Unique Alterations of Thyroid Hormone Indices in the Acquired Immunodeficiency Syndrome (AIDS)

LoPresti, Jonathan S.; Fried, Jeffrey; Spencer, Carole A.; Nicoloff, John T.

doi:10.7326/0003-4819-110-12-970

Cited by 126 publications

(47 citation statements)

References 21 publications

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“…Euthyroid sick syndrome is characterized by normal or low FT 4 levels, low T 3 levels, elevated reverse T 3 (rT 3 ) levels and low or normal TSH levels (31). This is a physiological adaptive phenomenon of the body to conserve energy during periods of extreme stress and during an infection.…”

Section: Introductionmentioning

confidence: 99%

Association between antiretrovirals and thyroid diseases: a cross-sectional study

Silva

Andrade

Sugui

et al. 2015

Arch. Endocrinol. Metab.

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Objective: This study aims to estimate the prevalence of thyroid diseases and anti-TPO status. We searched for an association among presence of immune reconstitution and use of stavudine, didanosine and protease inhibitors with thyroid diseases. Materials and methods: A cross-sectional study was performed to analyze the records of 117 HIV-infected patients who had their CD4 + cell count, viral load, anti-TPO, TSH and free T 4 levels collected on the same day. Immune reconstitution was considered in those whose T CD4 + count was below 200 cells/mm³, but these values increased above 200 cells/mm³ after the use of antiretrovirals. The odds ratio obtained by a 2x2 contingency table and a chi-square test were used to measure the association between categorical variables. Results: The prevalence of thyroid disease was 34.18%; of these, 4.34% were positive for anti-TPO. There was an association of risk between stavudine use and subclinical hypothyroidism (OR = 4.19, 95% CI: 1.29 to 13.59, X² = 6.37, p = 0.01). Immune reconstitution achieved protection associated with thyroid disease that was near statistical significance OR = 0.45, 95% CI: 0.19 to 1.04, X² = 3.55, p = 0.059. Conclusion:The prevalence of thyroid disease in the sample studied was higher than what had been found in the literature, with a low positive anti-TPO frequency. The historical use of stavudine has an association of risk for the presence of subclinical hypothyroidism, and immune reconstitution has trends towards protection for the presence of thyroid diseases. Arch Endocrinol Metab. 2015;59(2):116-22

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Section: Introductionmentioning

confidence: 99%

Association between antiretrovirals and thyroid diseases: a cross-sectional study

Silva

Andrade

Sugui

et al. 2015

Arch. Endocrinol. Metab.

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“…Thyroid hormone (T 3 ) and its receptors (TRs) have been suggested to play a role in HIV development. First, AIDS or ARC patients have multiple endocrine abnormalities and their serum T3 levels are often altered [3], [4]. Low levels of T3 often correlate with survival rate, and in all levels of illness, there is an increase in T3-binding globulin levels.…”

Section: Introductionmentioning

confidence: 99%

Involvement of chromatin and histone acetylation in the regulation of HIV-LTR by thyroid hormone receptor

2001

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The HIV-1 LTR controls the expression of HIV-1 viral genes and thus is critical for viral propagation and pathology. Numerous host factors have been shown to participate in the regulation of the LTR promoter. Among them is the thyroid hormone (T 3 ) receptor (TR). TR has been shown to bind to the critical region of the promoter that contain the NF B and Sp1 binding sites. Interestingly, earlier transient transfection studies in tissue culture cells have yielded contradicting conclusions on the role of TR in LTR regulation, likely due to the use of different cell types and/or lack of proper chromatin organization. Here, using the frog oocyte as a model system that allows replication-coupled chromatin assembly, mimicking that in somatic cells, we demonstrate that unliganded heterodimers of TR and RXR (9-cis retinoic acid receptor) repress LTR while the addition of T3 relieves the repression and further activates the promoter. More importantly, we show that chromatin and unliganded TR/RXR synergize to repress the promoter in a histone deacetylase-dependent manner.

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“…In addition, it has been also suggested a role for the T3 in HIV-1 LTR regulation, revealing the existence of binding sites for the T3 receptor (T3R) in different regions of the LTR sequence (Sawaya et al 1996, Xu et al 1996, Recio et al 2000, Hsia & Shi 2002. In this sense, previous studies have revealed that different hormones, such as T3, may have a role in AIDS development (LoPresti et al 1989), and a therapeutic use of retinoic antagonists has been already proposed to repress viral replication by inhibiting retinoid-dependent transcription (Lee et al 1994, Hanley et al 2004.…”

Section: Discussionmentioning

confidence: 99%

“…So far, the genetic predisposition of the host and the virus is the most important determinant for prediction and understanding the course of HIV infection and progression to AIDS. At this respect, previous studies have revealed that ligands of nuclear receptors such as thyroid hormones (T3) may have a role in AIDS development (LoPresti et al 1989). In fact, data from our laboratory, among others, have demonstrated a role for T3 and retinoic acid (RA), other nuclear receptor ligands, on HIV-1 LTR regulation, demonstrating the binding of RA receptors (RARs) and T3 receptors (TRs) to different LTR regions (Desai-Yajnik & Samuels 1993, Sawaya et al 1996, Xu et al 1996, Recio et al 2000, Hsia & Shi 2002.…”

Section: Introductionmentioning

confidence: 99%

Activation of the human immunodeficiency virus type I long terminal repeat by 1α,25-dihydroxyvitamin D3

Nevado¹,

Tenbaum²,

Castillo³

et al. 2007

Journal of Molecular Endocrinology

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The genetic predisposition of the host and the virus is the most important determinant for prediction of the course of human immunodeficiency virus type I (HIV-1) viral infection and acquired immune deficiency syndrome (AIDS) progression. Transcription from the HIV-1 long terminal repeat (LTR) is a crucial step for viral replication. Here, we describe a stimulatory role of the vitamin D receptor (VDR) on HIV-1 LTR transactivation. Transient transfections reveal that VDR activates the LTR in HeLa, U937, and Cos-1 cells in a ligand-dependent manner. 1a,25-Dihydroxyvitamin D3 (vitD3) promotes activation of a minimal LTR construct (from nucleotides K35 to C89), lacking a previously described hormone response element that binds several nuclear receptors. NF-kB (nuclear factor-kappa B) and Sp1-binding sites, which are responsible for most basal LTR activity in HeLa cells, are also dispensable for vitD3-dependent HIV-1 transcription. Although the tat response element element is not required for VDR-mediated HIV-1 gene expression, the viral protein Tat acts in a synergistic manner with the receptor to stimulate LTR activity. Furthermore, our data also show cooperation of the receptor with various cellular coactivators for HIV-1 transactivation by vitD3. Paradoxically, mutations in the VDR ligand-dependent transcriptional activation function-2 that abrogate vitD3-dependent stimulation through classical vitamin D response elements, do not reduce vitD3-mediated LTR transactivation. Furthermore, point mutations in the DNA-binding domain that abolish receptor binding to consensus DNA sequences do not affect ligand-dependent HIV-1 stimulation. These results show that VDR activates the HIV-1 LTR through different mechanisms, including nonclassical nuclear receptor transcriptional actions that may ensure viral transcription under different physiological scenarios.

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Unique Alterations of Thyroid Hormone Indices in the Acquired Immunodeficiency Syndrome (AIDS)

Cited by 126 publications

References 21 publications

Association between antiretrovirals and thyroid diseases: a cross-sectional study

Association between antiretrovirals and thyroid diseases: a cross-sectional study

Involvement of chromatin and histone acetylation in the regulation of HIV-LTR by thyroid hormone receptor

Activation of the human immunodeficiency virus type I long terminal repeat by 1α,25-dihydroxyvitamin D3

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