Oncogenic Effects of HIV-1 Proteins, Mechanisms Behind

Maria Isaguliants (Coresponding Author), Ekaterina Bayurova, Darya Avdoshina, Alla Kondrashova, Francesca Chiodi, Joel M. Palefsky

    Research output: Contribution to journalReview articlepeer-review

    10 Citations (Scopus)
    3 Downloads (Pure)

    Abstract

    People living with human immunodeficiency virus (HIV-1) are at increased risk of developing cancer, such as Kaposi sarcoma (KS), non-Hodgkin lymphoma (NHL), cervical cancer, and other cancers associated with chronic viral infections. Traditionally, this is linked to HIV-1-induced immune suppression with depletion of CD4+ T-helper cells, exhaustion of lymphopoiesis and lymphocyte dysfunction. However, the long-term successful implementation of antiretroviral therapy (ART) with an early start did not preclude the oncological complications, implying that HIV-1 and its antigens are directly involved in carcinogenesis and may exert their effects on the background of restored immune system even when present at extremely low levels. Experimental data indicate that HIV-1 virions and single viral antigens can enter a wide variety of cells, including epithelial. This review is focused on the effects of five viral proteins: envelope protein gp120, accessory protein negative factor Nef, matrix protein p17, transactivator of transcription Tat and reverse transcriptase RT. Gp120, Nef, p17, Tat, and RT cause oxidative stress, can be released from HIV-1-infected cells and are oncogenic. All five are in a position to affect “innocent” bystander cells, specifically, to cause the propagation of (pre)existing malignant and malignant transformation of normal epithelial cells, giving grounds to the direct carcinogenic effects of HIV-1.

    Original languageEnglish
    Article number305
    Pages (from-to)1-24
    Number of pages24
    JournalCancers
    Volume13
    Issue number2
    DOIs
    Publication statusPublished - 2 Jan 2021

    Keywords*

    • human immunodeficiency virus type 1
    • epithelial cells
    • carcinogenicity
    • oxidative stress
    • reactive oxygen species
    • gp120
    • Tat
    • Nef
    • matrix protein p17
    • reverse transcriptase

    Field of Science*

    • 3.2 Clinical medicine

    Publication Type*

    • 1.1. Scientific article indexed in Web of Science and/or Scopus database

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