Reactivation of latent DNA viruses during immunosuppression: basic contemplation

Immunosuppression (ISP) affects the outcome of acute virus primoinfection as well as the course of virus latency. ISP may result from viral infection of the immune cells. This infection can be either transient, as in measles virus infection, or progressive as in Human immunodeficiency virus (HIV-1, 2) infections, which proceed to acquired immunodeficiency syndrome (AIDS). Innate ISP occurs due to various congenital defects of cells, participating within immune response. In the majority of cases, ISP may be initiated by physical causes (e.g. irradiation) or by chemical substances including drugs used for post-transplantation therapeutic regimens. The hallmark of ISP is the impairment of B or T lymphocyte functions. Helper T lymphocytes produce a great variety of cytokines providing B lymphocyte proliferation and cytotoxic T cell maturation. The mature and/or activated memory cytotoxic T lymphocytes destroy the target cells, which synthesize virus-specific proteins. Since many ISP drugs hamper or downregulate the proliferation of B and T lymphocytes, their administration creates favorable conditions for the replication of reactivated DNA viruses otherwise produced in low amounts. Thus, ISP causes an extensive increase in the low-grade production of persisting virus, which might regularly occur during latency. In addition to reactivation of virus latency, ISP potentiates the replication and spread of any intercurrent infectious agent, whether bacterial, parasitic, yeast or fungal origin.