PMID- 30641912 OWN - NLM STAT- MEDLINE DCOM- 20190501 LR - 20200225 IS - 1422-0067 (Electronic) IS - 1422-0067 (Linking) VI - 20 IP - 2 DP - 2019 Jan 11 TI - CMV-Specific Immune Response-New Patients, New Insight: Central Role of Specific IgG during Infancy and Long-Lasting Immune Deficiency after Allogenic Stem Cell Transplantation. LID - 10.3390/ijms20020271 [doi] LID - 271 AB - Although the existing paradigm states that cytomegalovirus (CMV) reactivation is under the control of the cellular immune response, the role of humoral and innate counterparts are underestimated. The study analyzed the host(-)virus interaction i.e., CMV-immune response evolution during infection in three different clinical situations: (1) immunodeficient CMV-positive human leukocyte antigen (HLA)-matched bone marrow recipients after immunoablative conditioning as well as immunocompetent, (2) adult, and (3) infant with primary immune response. In the first situation, a fast and significant decrease of specific immunity was observed but reconstitution of marrow-derived B and natural killer (NK) cells was observed prior to thymic origin of T cells. The lowest CMV-IgG (93.2 RU/mL) was found just before CMV viremia. It is noteworthy that the sole and exclusive factor of CMV-specific immune response is a residual recipient antibody class IgG. The CMV-quantiferon increase was detected later, but in the first phase, phytohemagglutinin (PHA)-induced IFN-gamma release was significantly lower than that of CMV-induced ("indeterminate" results). It corresponds with the increase of NK cells at the top of lymphocyte reconstitution and undetected CMV-specific CD8 cells using a pentamer technique. In immunocompetent adult (CMV-negative donor), the cellular and humoral immune response increased in a parallel manner, but symptoms of CMV mononucleosis persisted until the increase of specific IgG. During infancy, the decrease of the maternal CMV-IgG level to 89.08 RU/mL followed by clinical sequel, i.e., CMV replication, were described. My observations shed light on a unique host-CMV interaction and CMV-IgG role: they indicate that its significant decrease predicts CMV replication. Before primary cellular immune response development, the high level of residual CMV-IgG (about >100 R/mL) from mother or recipient prevents virus reactivation. The innate immune response and NK-dependent IFN-secretion should be further investigated. FAU - Zdziarski, Przemyslaw AU - Zdziarski P AUID- ORCID: 0000-0002-5692-4734 AD - Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, 53-114 Wroclaw, Poland. zdziarski@oil.org.pl. AD - Department of Clinical Immunology and Hospital Infection Control Team, Lower Silesian Center for Cellular Transplantation, 53-439 Wroclaw, Poland. zdziarski@oil.org.pl. AD - Military Institute WITI Wroclaw; 136 Obornicka Str., 50-961 Wroclaw, Poland. zdziarski@oil.org.pl. LA - eng GR - 2014/2018/Leading National Research Centre (KNOW) Wroclaw Centre of Biotechnology/ PT - Journal Article DEP - 20190111 PL - Switzerland TA - Int J Mol Sci JT - International journal of molecular sciences JID - 101092791 RN - 0 (Antibodies, Viral) RN - 0 (Immunoglobulin G) SB - IM MH - Antibodies, Viral/metabolism MH - B-Lymphocytes/metabolism MH - Cytomegalovirus/*immunology MH - Cytomegalovirus Infections/*immunology MH - Female MH - Hematopoietic Stem Cell Transplantation/*adverse effects MH - Humans MH - Immunity, Cellular MH - Immunity, Humoral MH - *Immunocompetence MH - *Immunocompromised Host MH - Immunoglobulin G/*metabolism MH - Infant MH - Killer Cells, Natural/metabolism MH - Male MH - Middle Aged PMC - PMC6358762 OTO - NOTNLM OT - CMV-specific IgG OT - QuantiFERON OT - adoptive/acquired, innate immune response OT - cytomegalovirus (CMV) OT - epidemiology OT - epitope engineering OT - hematopoietic stem cell transplantation (HSCT) OT - host-virus interaction OT - natural killer (NK) cells OT - pentamer OT - protective IgG level OT - secondary immunodeficiency OT - beta2-microglobulin COIS- The author declares no conflict of interest. EDAT- 2019/01/16 06:00 MHDA- 2019/05/02 06:00 PMCR- 2019/01/01 CRDT- 2019/01/16 06:00 PHST- 2018/12/19 00:00 [received] PHST- 2019/01/02 00:00 [revised] PHST- 2019/01/03 00:00 [accepted] PHST- 2019/01/16 06:00 [entrez] PHST- 2019/01/16 06:00 [pubmed] PHST- 2019/05/02 06:00 [medline] PHST- 2019/01/01 00:00 [pmc-release] AID - ijms20020271 [pii] AID - ijms-20-00271 [pii] AID - 10.3390/ijms20020271 [doi] PST - epublish SO - Int J Mol Sci. 2019 Jan 11;20(2):271. doi: 10.3390/ijms20020271.