Abstract
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-γ 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.
Highlights
IntroductionCytomegalovirus (CMV) is the most common cause of host–virus interaction (named here host-CMV balance), it appears to be an important problem in the clinical practice of infectious disease immunology
Cytomegalovirus (CMV) is the most common cause of host–virus interaction, it appears to be an important problem in the clinical practice of infectious disease immunology
This might be due to the presence of several confounding factors (e.g., CMV-antigen types, immunoparameters, immunosuppressive therapy, and immunogenetic background with inter-individual variation presented in Supplementary Material Table S1). It may bias the final results in multicenter U.S National Marrow Donor Program (NMDP) and European Group for Blood and Marrow Transplantation (EBMT) studies [5,6]
Summary
Cytomegalovirus (CMV) is the most common cause of host–virus interaction (named here host-CMV balance), it appears to be an important problem in the clinical practice of infectious disease immunology It may be strictly local, e.g., CMV retinitis, hearing loss [1], mental retardation, cognitive defects, and neurodevelopmental abnormalities [2]. Unique conditions of the affected patients and diversity of clinical manifestations of cytomegalovirus infection do not allow formation of real comparable cohort of patients without distinguishing different clinical host–virus constellation for example presented in table in discussion section (see below) This might be due to the presence of several confounding factors (e.g., CMV-antigen types, immunoparameters, immunosuppressive therapy, and immunogenetic background with inter-individual variation presented in Supplementary Material Table S1). Differential diagnosis and classification of CD8 T cell infiltration were quite difficult in histological examination depending on whether it was Graft-versus-host (GvH)- or virus-related cellular cytotoxicity
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