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<p>Human retroviruses such as HIV-1 and HTLV-1 hijack host cellular mechanisms for their replication, survival, and pathogenesis, often causing profound genomic instability. This review explores the dual role of homologous recombination (HR), explicitly mediated by the recombinase RAD51, in the context of retroviral infections. RAD51 is central to high-fidelity repair of DNA double-strand breaks, yet its activity is manipulated differently by HIV-1 and HTLV-1. In HIV-1 infection, RAD51 expression is elevated by viral proteins like Tat and Vpr, promoting DNA repair and enhancing viral transcription through interactions with NF-κB, thereby supporting viral persistence. Conversely, HTLV-1 suppresses RAD51-mediated HR via viral proteins such as p30 and Tax, promoting error-prone DNA repair pathways that contribute to oncogenesis. These contrasting effects may underscore RAD51's functional plasticity as both a facilitator of viral replication and a potential antiviral restriction factor. Furthermore, the therapeutic modulation of RAD51 activity-especially in combination with PARP inhibitors offers promising avenues for treating retrovirus-associated malignancies such as adult T-cell leukemia/lymphoma. This review highlights RAD51 as a pivotal connection in the interplay between genome stability and retroviral pathobiology.</p>

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The role of homologous recombination in human retrovirus-associated diseases

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年12月20日

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  • Mohammad Mehdi Akbarin,
  • Zahra Farjami,
  • Gabriel Eduardo Acevedo-Jiménez,
  • Cecilia Rodríguez Murillo,
  • Víctor David González-Fernández,
  • Lucero de María Ávila-De la Vega,
  • Hugo Ramírez Álvarez

摘要

Human retroviruses such as HIV-1 and HTLV-1 hijack host cellular mechanisms for their replication, survival, and pathogenesis, often causing profound genomic instability. This review explores the dual role of homologous recombination (HR), explicitly mediated by the recombinase RAD51, in the context of retroviral infections. RAD51 is central to high-fidelity repair of DNA double-strand breaks, yet its activity is manipulated differently by HIV-1 and HTLV-1. In HIV-1 infection, RAD51 expression is elevated by viral proteins like Tat and Vpr, promoting DNA repair and enhancing viral transcription through interactions with NF-κB, thereby supporting viral persistence. Conversely, HTLV-1 suppresses RAD51-mediated HR via viral proteins such as p30 and Tax, promoting error-prone DNA repair pathways that contribute to oncogenesis. These contrasting effects may underscore RAD51's functional plasticity as both a facilitator of viral replication and a potential antiviral restriction factor. Furthermore, the therapeutic modulation of RAD51 activity-especially in combination with PARP inhibitors offers promising avenues for treating retrovirus-associated malignancies such as adult T-cell leukemia/lymphoma. This review highlights RAD51 as a pivotal connection in the interplay between genome stability and retroviral pathobiology.