ArticleProceedings of the National Academy of Sciences of the United States of America2005
Resting naive CD4+ T cells are massively infected and eliminated by X4-tropic simian-human immunodeficiency viruses in macaques.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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Who cites it
65 citing papers in PubMed, 102 citations in OpenAlex.
- Ultrasensitive single-genome sequencing reveals strong purifying selection in acute HIV-1 infection.bioRxiv : the preprint server for biology · 2026Article
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- Transmission of highly virulent CXCR4 tropic HIV-1 through the mucosal route in an individual with a wild-type CCR5 genotype.EBioMedicine · 2024Article
- Transmission of highly virulent CXCR4 tropic HIV-1 through the mucosal route in an individual with a wild-type CCR5 genotype.Research square · 2023Article
- Intestinal endothelial cells increase HIV infection and latency in resting and activated CD4 + T cells, particularly affecting CCR6 + CD4 + T cells.Retrovirology · 2023Article
- Endothelial Cells Promote Productive HIV Infection of Resting CD4AIDS research and human retroviruses · 2022Article
- TLR7 agonist, N6-LS and PGT121 delayed viral rebound in SHIV-infected macaques after antiretroviral therapy interruption.PLoS pathogens · 2021Article
- Gut Microbiome Homeostasis and the CD4 T- Follicular Helper Cell IgA Axis in Human Immunodeficiency Virus Infection.Frontiers in immunology · 2021Review
- An Evolutionary Model of Progression to AIDS.Microorganisms · 2020Article
- Microbial Dysbiosis During Simian Immunodeficiency Virus Infection is Partially Reverted with Combination Anti-retroviral Therapy.Scientific reports · 2020Article
- Disparate impact on CD4 T cell count by two distinct HIV-1 phylogenetic clusters from the same clade.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Lymphatic endothelial cells promote productive and latent HIV infection in resting CD4+ T cells.Virology journal · 2018Article
- Potent Inhibition of HIV-1 Replication in Resting CD4 T Cells by Resveratrol and Pterostilbene.Antimicrobial agents and chemotherapy · 2017Article
- A highly pathogenic simian/human immunodeficiency virus effectively produces infectious virions compared with a less pathogenic virus in cell culture.Theoretical biology & medical modelling · 2017Article
- Soluble Factors Secreted by Endothelial Cells Allow for Productive and Latent HIV-1 Infection in Resting CD4AIDS research and human retroviruses · 2017Article
- TheInternational scholarly research notices · 2017Article
- Pathophysiology of CD4+ T-Cell Depletion in HIV-1 and HIV-2 Infections.Frontiers in immunology · 2017Review
- Deep Sequencing of the HIV-1 env Gene Reveals Discrete X4 Lineages and Linkage Disequilibrium between X4 and R5 Viruses in the V1/V2 and V3 Variable Regions.Journal of virology · 2016Article
- HIV-1 and HIV-2 exhibit divergent interactions with HLTF and UNG2 DNA repair proteins.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
5 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Unlike HIV-1 and simian immunodeficiency virus (SIV), which induce a slow, unrelenting loss of immune function spanning several years, highly pathogenic simian-human immunodeficiency viruses (SHIVs) induce a rapid, complete, and irreversible depletion of CD4(+) T lymphocytes in rhesus monkeys within weeks of infection, leading to death from immunodeficiency. We recently reported that, because these SHIVs exclusively use the CXCR4 coreceptor for cell entry, they target naive CD4(+) T cells for depletion in infected monkeys, whereas SIVs, which use CCR5, not CXCR4, cause the selective loss of memory CD4(+) T lymphocytes in vivo. Here we show both by DNA PCR analyses and infectivity assays, using live sorted CD4(+) T lymphocyte subsets, that 30-90% of circulating naive cells were productively infected by day 10 after inoculation. This result implies that direct cell killing, not bystander apoptosis, is responsible for the massive loss of CD4(+) T cells in the X4-tropic SHIV model. Furthermore, we directly demonstrate that >96% of virus producing cells did not express the Ki-67 proliferation marker on day 10 after inoculation using confocal microscopic analysis of lymph nodes samples. This finding is consistent with the prodigious levels of plasma viremia measured during acute X4-tropic SHIV infections of macaques being generated almost entirely by resting naive CD4(+) T cells.
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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.