日大医学雑誌

ヘルペスウイルス感染症の制御―Epstein-Barr
ウイルス感染と免疫機構を支える遺伝子 (SAP/SH2D1A)

総説

著者

武井 正美1)  石渡 哲義3)  三田村 巧1)  山上 賢治1)
澤田 滋正1, 2)
1)日本大学医学部内科学講座血液膠原病内科部門 
2)日本大学医学部練馬光が丘病院内科
3)協和発酵工業東京研究所

要旨

Herpes virus group viruses include cytomegalovirus (CMV), Epstein-Barr virus (EBV), herpes simplex virus 1 or 2(HSV), varicella zoster virus (VZV), and human herpes virus-6, 7, and 8. These herpes viruses are transmitted by humancontact, cause primary infection, and may exist for several years in a latent state in healthy individuals. These viruses maybe reactivated by the dysregulation of the host immune system or possibly by virus mutation. In the present paper, wedescribe the treatment and diagnosis of HSV, VZV, CMV, and EBV infection and discuss possible future treatments. Ourproposed therapy is based on SAP (signaling lymphocytic-activation molecule associated protein) or SH2D1A (Src homology2 domain-containing protein). SAP (or SH2D1A), an adaptor-like molecule expressed in immune cells, is composedalmost exclusively of a Src homology 2 (SH2) domain. In humans, SAP is mutated and either absent or nonfunctionalin X-linked lymphoproliferative (XLP) syndrome (Duncan disease), a disease characterized by an inappropriateresponse to EBV infection. SAP is essential for late B cell help and the development of long-term humoral immunity.The regulation of this molecule (SAP) could become the basis of a new therapeutic approach to the treatment of infectionscaused by the herpes virus group.

keyword

signaling lymphocytic-activation molecule associated protein (SAP)
ヘルペスウイルス感染症,Epstein-Barr ウイルス