Abstract
Viruses and natural killer (NK) cells have a long co-evolutionary history, evidenced by patterns of specific NK gene frequencies in those susceptible or resistant to infections. The killer immunoglobulin-like receptors (KIR) and their human leukocyte antigen (HLA) ligands together form the most polymorphic receptor-ligand partnership in the human genome and govern the process of NK cell education. The KIR and HLA genes segregate independently, thus creating an array of reactive potentials within and between the NK cell repertoires of individuals. In this review, we discuss the interplay between NK cell education and adaptation with virus infection, with a special focus on three viruses for which the NK cell response is often studied: human immunodeficiency virus (HIV), hepatitis C virus (HCV) and human cytomegalovirus (HCMV). Through this lens, we highlight the complex co-evolution of viruses and NK cells, and their impact on viral control.
Highlights
Persons lacking natural killer (NK) cells or with defects in NK cell function present with recurrent viral infections, highlighting the crucial role of this population in virus control [1]
We focus on the impact of NK cell
Persons succumbing to Lassa virus infection are enriched for the educating partnership of KIR2DL2 and human leukocyte antigen (HLA)-C1 compared with healthy controls and infected survivors, which suggests that inhibitory peptides encoded by Lassa and presented on HLA-C1 can inhibit or slow antiviral NK cell responses [107]
Summary
Persons lacking natural killer (NK) cells or with defects in NK cell function present with recurrent viral infections, highlighting the crucial role of this population in virus control [1]. The hallmark function of NK cells is their ability to sense and eliminate targets based on a lack of “self” human leukocyte antigen (HLA) class I proteins (hereafter referred to as HLA). The ability of NK cells to kill tumour cells without prior sensitization was initially described in mice, and quickly recognized thereafter in humans [7] This is remarkable: major histocompatibility complex molecules (MHC) in mice and humans (i.e., HLA) are extremely diverse, and the genes for the Ly49 (mouse) and killer immunoglobulin-like receptor (KIR) receptors that bind them derive from different founder genes [8,9]. NK cell receptors are expressed and co-expressed codominantly within the NK cell repertoire, creating an array of NK cells with differing patterns of education and reactive potential
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