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Blood, 1 July 2006, Vol. 108, No. 1, pp. 8. This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Lemas, M. V. Articles by Ambinder, R. F. Search for Related Content PubMed Articles by Lemas, M. V. Articles by Ambinder, R. F. Related Collections Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Comment on Sauce et al, page 11 The kiss that scars M. Victor Lemas, and Richard F. Ambinder JOHNS HOPKINS SCHOOL OF MEDICINE In their article in this issue, Sauce and colleagues report that the syndrome of acute infectious mononucleosis leaves an immune scar that endures for years. The syndrome of acute infectious mononucleosis (pharyngitis, fever, activated lymphocytosis) and its mode of transmission (kissing) were recognized long before the etiologic agent, Epstein-Barr virus (EBV), was first identified. Although the syndrome is common, the virus is much more common and asymptomatic infection is the rule. People with a history of acute infectious mononucleosis lack T cells expressing IL-15R. Other infections are associated with temporary depletion of IL-15R and IL-7R, but over time there is recovery. Only EBV-associated infectious mononucleosis—and not asymptomatic primary infection and not a similar symptomatic primary infection associated with cytomegalovirus—leads to this particular scar. Other investigators have failed to identify immunologic parameters that distinguish people with history of asymptomatic versus symptomatic primary infection.1 EBV has been linked with a multitude of disorders including lymphoma, carcinoma, and a variety of autoimmune disorders that occur months or years after the acute phase of the infection. Hodgkin disease is of special interest here because it has been linked to the virus (viral DNA, RNA, and proteins are readily detected in at least a third of cases in tumor cells), and the syndrome per se is linked to the tumor. Thus, laboratory-confirmed symptomatic infectious mononucleosis is associated with an increased risk of developing EBV-associated Hodgkin disease.2 But we know very little of the determinants of symptomatic infection. Are age of the host, the size of the viral innoculum, the strain or strains of infecting virus, or host genetics important determinants? Can symptomatic infection and its consequences be altered? These questions are very much at the forefront in research and clinical care. A vaccine designed to modify the natural history of primary infection in seronegative university students is presently in trials in Belgium.3 In patients with a special susceptibility to fatal primary EBV infection (X-linked lymphoproliferative syndrome), the use of rituximab at the first sign of infection may have blunted the course of the illness.4 A multitude of other approaches to treating EBV-associated Hodgkin disease, including the use adoptive T-cell therapy and therapeutic vaccines designed to target cells expressing particular viral antigens, are being explored. The present report offers the possibility of an immunologic handle on the consequences of symptomatic infection versus asymptomatic infection. Questions brought to mind include the following: Do patients with a variety of diseases show the scar described in the present paper (EBV-Hodgkin, other EBV-associated tumors, multiple sclerosis, lupus, etc)? Do interventions such as vaccines, chemotherapies, anti-inflammatories, or adoptive cellular therapies change the long-term manifestations in terms of IL-15R-bearing T cells? Will such changes alter disease associations? References Cameron B, Bharadwaj M, Burrows J, et al. Prolonged illness after infectious mononucleosis is associated with altered immunity but not with increased viral load. J Infect Dis. 2006;193: 664-671.[CrossRef][Medline] [Order article via Infotrieve] Hjalgrim H, Askling J, Rostgaard K, et al. Characteristics of Hodgkin's lymphoma after infectious mononucleosis. N Engl J Med. 2003;349: 1324-1332.[Abstract/Free Full Text] Williams H, Crawford DH. Epstein-Barr virus: the impact of scientific advances on clinical practice. Blood. 2006;107: 862-869.[Abstract/Free Full Text] Milone MC, Tsai DE, Hodinka RL, et al. Treatment of primary Epstein-Barr virus infection in patients with X-linked lymphoproliferative disease using B-cell-directed therapy. Blood. 2005;105: 994-996.[Abstract/Free Full Text] CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: EBV-associated mononucleosis leads to long-term global deficit in T-cell responsiveness to IL-15 Delphine Sauce, Martin Larsen, S. John Curnow, Alison M. Leese, Paul A. H. Moss, Andrew D. Hislop, Michael Salmon, and Alan B. Rickinson Blood 2006 108: 11-18. [Abstract] [Full Text] [PDF] This article has been cited by other articles: R. L. Levine and G. Wernig Role of JAK-STAT Signaling in the Pathogenesis of Myeloproliferative Disorders Hematology, January 1, 2006; 2006(1): 233 - 239. [Abstract] [Full Text] [PDF] This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Lemas, M. V. Articles by Ambinder, R. F. Search for Related Content PubMed Articles by Lemas, M. V. Articles by Ambinder, R. F. Related Collections Related Article in Blood Online Social Bookmarking                   What's this?

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