Mitochondrial Proteins Coded by Human Tumor Viruses

Research output: Contribution to journalReview article

Abstract

Viruses must exploit the cellular biosynthetic machinery and evade cellular defense systems to complete their life cycles. Due to their crucial roles in cellular bioenergetics, apoptosis, innate immunity and redox balance, mitochondria are important functional targets of many viruses, including tumor viruses. The present review describes the interactions between mitochondria and proteins coded by the human tumor viruses human T-cell leukemia virus type 1, Epstein-Barr virus, Kaposi's sarcoma-associated herpesvirus, human hepatitis viruses B and C, and human papillomavirus, and highlights how these interactions contribute to viral replication, persistence and transformation.

Original languageEnglish
Pages (from-to)81
JournalFrontiers in Microbiology
Volume9
DOIs
Publication statusPublished - 2018

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Oncogenic Viruses
Mitochondrial Proteins
Mitochondria
Viruses
Deltaretrovirus
Human Herpesvirus 8
Life Cycle Stages
Human Herpesvirus 4
Innate Immunity
Hepatitis B virus
Hepacivirus
Energy Metabolism
Oxidation-Reduction
Apoptosis
Proteins

Cite this

Mitochondrial Proteins Coded by Human Tumor Viruses. / Cavallari, Ilaria; Scattolin, Gloria; Silic-Benussi, Micol; Raimondi, Vittoria; D'Agostino, Donna M; Ciminale, Vincenzo.

In: Frontiers in Microbiology, Vol. 9, 2018, p. 81.

Research output: Contribution to journalReview article

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AB - Viruses must exploit the cellular biosynthetic machinery and evade cellular defense systems to complete their life cycles. Due to their crucial roles in cellular bioenergetics, apoptosis, innate immunity and redox balance, mitochondria are important functional targets of many viruses, including tumor viruses. The present review describes the interactions between mitochondria and proteins coded by the human tumor viruses human T-cell leukemia virus type 1, Epstein-Barr virus, Kaposi's sarcoma-associated herpesvirus, human hepatitis viruses B and C, and human papillomavirus, and highlights how these interactions contribute to viral replication, persistence and transformation.

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