as they lack mature B cells (and so HLA co-receptors) needed for the viral infection. Patients with XLA are also more likely to have a history of septic arthritis. It is not known if XLA patients are able to generate an allergic reaction, as they lack functional IgE antibodies. There is no special hazard for XLA patients in dealing with pets or outdoor activities. Unlike in other primary immunodeficiencies XLA patients are at no greater risk for developing autoimmune illnesses. Agammaglobulinemia (XLA) is similar to the primary immunodeficiency disorder Hypogammaglobulinemia (CVID), and their clinical conditions and treatment are almost identical. However, while XLA is a congenital disorder, with known genetic causes, CVID may occur in adulthood and its causes are not yet understood. In addition, to X-linked agammaglobulinemia a couple of autosomal recessive agammaglobulinemia gene mutations have been described including mutations in IGHM, IGLL1, CD79A/B, BLNK and deletion of the deletion of the terminal 14q32.33 chromosom. XLA was also historically mistaken as Severe Combined Immunodeficiency (SCID), a much more severe immune deficiency ("Bubble boys").A strain of laboratory mouse, XID, is used to study XLA. These mice have a mutated version of the mouse Btk gene, and exhibit a similar, yet milder, immune deficiency as in XLA. See also Hypogammaglobulinemia (CVID) Intravenous immunoglobulin (IVIg) References External links GeneReviews/NCBI/NIH/UW entry on X-Linked Agammaglobulinemia Predominantly antibody deficiencies Neurocutaneous conditions X-linked recessive disorders