LEADER 00547nam 2200193zu 450 001 9910987990603321 005 20250327175613.0 035 $a(CKB)38094159800041 035 $a(EXLCZ)9938094159800041 100 $a20250327|2024uuuu || | 101 0 $aeng 135 $aur||||||||||| 200 10$aAdjarian?s Armenian dialectology (1911) 210 $cLanguage Science Press$d2024 700 $aDolatian$b Hossep$01800746 906 $aBOOK 912 $a9910987990603321 996 $aAdjarian?s Armenian dialectology (1911)$94345677 997 $aUNINA LEADER 03073nam 2200433z- 450 001 9910557221503321 005 20211118 035 $a(CKB)5400000000041729 035 $a(oapen)https://directory.doabooks.org/handle/20.500.12854/73723 035 $a(oapen)doab73723 035 $a(EXLCZ)995400000000041729 100 $a20202111d2020 |y 0 101 0 $aeng 135 $aurmn|---annan 181 $ctxt$2rdacontent 182 $cc$2rdamedia 183 $acr$2rdacarrier 200 00$aEBV Infection and Human Primary Immune Deficiencies 210 $cFrontiers Media SA$d2020 215 $a1 online resource (132 p.) 311 08$a2-88963-571-6 330 $aEpstein-Barr virus (EBV) is a ubiquitous virus that infects 95% of adults worldwide; the vast majority of persons have asymptomatic or non-specific primary infection and no complications associated with EBV during their lifetime. Some persons, particularly those who are infected as adolescents or young adults, develop infectious mononucleosis. EBV infects resting B cells and infection in vitro results in transformation and continuous proliferation of the cells, whereas infection in vivo results in a latent infection in which proliferation of the cells is controlled by virus-specific T cells and NK cells. Certain persons have mutations in genes that result in impaired cellular immunity involving the function of cytotoxic T cells or NK cells that result in impaired responses and failure to control EBV. These persons are at risk for fulminant infectious mononucleosis, EBV-associated hemophagocytosis, EBV B or T cell lymphoma, or other opportunistic infections. These genes encode proteins that are important for a variety of NK and T cell activities: T cell interactions with B cells, NK and T cell activation, NK and T cell cytotoxicity, priming and expansion of virus-specific T cells, and control of T cell apoptosis. For most of these diseases, hematopoietic stem cell transplantation has been the only curative therapy. However, identification of certain immune deficiencies has led to new approaches to therapy such as drugs to inhibit overactive signaling pathways or supplemental magnesium for patients with mutations in a magnesium transporter. The study of these EBV-associated immune deficiencies identifies the importance of these proteins for the function of T and NK cells and may lead to novel approaches to therapy for EBV diseases. 606 $aImmunology$2bicssc 606 $aMedicine and Nursing$2bicssc 610 $aB-cell lymphoma 610 $aEpstein-Barr virus 610 $ahemophagocytic lymphohistiocytosis 610 $aimmune deficiency 610 $alymphoproliferative disease 615 7$aImmunology 615 7$aMedicine and Nursing 700 $aMeyts$b Isabelle$4edt$01317939 702 $aCohen$b Jeffrey I$4edt 702 $aMeyts$b Isabelle$4oth 702 $aCohen$b Jeffrey I$4oth 906 $aBOOK 912 $a9910557221503321 996 $aEBV Infection and Human Primary Immune Deficiencies$93033114 997 $aUNINA