ReviewMicrobiological reviews1996
T helper cell activation and human retroviral pathogenesis.
Review in Microbiological reviews, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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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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.
Who cites it
13 citing papers in PubMed, 66 citations in OpenAlex.
- Influence of hepatitis C virus coinfection on failure of HIV-infected patients receiving highly active antiretroviral therapy to achieve normal serum beta2microglobulin levels.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2003Trial
- Article
- Human Codon Usage: The Genetic Basis of Pathogen Latency.Global medical genetics · 2021Article
- Systemic Immune Activation and HIV Shedding in the Female Genital Tract.Journal of acquired immune deficiency syndromes (1999) · 2016Article
- Increased expression of OX40 is associated with progressive disease in patients with HTLV-1-associated myelopathy/tropical spastic paraparesis.Retrovirology · 2013Article
- Variable effect of co-infection on the HIV infectivity: within-host dynamics and epidemiological significance.Theoretical biology & medical modelling · 2012Article
- Co-infection by human immunodeficiency virus type 1 (HIV-1) and human T cell leukemia virus type 1 (HTLV-1): does immune activation lead to a faster progression to AIDS?BMC infectious diseases · 2009Article
- Tetraspanin CD81 provides a costimulatory signal resulting in increased human immunodeficiency virus type 1 gene expression in primary CD4+ T lymphocytes through NF-kappaB, NFAT, and AP-1 transduction pathways.Journal of virology · 2005Article
- Reduced cell turnover in bovine leukemia virus-infected, persistently lymphocytotic cattle.Journal of virology · 2003Article
- Impaired recovery of CD4+ cell counts following highly active antiretroviral therapy in drug-naïve patients coinfected with human immunodeficiency virus and hepatitis C virus.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2003Article
- Characteristics of bursal T lymphocytes induced by infectious bursal disease virus.Journal of virology · 2000Article
- Mechanisms of T-cell activation by human T-cell lymphotropic virus type I.Microbiology and molecular biology reviews : MMBR · 1999Review
- Interleukin-12 p40 mRNA expression in bovine leukemia virus-infected animals: increase in alymphocytosis but decrease in persistent lymphocytosis.Journal of virology · 1998Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
T helper (Th) cells are of central importance in regulating many critical immune effector mechanisms. The profile of cytokines produced by Th cells correlates with the type of effector cells induced during the immune response to foreign antigen. Th1 cells induce the cell-mediated immune response, while Th2 cells drive antibody production. Th cells are the preferential targets of human retroviruses. Infections with human T-cell leukemia virus (HTLV) or human immunodeficiency virus (HIV) result in the expansion of Th cells by the action of HTLV (adult T-cell leukemia) or the progressive loss of T cells by the action of HIV (AIDS). Both retrovirus infections impart a high-level activation state in the host immune cells as well as systemically. However, diverging responses to this activation state have contrasting effects on the Th-cell population. In HIV infection, Th-cell loss has been attributed to several mechanisms, including a selective elimination of cells by apoptosis. The induction of apoptosis in HIV infection is complex, with many different pathways able to induce cell death. In contrast, infection of Th cells with HTLV-1 affords the cell a protective advantage against apoptosis. This advantage may allow the cell to escape immune surveillance, providing the opportunity for the development of Th-cell cancer. In this review, we will discuss the impact of Th-cell activation and general immune activation on human retrovirus expression with a focus upon Th-cell function and the progression to disease.
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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.