Immunoreactivation of Epstein-Barr virus due to cytomegalovirus primary infection

Abstract

Serological diagnosis of herpes virus infections is hampered by concurrent expression of IgM for heterologous members of this virus family. To assess the frequency of such multiple diagnostic findings and to understand their etiology, we sought by using IgG, IgM, and IgG avidity test serodiagnoses for Epstein-Barr virus (EBV) among immunocompetent or immune-suppressed patients with well-documented cytomegalovirus (CMV) primary infection. Controls had primary infection by EBV or had acute septic or severe respiratory infection. Among EBV-seropositive patients with CMV primary infection, a large proportion (13/56, 23%) showed antibody profiles of EBV reactivation: seroconversion of VCA IgM and/or > or = fourfold rise of VCA IgG, together with high or intermediate avidity of VCA IgG. Most of the CMV patients with EBV serodiagnosis showed also diagnostic HHV-6 antibody rises. In contrast to the frequently occurring CMV-induced EBV immunoreactivation, EBV primary infections did not appear to induce immunoreactivations of CMV (0/22). Only one (2%) CMV patient had a significant varicella zoster virus (VZV) antibody rise. The studies show that CMV is a particularly active inducer of some, but not all, members of the herpes virus family and suggest that the in vivo interplay between CMV and EBV occurs unidirectionally. The high frequency of heterologous herpes virus immunoreactivations poses demands on laboratory diagnosis.

Epstein-Barr virus and cytomegalovirus infections and their clinical relevance in Egyptian leukemic pediatric patients

“…Earlier, Drouct and colleagues had briefly reported signs of CMV and EBV co-infections in graft recipients and suggested that CMV might encourage EBV replication and dissemination [29]. Moreover, Aalto and team work have suggested that CMV may induce EBV immune reactivation following stimulation of EBV-specific memory B-cells due to iterated EBV replication [30]. EBV may require another virus like CMV to increase immunosuppressive status and mediate a suitable environment for EBV reactivation as previously reported [30, 31].…”

Clinical characteristics of patients with Epstein Barr virus in cerebrospinal fluid

“…When available, results of EBV serology including VCA-IgG, IgM and IgG avidity [10] were recorded to assess whether the patient had primary infection or reactivation.…”

The role of EBV in post-transplant malignancies: a review

“…70 This may simply reflect the combined loss of immune control for cytomegalovirus and EBV with high dose immunosuppression, but it is also possible that reactivation of cytomegalovirus has profound eVects on the immune system by inducing cytokine production which directly transactivate EBV genes. 71 In tumour biopsy material, EBV positive cells often make up only a modest proportion of the tumour mass, with an extensive EBV negative lymphoid infiltrate comprising predominantly CD4+ T lymphocytes. 72 In vivo experiments in severe combined immunodeficient (SCID) mice, where PTLD-like tumours can be generated following injection of human peripheral blood mononuclear cells, show that T cells are necessary for establishment of these tumours.…”