Evidence map›Paper›PMID 37267224›Full record

ArticlePloS one2023

Differing natural killer cell, T cell and antibody profiles in antiretroviral-naive HIV-1 viraemic controllers with and without protective HLA alleles.

Ana Moyano, Bongiwe Ndlovu, Msizi Mbele, Kewreshini Naidoo, Nasreen Khan, Jaclyn K Mann, Thumbi Ndung'u

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.5field-weighted citation impact, top 31% 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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. 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

7 authors at 3 institutions in 3 countries.

Ana MoyanoAfrica Health Research Institute, KwaZulu-Natal, South Africa, Durban, South Africa.
Bongiwe NdlovuHIV Pathogenesis Programme, The Doris Duke Medical Research Institute, School of Laboratory Medicine and Medical Sciences, University of KwaZulu-Natal, Durban, South Africa.
Msizi MbeleHIV Pathogenesis Programme, The Doris Duke Medical Research Institute, School of Laboratory Medicine and Medical Sciences, University of KwaZulu-Natal, Durban, South Africa.
Kewreshini NaidooHIV Pathogenesis Programme, The Doris Duke Medical Research Institute, School of Laboratory Medicine and Medical Sciences, University of KwaZulu-Natal, Durban, South Africa.
Nasreen KhanHIV Pathogenesis Programme, The Doris Duke Medical Research Institute, School of Laboratory Medicine and Medical Sciences, University of KwaZulu-Natal, Durban, South Africa.
Jaclyn K MannHIV Pathogenesis Programme, The Doris Duke Medical Research Institute, School of Laboratory Medicine and Medical Sciences, University of KwaZulu-Natal, Durban, South Africa.ORCID 0000-0002-2398-1273
Thumbi Ndung'uAfrica Health Research Institute, KwaZulu-Natal, South Africa, Durban, South Africa.ORCID 0000-0003-2962-3992
University of KwaZulu-Natal · ZAAfrica Health Research Institute · ZARagon Institute of MGH, MIT and Harvard · US

Funding

Wellcome Trust DEL-15-006
6 · The paper itself

Abstract

Previous work suggests that HIV controllers with protective human leukocyte antigen class I alleles (VC+) possess a high breadth of Gag-specific CD8+ T cell responses, while controllers without protective alleles (VC-) have a different unknown mechanism of control. We aimed to gain further insight into potential mechanisms of control in VC+ and VC-. We studied 15 VC+, 12 VC- and 4 healthy uninfected individuals (UI). CD8+ T cell responses were measured by ELISpot. Flow cytometry was performed to analyse surface markers for activation, maturation, and exhaustion on natural killer (NK) cell and T cells, as well as cytokine secretion from stimulated NK cells. We measured plasma neutralization activity against a panel of 18 Env-pseudotyped viruses using the TZM-bl neutralization assay. We found no significant differences in the magnitude and breadth of CD8+ T cell responses between VC+ and VC-. However, NK cells from VC- had higher levels of activation markers (HLA-DR and CD38) (p = 0.03), and lower cytokine expression (MIP-1β and TNF-α) (p = 0.05 and p = 0.04, respectively) than NK cells from VC+. T cells from VC- had higher levels of activation (CD38 and HLA-DR co-expression) (p = 0.05), as well as a trend towards higher expression of the terminal differentiation marker CD57 (p = 0.09) when compared to VC+. There was no difference in overall neutralization breadth between VC+ and VC- groups, although there was a trend for higher neutralization potency in the VC- group (p = 0.09). Altogether, these results suggest that VC- have a more activated NK cell profile with lower cytokine expression, and a more terminally differentiated and activated T cell profile than VC+. VC- also showed a trend of more potent neutralizing antibody responses that may enhance viral clearance. Further studies are required to understand how these NK, T cell and antibody profiles may contribute to differing mechanisms of control in VC+ and VC-.

Indexed as

HIV-1HIV InfectionsAllelesCD8-Positive T-LymphocytesCytokinesHIV Non-ProgressorsHLA-DR AntigensHumansKiller Cells, NaturalCytokinesHLA-DR Antigens

Identifiers

PMID37267224
PMCPMC10237385
OpenAlexW4379197407

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.