Cellular proteins as potential targets for antiretroviral therapy

Vopr Virusol. 2023 Dec 26;68(6):488-504. doi: 10.36233/0507-4088-207.

Abstract

The review article conducts an in-depth analysis of information gleaned from a comprehensive literature search across Scopus, Web of Science, and MedLine databases. The focal point of this search revolves around the identification and exploration of the mechanisms orchestrated by host cell factors in the replication cycle of the human immunodeficiency virus (HIV-1, Retroviridae: Orthoretrovirinae: Lentivirus: Human immunodeficiency virus-1). The article delves into two primary categories of proteins, namely HIV dependence factors (such as CypA, LEDGF, TSG101) and restriction factors (including SERINС5, TRIM5α, APOBEC3G), providing illustrative examples. The current understanding of the functioning mechanisms of these proteins is elucidated, and an evaluation is presented on the potential development of drugs for treating HIV infection. These drugs aim to either inhibit or stimulate the activity of host factors, offering insights into promising avenues for future research and therapeutic advancements.

Обзорная статья содержит анализ информации, полученной в результате поиска литературы по базам данных Scopus, Web of Science, MedLine. Тема поиска – идентификация и изучение механизмов действия факторов хозяйской клетки, участвующих в цикле репликации вируса иммунодефицита человека (ВИЧ, Retroviridae: Orthoretrovirinae: Lentivirus: Human immunodeficiency virus-1). Приведены примеры двух основных групп белков – факторов зависимости ВИЧ (CypA, LEDGF, TSG101 и др.) и факторов рестрикции (SERINС5, TRIM5α, APOBEC3G и др.); описано современное состояние представлений о механизмах их функционирования. Дана оценка перспектив разработки лекарственных средств для лечения ВИЧ-инфекции, направленных на ингибирование либо стимуляцию активности хозяйских факторов.

Keywords: HIV; dependence factors; host proteins; restriction factors; review.

Publication types

  • Review

MeSH terms

  • Cell Line
  • HIV Infections* / drug therapy
  • HIV-1* / genetics
  • Humans
  • Ubiquitin-Protein Ligases
  • Virus Replication

Substances

  • Ubiquitin-Protein Ligases