Erratum to: Antiviral therapy in acute viral hepatitis B: why and when

Morelli, Giuseppe; Perrella, Alessandro; Sbreglia, Costanza; Bellopede, Pasquale; Riccio, Vincenzo; Antonio, Miguel; Perrella, Oreste

doi:10.1186/1750-9378-4-5

Cited by 2 publications

(2 citation statements)

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“…After publication of this work [ 1 ], we noted that we inadvertently failed to include the complete list of all coauthors. The full list of authors has now been corrected here and the Authors' contributions and Competing interests section modified accordingly (see below).…”

Section: Correctionmentioning

confidence: 99%

Erratum to: Antiviral therapy in acute viral hepatitis B: why and when

Morelli

Perrella

Sbreglia

et al. 2009

Infect Agents Cancer

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Section: Correctionmentioning

confidence: 99%

Erratum to: Antiviral therapy in acute viral hepatitis B: why and when

Morelli

Perrella

Sbreglia

et al. 2009

Infect Agents Cancer

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“…Human papillomaviruses (HPV) are classified group 1 human carcinogens (IARC, International Agency for Research on Cancer) extensively studied for their role in cervical cancer [ 1 ]. HPV are double-stranded DNA viruses with a well-defined affinity for epithelial cells.…”

Section: Introductionmentioning

confidence: 99%

Selenium Attenuates HPV-18 Associated Apoptosis in Embryo-Derived Trophoblastic Cells but Not Inner Cell Mass In Vitro

Tolen

Duerksen-Hughes

Lau

et al. 2015

International Journal of Reproductive Medicine

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Objectives. Human papillomaviruses (HPV) are associated with cell cycle arrest. This study focused on antioxidant selenomethionine (SeMet) inhibition of HPV-mediated necrosis. The objectives were to determine HPV-18 effects on embryonic cells and to evaluate SeMet in blocking HPV-18 effects. Methods. Fertilized mouse embryos were cultured for 5 days to implanted trophoblasts and exposed to either control medium (group 1), HPV-18 (group 2), combined HPV-18 and 0.5 µM SeMet (group 3), or combined HPV-18 and 5.0 µM SeMet (group 4). After 48 hrs, trophoblast integrity and, apoptosis/necrosis were assessed using morphometric and dual-stain fluorescence assays, respectively. Results. HPV-18 exposed trophoblasts nuclei (253.8 ± 28.5 sq·µ) were 29% smaller than controls (355.6 ± 35.9 sq·µ). Supplementation with 0.5 and 5.0 µM SeMet prevented nuclear shrinkage after HPV-18 exposure. HPV-18 infected trophoblasts remained larger with SeMet supplementation. HPV-18 decreased cell viability by 44% but SeMet supplementation sustained cell viability. Apoptosis was lower when SeMet was present. HPV-18 decreased inner cell mass (ICM) viability by over 60%. Conclusions. HPV-18 decreased nuclear size and trophoblast viability but these effects were attenuated by the antioxidant SeMet. SeMet blocked HPV-18 associated apoptosis process in trophoblasts but not ICM cells suggesting involvement of different oxidative stress pathways.

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Erratum to: Antiviral therapy in acute viral hepatitis B: why and when

Abstract: Correction to Morelli G, Perrella A, Sbreglia C, Bellopede P, Riccio V, Perrella O: Antiviral therapy in acute viral hepatitis B: why and when. Infectious Agents and Cancer 2009, 4:2.

Cited by 2 publications

References 2 publications

Erratum to: Antiviral therapy in acute viral hepatitis B: why and when

Erratum to: Antiviral therapy in acute viral hepatitis B: why and when

Selenium Attenuates HPV-18 Associated Apoptosis in Embryo-Derived Trophoblastic Cells but Not Inner Cell Mass In Vitro

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