ArticleThe Journal of infectious diseases2012
HTLV-2 APH-2 expression is correlated with proviral load but APH-2 does not promote lymphocytosis.
Article in The Journal of infectious diseases, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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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.
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Who cites it
25 citing papers in PubMed, 33 citations in OpenAlex.
- TRIM13 Positively Regulates the NF-κB Signaling Pathway Induced by Encephalomyocarditis Virus.Viruses · 2026Article
- HTLV-I Basic Leucine Zipper Factor (sHBZ) Actively Associates with Nucleophosmin (B23) in the Nucleolus.Viruses · 2025Article
- Vulnerability to APOBEC3G linked to the pathogenicity of deltaretroviruses.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- A newly identified interaction between nucleolar NPM1/B23 and the HTLV-I basic leucine zipper factor in HTLV-1 infected cells.Frontiers in microbiology · 2022Article
- Article
- The ESCRT-0 Protein HRS Interacts with the Human T Cell Leukemia Virus Type 2 Antisense Protein APH-2 and Suppresses Viral Replication.Journal of virology · 2019Article
- Silencers of HTLV-1 and HTLV-2: the pX-encoded latency-maintenance factors.Retrovirology · 2019Review
- HTLV-1 as a Model for Virus and Host Coordinated Immunoediting.Frontiers in immunology · 2019Article
- TRAF3 Is Required for NF-κB Pathway Activation Mediated by HTLV Tax Proteins.Frontiers in microbiology · 2019Article
- Stability of HTLV-2 antisense protein is controlled by PML nuclear bodies in a SUMO-dependent manner.Oncogene · 2018Article
- HTLV Deregulation of the NF-κB Pathway: An Update on Tax and Antisense Proteins Role.Frontiers in microbiology · 2018Review
- Human T-cell leukaemia virus type 1: parasitism and pathogenesis.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017Review
- Multifaceted functions and roles of HBZ in HTLV-1 pathogenesis.Retrovirology · 2016Review
- Functional Comparison of HBZ and the Related APH-2 Protein Provides Insight into Human T-Cell Leukemia Virus Type 1 Pathogenesis.Journal of virology · 2016Article
- Human T-cell leukemia virus type 3 (HTLV-3) and HTLV-4 antisense-transcript-encoded proteins interact and transactivate Jun family-dependent transcription via their atypical bZIP motif.Journal of virology · 2014Article
- HTLV-1 and HTLV-2: highly similar viruses with distinct oncogenic properties.Frontiers in microbiology · 2014Review
- HTLV-1 bZIP factor supports proliferation of adult T cell leukemia cells through suppression of C/EBPα signaling.Retrovirology · 2013Article
- HTLV-3/4 and simian foamy retroviruses in humans: discovery, epidemiology, cross-species transmission and molecular virology.Virology · 2013Review
- Functional comparison of antisense proteins of HTLV-1 and HTLV-2 in viral pathogenesis.Frontiers in microbiology · 2013Article
- Interplay between the HTLV-2 Tax and APH-2 proteins in the regulation of the AP-1 pathway.Retrovirology · 2012Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
Abstract
We recently discovered the antisense protein of human T-cell leukemia virus (HTLV) type 2 (APH-2), whose messenger RNA is encoded by the antisense strand of the HTLV-2 genome. We quantified proviral load, level of tax, and APH-2 in a series of blood samples obtained from a cohort of HTLV-2 carriers. We determined whether APH-2 promotes cell proliferation. APH-2 was detectable in most samples tested and was correlated with proviral load. APH-2 levels were not correlated with lymphocyte count in vivo, consistent with the inability of APH-2 to promote cell proliferation in vitro. APH-2 does not promote cell proliferation and does not cause lymphocytosis.
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Registered trials
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.