Polymorphism in the Interleukin‐10 Promoter Affects Both Provirus Load and the Risk of Human T Lymphotropic Virus Type I–Associated Myelopathy/Tropical Spastic Paraparesis

Sabouri, Amir H.; Saito, Mineki; Lloyd, Alun L.; Vine, Alison M.; Witkover, Aviva W.; Furukawa, Yoshitaka; Izumo, Shuji; Arimura, Kimiyoshi; Marshall, Sara E.; Usuku, Koichiro; Bangham, Charles R. M.; Osame, Mitsuhiro

doi:10.1086/423942

Cited by 50 publications

(43 citation statements)

References 33 publications

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“…Conversely, a Caribbean study that examined SNPs in 38 gene candidates found that SNPs in the coding regions of IL13 (A98G) and VCAM1 (G149A)—both of which are known to be upregulated in HTLV-1-infected T cells—were associated with decreased risk for ATL development (161). In HAM/TSP patients, expansions of a CA repeat polymorphism in the MMP9 gene correlate with development of disease (78), and individual SNPs in the immunity-related cytokine genes IL18, IFNG, IL28B, and IL10 have each been associated with higher proviral load (5, 127, 128). Such findings further highlight the genetic complexity underlying HTLV-1-mediated disease.…”

Section: Human T Cell Leukemia Virus Typementioning

confidence: 99%

Human Genetic Determinants of Viral Diseases

et al. 2017

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Much progress has been made in the identification of specific human gene variants that contribute to enhanced susceptibility or resistance to viral diseases. Herein we review multiple discoveries made with genome-wide or candidate gene approaches that have revealed significant insights into virus–host interactions. Genetic factors that have been identified include genes encoding virus receptors, receptor-modifying enzymes, and a wide variety of innate and adaptive immunity-related proteins. We discuss a range of pathogenic viruses, including influenza virus, respiratory syncytial virus, human immunodeficiency virus, human T cell leukemia virus, human papilloma virus, hepatitis B and C viruses, herpes simplex virus, norovirus, rotavirus, parvovirus, and Epstein-Barr virus. Understanding the genetic underpinnings that affect infectious disease outcomes should allow tailored treatment and prevention approaches in the future.

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Section: Human T Cell Leukemia Virus Typementioning

confidence: 99%

Human Genetic Determinants of Viral Diseases

et al. 2017

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“…In the same cohort, the host genotype was determined (Vine et al, 2002;Kodama et al, 2004;Sabouri et al, 2004) at over 70 single-nucleotide polymorphisms (SNPs) in over 50 loci outside HLA class 1. Of these, polymorphisms at four loci (TNFA, IL-15, SDF-1 and IL-10) had statistically significant independent effects on the proviral load or the risk of HAM/TSP, or both.…”

Section: Htlv-1-specific Ctls Must Be Highly Active In Vivomentioning

confidence: 99%

Cellular immune response to HTLV-1

2005

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There is strong evidence at the individual level and the population level that an efficient cytotoxic T lymphocyte (CTL) response to HTLV-1 limits the proviral load and the risk of associated inflammatory diseases such as HAM/TSP. This evidence comes from host population genetics, viral genetics, DNA expression microarrays and assays of lymphocyte function. However, until now there has been no satisfactory and rigorous means to define or to measure the efficiency of an antiviral CTL response. Recently, methods have been developed to quantify lymphocyte turnover rates in vivo and the efficiency of anti-HTLV-1 CTLs ex vivo. Data from these new techniques appear to substantiate the conclusion that variation between individual hosts in the rate at which a single CTL kills HTLV-1-infected lymphocytes is an important determinant, perhaps the decisive determinant, of the proviral load and the risk of HAM/ TSP. With these experimental data, it is becoming possible to refine, parameterize and test mathematical models of the immune control of HTLV-1, which are a necessary part of an understanding of this complex dynamic system.

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“…The final published version may differ from this proof. In this context, many studies have demonstrated an association between mutations in human genes, diseases manifestation and viral infections influence [34][35][36] .…”

Section: Resultsmentioning

confidence: 99%

Amino- and Carboxyl-Terminal CCR5 Mutations in Brazilian HIV-1-Infected Women and Homology Model of p.L55Q CCR5 Mutant

Costa

Nunes

Jesus

et al. 2015

AIDS Research and Human Retroviruses

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Genetic factors from an HIV-1 host can affect the rate of progression to AIDS and HIV infection. To investigate the frequency of mutations in the CCR5 gene, HIV-1 samples from infected women and uninfected individuals were selected for sequencing of the CCR5 gene regions encoding the N- and C-terminal protein domains. Physicochemical CCR5 modeling and potential protein domain analysis were performed in order to evaluate the impact of the mutations found in the properties and structure of CCR5. The p.L55Q mutation in the N-terminal protein domain was observed only in uninfected individuals, with an allelic frequency of 1.8%. Physicochemical analysis revealed that the p.L55Q mutation magnified the flexibility and accessibility profiles and the modeling of CCR5 structures showed resulting in a small deviation to the right, as well as a hydrophobic to hydrophilic property alteration. The p.L55Q mutation also resulted in a slight modification of the electrostatic load of this region. Additionally, three novel silent mutations were found at the C-terminal coding region among HIV-1-infected women. The results suggest that the p.L55Q mutation might alter CCR5 conformation. Further studies should be conducted to verify the role of this mutation in HIV-1 susceptibility.

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Polymorphism in the Interleukin‐10 Promoter Affects Both Provirus Load and the Risk of Human T Lymphotropic Virus Type I–Associated Myelopathy/Tropical Spastic Paraparesis

Cited by 50 publications

References 33 publications

Human Genetic Determinants of Viral Diseases

Human Genetic Determinants of Viral Diseases

Cellular immune response to HTLV-1

Amino- and Carboxyl-Terminal CCR5 Mutations in Brazilian HIV-1-Infected Women and Homology Model of p.L55Q CCR5 Mutant

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