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Epstein-Barr virus related to Hodgkin's lymphoma

Researchers at the National Institutes of Health (NIH), along with international colleagues, identify a genetic immune disorder that increases susceptibility to Epstein-Barr virus (EBV) and an associated cancer — Hodgkin's lymphoma.

Studying two unrelated sets of siblings with similar immune problems, researchers determined their symptoms were the result of a lack of the protein CD70. CD70 is found on the surface of several types of immune cells. Scientists at the National Institute of Allergy and Infectious Diseases (NIAID), a part of the National Institutes of Health or NIH, conducted the research with an international team of collaborators.

The work appears in the Journal of Experimental Medicine.

Both sets of siblings had evidence for uncontrolled infection by Epstein-Barr virus. EBV is a common and usually mild virus, which developed into Hodgkin's lymphoma in three of the children. Each infected child also had other immune symptoms, reduced activity of pathogen-fighting T cells, low production of antibodies, and poor activation of antibody-producing B cells.

Researchers analyzed the genomes of all four children and found each had two mutated copies of the CD70 gene, resulting in nonfunctioning or nonexistent CD70 proteins.

All four parents had healthy immune systems, but had only one copy of the mutation — indicating CD70 deficiency follows a pattern of autosomal recessive inheritance. This means affected individuals receive a flawed gene from each parent.

While no specific treatment for CD70 deficiency currently exists, each of the four children recovered from Hodgkin's lymphoma and receives antibody infusions to help bolster their immune systems.

The research also offers insight into the normal role of CD70. Previous studies showed that CD70 interacts with another immune cell protein called CD27. The interaction of these two proteins may be important for the proper function of lymphocytes — the white blood cells with a single round nucleus found in the lymphatic system.

This idea is confirmed by the latest findings on CD70 deficiency. As the research indicated, investigators testing experimental medications that decrease CD70 or CD27 activity as a possible strategy for combatting autoimmune disease — may also increase a possible risk of EBV-related complications.

In this study, we describe four patients from two unrelated families of different ethnicities with a primary immunodeficiency, predominantly manifesting as susceptibility to Epstein-Barr virus (EBV)–related diseases. Three patients presented with EBV-associated Hodgkin’s lymphoma and hypogammaglobulinemia; one also had severe varicella infection. The fourth had viral encephalitis during infancy. Homozygous frameshift or in-frame deletions in CD70 in these patients abolished either CD70 surface expression or binding to its cognate receptor CD27. Blood lymphocyte numbers were normal, but the proportions of memory B cells and EBV-specific effector memory CD8+ T cells were reduced. Furthermore, although T cell proliferation was normal, in vitro–generated EBV-specific cytotoxic T cell activity was reduced because of CD70 deficiency. This reflected impaired activation by, rather than effects during killing of, EBV-transformed B cells. Notably, expression of 2B4 and NKG2D, receptors implicated in controlling EBV infection, on memory CD8+ T cells from CD70-deficient individuals was reduced, consistent with their impaired killing of EBV-infected cells. Thus, autosomal recessive CD70 deficiency is a novel cause of combined immunodeficiency and EBV-associated diseases, reminiscent of inherited CD27 deficiency. Overall, human CD70–CD27 interactions therefore play a nonredundant role in T and B cell–mediated immunity, especially for protection against EBV and humoral immunity.

H Abolhassani et al. Combined Immunodeficiency and Epstein-Barr Virus-Induced B Cell Malignancy in Humans with Inherited CD70 Deficiency. Journal of Experimental Medicine DOI: 10.1084/jem.20160849 (2016).

Authors: Principal investigator Helen C. Su, M.D., Ph.D., Human Immunological Diseases Section Chief in the Laboratory of Host Defenses in NIAID's Division of Intramural Research, is available to comment.

NIAID conducts and supports research — at NIH, throughout the United States, and worldwide — to study the causes of infectious and immune-mediated diseases, and to develop better means of preventing, diagnosing and treating these illnesses. News releases, fact sheets and other NIAID-related materials are available on the NIAID website.

About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit http://www.nih.gov.
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Leukemia cells containing Epstein-Barr Virus
Image Credit: The Scientist



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