receptor CD28. Several studies have demonstrated that while Nef downregulates CD28 from the T cell surface, this ability is not completely conserved throughout the SIV/HIV phylogeny. In comparison, Nef-mediated CD3 downregulation is highly conserved in SIV derived from lower-order primates yet completely absent from SIVcpz/HIV-1. Here, we used Nef proteins previously generated via an ancestral reconstruction pipeline, corresponding to common ancestors in the SIV/HIV phylogeny leading to HIV-1 group M, and evaluated their ability to downregulate CD3ζ and CD28 in both expression and transduction systems. We observed that only the ancestral Nef of all primate lentiviruses efficiently downregulated both CD3ζ and CD28, while ancestors along the SIVcpz/HIV-1 lineage failed to downregulate CD3ζ and minimally recovered the ability to downregulate CD28 over time. Furthermore, we showed that the loss of CD3ζ and CD28 downregulation was associated with increased expression of cell surface T cell activation markers and inflammatory cytokines, consistent with a pathogenic infection. Altogether, this study illustrates the evolutionary dynamics of Nef modulation of T cell activation and its impact on pathogenesis in the SIV/HIV lineage.IMPORTANCEWe characterized ancestral Nef proteins derived from the lineage that gave rise to HIV-1 group M. We show that the loss of Nef-mediated CD3ζ and CD28 downregulation occurred in the common ancestor of the SIVcpz/HIV-1 lineage and coincided with increased T cell activation, a hallmark of pathogenicity. Moreover, this suggests that evolutionary changes to Nef-mediated immune modulation contributed to the emergence of pathogenic viruses like HIV-1. Together, these findings support the application of ancestral reconstruction to better understand the functional evolution of viral proteins, particularly in the context of cross-species transmission.

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame machine prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.001
Version: metacan-v3-hybrid-931329e0061cValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Bench or experimental · Consensus signal: Bench or experimental
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.002
Threshold uncertainty score0.006

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0000.001
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0000.000
Science and technology studies0.0000.000
Scholarly communication0.0010.000
Open science0.0000.000
Research integrity0.0000.001
Insufficient payload (model declined to judge)0.0020.000

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.014
GPT teacher head0.256
Teacher spread0.242 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
Study designBench or experimental
Domainnot available
GenreEmpirical

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

Quick stats

Citations0
Published2025
Admission routes2
Has abstractyes

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