Epstein–Barr virus and immunity

Epstein–Barr virus is the most widespread herpes virus in humans; the majority of the global population is infected by it. In children, the viral infection either lacks symptoms or leads to infectious mononucleosis. In a small percentage of people with latent infection, especially immunosuppressed patients, Epstein–Barr virus causes lymphoid and epithelial malignant neoplasms and a number of autoimmune diseases. Among other things, it is one of the causes of multiple sclerosis. Innate immunity is the primary protection from viruses, which the virus evades by using a number of strategies for successfully infecting people. It disrupts the innate immunity’s signaling pathways activated by Toll-, NOD-, RIG-I- and AIM2-like receptors, as well as cyclic GMP-AMP synthase. Epstein–Barr virus also counters the production and signaling of interferon, including JAK-STAT and TBK1-IRF3 pathways. Because of the differential modulation of the proviral and antiviral mechanisms of caspases and other cell cycle regulators at different infection stages, the virus actively interferes with the apoptosis and inflammation pathways to proceed infecting effectively. Using the activation of innate immunity to its advantage by triggering the pro-inflammatory response and the proteolytic cleavage of caspases which demonstrate proviral activity, the virus establishes latency and enters the phase of lytic reactivation. This promotes the development of serious life-threatening conditions, including cancer. The outcome of the infection is regulated by the delicate interaction between innate and adaptive immunity and the virus’ reproduction. In the absence of approved prophylactic vaccines, immunocorrection and antiviral therapy are the only possible methods of combating the virus and preventing the conditions associated with it. Understanding the mechanisms of various genes of Epstein–Barr virus involved in its life activity at different infection stages will help to find the right approach to developing preventive and curative treatments for this virus in the future.