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<p>Human cytomegalovirus (HCMV) is a betaherpesvirus that has evolved multiple defense mechanisms against host immunity. Most HCMV infections go unnoticed, but the reactivation of the latent virus can be life-threatening in immune-suppressed people. Over millions of years of coevolution with the human host, HCMV has adapted to evade both innate and adaptive immune responses through a dynamic host-pathogen arms race in which selective pressures from host immunity have driven the diversification and refinement of viral genes. This is particularly evident in the UL and US regions of the HCMV genome, which encode multiple proteins that interfere with antigen presentation and modulate immune receptor signaling. HCMV also employs molecular mimicry, encoding an MHC class I homolog, UL18, which binds to LIR-1 to inhibit NK cell activation, enabling immune evasion and persistent infection. This mini-review focuses on the key immunoevasive mechanisms by which HCMV gene products interfere with NK and T cell recognition and effector functions to modulate host immune responses. Elucidating these strategies is critical for identifying novel antiviral targets and informing the rational design of effective vaccines.</p>

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NK and T cell evasion mechanism of human cytomegalovirus

  • 期刊论文

  • 发表日期：

    2025年11月10日

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  • Animesh Sarker,
  • Joynab Binta Arafat

摘要

Human cytomegalovirus (HCMV) is a betaherpesvirus that has evolved multiple defense mechanisms against host immunity. Most HCMV infections go unnoticed, but the reactivation of the latent virus can be life-threatening in immune-suppressed people. Over millions of years of coevolution with the human host, HCMV has adapted to evade both innate and adaptive immune responses through a dynamic host-pathogen arms race in which selective pressures from host immunity have driven the diversification and refinement of viral genes. This is particularly evident in the UL and US regions of the HCMV genome, which encode multiple proteins that interfere with antigen presentation and modulate immune receptor signaling. HCMV also employs molecular mimicry, encoding an MHC class I homolog, UL18, which binds to LIR-1 to inhibit NK cell activation, enabling immune evasion and persistent infection. This mini-review focuses on the key immunoevasive mechanisms by which HCMV gene products interfere with NK and T cell recognition and effector functions to modulate host immune responses. Elucidating these strategies is critical for identifying novel antiviral targets and informing the rational design of effective vaccines.