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Infectious Mononucleosis and Malignant Neoplasia

  • Ian Magrath
Part of the Clinical Topics in Infectious Disease book series (CLIN.TOP.INFECT)

Abstract

Epstein-Barr virus (EBV) infection is ubiquitous, but is usually asymptomatic except in teenagers and young adults, some 50 percent of whom experience the syndrome of acute infectious mononucleosis at the time of primary infection. Although the virus establishes a permissive infection in a number of cell types in the mouth and pharynx, including the ductal cells of the salivary glands, it is the proliferation of latently infected (i.e., nonpermissive for viral replication) B lymphocytes in lymphoid tissue and the resultant cellular immune reaction against these EBV-infected cells which give rise to the syndrome of infectious mononucleosis described elsewhere in this book. EBV gains access to B lymphocytes via the surface receptor for the complement component C3d (CR2) (Nemerow et al. 1987), also known as CD21, and transforms them into lymphoblasts capable of indefinite proliferation in vitro. This capacity is conferred on the cell via a small set of EBV genes which are expressed in the absence of viral replication. In addition to "immortalizing" the cell, however, some of these latent genes induce an immune response against the EBV-infected cells which leads to their destruction. Destruction is accomplished initially by NK cells and nonspecifically reactive T cells which probably respond to EBV-induced activation antigens, and later by specifically reactive cytotoxic T lymphocytes which recognize virally coded proteins on the cell surface in the context of HLA class 1 antigens. The clinical syndrome of infectious mononucleosis, if it occurs at all, is thus limited in duration and rarely fatal. These two points— the potentially unUmited proliferation of EBV-infected B lymphocytes, and their control by immune mechanisms—are crucial and worthy of emphasis; for in the absence of an effective immune response, the stage is set for the progressive and inexorable accumulation of EBV-infected cells which, unchecked, will result in the death of the host. Intuitively, it would seem that the complete lack of an ability to control the proliferation of EBV-infected cells would resuh in a fatal lymphoproliferative process soon after primary EBV infection, whereas lesser degrees of impairment could result in the establishment of a more chronic or more localized process, or possibly of uncontrolled proliferation in immunoprivileged sites such as the brain. Penetration into these special sites may result from the presence of a persistently higher body burden of EBV-infected cells.

Keywords

Latent Membrane Protein Infectious Mononucleosis Malignant Neoplasia Aotus Trivirgatus Tious Mononucleosis 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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  • Ian Magrath

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