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EBNA1 is required for that automantenga DNA in lymphocytes that are activated and allows the virus to remain LPM2 limiting latent gene expression in the membrane. This minimal expression of the repertoire of viral proteins allows the virus to minimize the number of targets for the immune system.

Another defense mechanism is BCRF1 gene expression that produces a protein, EBV IL-10, similar in 80% of interleukin 10 (IL-10). Thus, the virus inhibits the production of interferon and synthesis of IL-1 and IL-12, thus altering the differentiation of B lymphocytes. The third mechanism that can be used for persisting EBV is its ability to decrease the production and expression of HLA I and also of “carrier proteins” in the infected cells also appears that EBNA1 can inhibit the mechanism of processing of viral antigens. This will achieve a reduction in antigen expression on cell membranes and protection against the destructive power of T8 lymphocytes.

Epidemiology

It is a widely distributed virus, estimated that about 90% of adults have been infected. It is thought that 70% of the population is infected before age 30. The seroepidemiology has shown that in underdeveloped countries asymptomatic infection in early life is more often while on the contrary, in countries with better standard of living many individuals escape from primary infection until adolescence . When primary infection is delayed virus tends to cause symptoms.

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