Abstract
Epstein–Barr virus (EBV) is a potent B cell transforming pathogen in humans. In most persistently EBV-infected individuals, potent cytotoxic lymphocyte responses prevent EBV-associated pathologies. In addition to comprehensive adaptive T cell responses, several innate lymphocyte populations seem to target different stages of EBV infection and are compromised in primary immunodeficiencies that render individuals susceptible to symptomatic EBV infection. In this mini-review, I will highlight the functions of natural killer, γδ T cells, and natural killer T cells during innate immune responses to EBV. These innate lymphocyte populations seem to restrict both lytic replication and transforming latent EBV antigen expression. The mechanisms underlying the recognition of these different EBV infection programs by the respective innate lymphocytes are just starting to become unraveled, but will provide immunotherapeutic strategies to target pathologies that are associated with the different EBV infection programs.
Highlights
ON INNATE LYMPHOCYTESEpstein–Barr virus (EBV) is a common human γ-herpesvirus that persistently infects more than 90% of the human adult population
This peaceful coexistence is thought to be maintained by cytotoxic lymphocytes, which massively expand during symptomatic primary EBV infection, called infectious mononucleosis (IM), can be used to treat some EBV-associated malignancies and are affected by primary or secondary immunodeficiencies that predispose for EBV-driven pathologies, such as human immunodeficiency virus-associated lymphomas [5,6,7]
The above discussed studies seem to indicate that several human innate lymphocyte subsets target different stages of EBV infection with natural killer (NK) cells recognizing lytic replication, Vγ9Vδ2 T cells reacting to EBV latency I and maybe III, and natural killer T (NKT) cells providing restriction of EBV latency II
Summary
In addition to comprehensive adaptive T cell responses, several innate lymphocyte populations seem to target different stages of EBV infection and are compromised in primary immunodeficiencies that render individuals susceptible to symptomatic EBV infection. In this mini-review, I will highlight the functions of natural killer, γδ T cells, and natural killer T cells during innate immune responses to EBV. These innate lymphocyte populations seem to restrict both lytic replication and transforming latent EBV antigen expression.
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