Abstract
Natural killer (NK) cells are essential in the early immune response against viral infections, in particular through clearance of virus-infected cells. In return, viruses have evolved multiple mechanisms to evade NK cell-mediated viral clearance. Several unrelated viruses, including influenza virus, respiratory syncytial virus, and human immunodeficiency virus, can directly interfere with NK cell functioning through infection of these cells. Viral infection can lead to immune suppression, either by downregulation of the cytotoxic function or by triggering apoptosis, leading to depletion of NK cells. In contrast, some viruses induce proliferation or changes in the morphology of NK cells. In this review article, we provide a comprehensive overview of the viruses that have been reported to infect NK cells, we discuss their mechanisms of entry, and describe the interference with NK cell effector function and phenotype. Finally, we discuss the contribution of virus-infected NK cells to viral load. The development of specific therapeutics, such as viral entry inhibitors, could benefit from an enhanced understanding of viral infection of NK cells, opening up possibilities for the prevention of NK cell infection.
Highlights
Natural killer (NK) cells are innate lymphocytes that represent the first line of defense against tumor cells and viral infections [1,2]
This study proposes that FcγRIIIA, the IgG-receptor expressed on NK cells, mediates binding to NK cells in the presence of virus-specific antibodies [42]
Depletion of NK cells during viral infections has been shown in clinical studies for influenza A virus (IAV) [51,52] and Respiratory syncytial virus (RSV) [51,58], but whether this is due to direct infection of NK cells is unknown
Summary
Natural killer (NK) cells are innate lymphocytes that represent the first line of defense against tumor cells and viral infections [1,2]. To mediate cytolysis through engagement of death receptors expressed on target cells, NK cells express multiple extracellular ligands, including Fas ligand (FasL) and the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) [5]. Some viruses are known to downregulate surface expression of MHC-I to interfere with the presentation of viral antigens, thereby escaping detection by the adaptive immune system [8]. This immune evasion strategy is effective in preventing recognition by T cells, decreased. Due to the important role of NK cells in the early antiviral immune response, viruses have evolved numerous strategies to evade NK cell effector functions One of these evasion strategies is the manipulation of NK cells through direct infection.
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