Acceleration of Adenovirus Replication and Increased Virion Production by Treatment with the Steroid Hormone 17 Beta‐Estradiol

James, Calvin; Vanderpool, Eustace A.; Roane, Philip R.

doi:10.1111/j.1348-0421.1992.tb01646.x

Cited by 5 publications

(3 citation statements)

References 8 publications

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“…It also inhibits hepatitis B virus (HBV) transcription (Wang et al, 2012), limits herpes simplex virus (HSV) primary infection and reactivation (Gillgrass et al, 2010; Vicetti Miguel et al, 2010), and inhibits rubella virus replication(Roehrig, Brawner, and Riggs, 1979). 17β-estradiol, on the other hand, promotes the replication of adenovirus type 12 (James, Vanderpool, and Roane, 1992). The signal transduction cascade of estrogen is complex and can be engaged by multiple pathways.…”

Section: Introductionmentioning

confidence: 99%

17β-Estradiol inhibits HIV-1 by inducing a complex formation between β-catenin and estrogen receptor α on the HIV promoter to suppress HIV transcription

2013

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Human Immunodeficiency virus type 1 (HIV-1) disproportionately affects women, accounting for >50% of new HIV infections in adults worldwide. While multiple mechanisms may contribute to a greater degree of HIV infection in women than men, we evaluated the direct effect of 17β-estradiol, the most bioactive form of estrogen in women, on HIV replication in peripheral blood mononuclear cells (PBMCs). We demonstrate that 17β-estradiol, in an ERα dependent manner, inhibits HIV replication by activating β-catenin signaling. Specifically, we show for the first time that 17β-estradiol induces a complex formation between ERα and β-catenin which tether on the HIV LTR at −143 nt site from +1 start site of HIV transcription to repress HIV promoter activity. These studies define a role of 17β-estradiol in inhibiting HIV replication which may impact HIV pathogenesis in women and add to a growing list of viruses that are inhibited by 17β-estradiol through ERα engagment.

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Section: Introductionmentioning

confidence: 99%

17β-Estradiol inhibits HIV-1 by inducing a complex formation between β-catenin and estrogen receptor α on the HIV promoter to suppress HIV transcription

2013

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“…Previous studies with other human viruses have illustrated a stimulating or inhibiting role of steroid hormones on viral replication (herpes simplex virus type 2 [4], vaccinia virus [4], herpes simplex virus type 1 [64], Epstein-Barr virus [6], human immunodeficiency virus type 1 [56], human cytomegalovirus [46,79,80], and adenovirus [41]). In other human viruses, a GRE has been identified.…”

Section: Discussionmentioning

confidence: 99%

A steroid hormone response unit in the late leader of the noncoding control region of the human polyomavirus BK confers enhanced host cell permissivity

Moens

Subramaniam

Johansen

et al. 1994

J Virol

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The effect of steroid hormones on multiplication of the human polyomavirus BK (BKV) was studied. Physiological concentrations of the synthetic glucocorticoid dexamethasone, progesterone R5020, or estrogen 17,-estradiol enhanced the permissivity of the host cell for BKV, resulting in an up to 11-fold (dexamethasone), 5-fold (progesterone), or 3-fold (17I1-estradiol) higher virus yield. The increase in virus yield in dexamethasone-stimulated cells correlated with enhanced steady-state levels of viral transcripts. The late leader sequence of the BKV control region contains a hormone response unit composed of a nonconsensus glucocorticoid and/or progesterone response element (GRE/PRE) and a fully consensus estrogen response element (ERE). DNA-protein binding studies showed that the glucocorticoid receptor and the progesterone receptor bound to this BKV GRE/PRE-like sequence, while the estrogen receptor could bind to the BKV ERE motif. By transient transfection assays, we were able to show that these sequences can mediate steroid hormone-induced gene expression. However, no cooperative transactivation effect between the BKV GRE/PRElike motif and BKV ERE motif was observed. This BKV hormone response unit may play an important role in vivo by enhancing a productive BKV infection, and perhaps also by reactivating a latent infection, during physiological or pathological conditions accompanied by increased steroid hormone levels.

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“…The frequency of atypical thrombosis after vaccination has to be weighted with that of thrombosis in the general population [ 16 ], and the higher frequency of thrombosis in COVID-19 patients in emergency departments, which will be strongly reduced by vaccination [ 17 , 18 ]. Factors contributing to the preferential affection of female gender in the observed thromboses after AdV-S vaccination may include increased seasonal adenovirus production supported by beta-estradiol [ 19 ] and hormonal activation of thrombocytes [ 20 ]. There may be further some contribution to a tendency of hypercoagulation by genetic factors, since the kinetics of clot formation after vaccination is at least fivefold enhanced when there are mutations in von Willebrand factor cleaving protease deficiency G20210A (ADAMTS-13) [ 10 ], and presence of factor V Leiden mutation, enhanced by oral contraceptive use [ 21 – 23 ], which however were not an apparent cause of most of the so far observed cases of atypical thrombosis after vaccination [ 24 , 25 ].…”

mentioning

confidence: 99%

Cerebral venous thrombosis after COVID-19 vaccination: is the risk of thrombosis increased by intravascular application of the vaccine?

Gürtler

Seitz²,

Schramm

2021

Infection

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Keywords Venous thrombosis • SARS-CoV-2 vaccination • Adenovirus vector • PF4 antibody • ThrombocytopeniaCurrently, an unprecedented campaign of vaccination against COVID-19 is carried out worldwide, involving many millions of people. Pre-licensing clinical studies of new vaccines can include only a limited number of subjects; therefore rigorous pharmacovigilance is warranted to detect rare side effects.The surveillance of the recombinant adenovirus-based COVID-19 vaccine ChAdOx1-S (Oxford, Astra-Zeneca) which contains chimpanzee adenovirus (AdV) encoding the SARS-CoV-2 spike glycoprotein, revealed rare thromboses with concurrent thrombocytopenia, including venous thromboses in unusual sites such as cerebral venous sinus thrombosis (CVST), intestinal venous and arterial thromboses [1]. Soon thereafter, the Pharmacovigilance Risk Assessment Committee (PRAC) of the European Medicines Agency (EMA) reported also a signal concerning thromboembolic events with thrombocytopenia after vaccination with the Ad26.COV2-S COVID-19 vaccine (Johnson & Jonhnson) [2], which contains the cloned SARS-CoV-2 spike glycoprotein in AdV type 26. Both above-mentioned vaccines are abbreviated in the following as AdV-S. The above described thrombotic complications after AdV-S have in the meantime Rainer Seitz retired from Paul-Ehrlich-Institute.

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Acceleration of Adenovirus Replication and Increased Virion Production by Treatment with the Steroid Hormone 17 Beta‐Estradiol

Cited by 5 publications

References 8 publications

17β-Estradiol inhibits HIV-1 by inducing a complex formation between β-catenin and estrogen receptor α on the HIV promoter to suppress HIV transcription

17β-Estradiol inhibits HIV-1 by inducing a complex formation between β-catenin and estrogen receptor α on the HIV promoter to suppress HIV transcription

A steroid hormone response unit in the late leader of the noncoding control region of the human polyomavirus BK confers enhanced host cell permissivity

Cerebral venous thrombosis after COVID-19 vaccination: is the risk of thrombosis increased by intravascular application of the vaccine?

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