Mechanisms of Immunosuppression in Cytomegalovirus Mononucleosis. II. Virus-Monocyte Interactions

Abstract

Virus-monocyte interactions were evaluated in patients with mononucleosis due to cytomegalovirus (CMV). Group 1 patients studied about two weeks after the onset of symptoms had lymphocyte responses to concanavalin A (con A) that were maximally suppressed and unaffected by in vitro culture or reconstitution with monocytes. Lymphocytes from group 2 patients studied about three weeks after the onset of symptoms had less markedly suppressed responses, which were reversed by in vitro culture or by reconstitution with monocytes. Monocyte depletion resulted in a marked diminution of fresh lymphocyte responses of group 2 patients but not of group 1 patients. CMV was isolated from blood monocytes of four patients with mononucleosis; intact, infected monocytes were capable of suppressing responses of cultured autologous lymphocytes to con A. Monocytes from uninfected control donors were infected in vitro with CMV and evaluated for the induction of suppressor activity. CMV-infected monocytes were significantly more suppressive for autologous lymphocyte responses to con A than were uninfected monocytes.

Cavity Forming Pneumonia Due to Staphylococcus aureus Following Dengue Fever

“…Some viruses such as measles, cytomegalovirus, and influenza are known to induce transient in vitro and in vivo immunosuppression. 7,8 DENV is also thought to induce immunosuppression leading to concurrent bacterial infections. The mechanism has been investigated, supported by reports from literature, and proposed as follows: 1) DENV infects and replicates in human dendritic cells and has been shown to block interferon (IFN)-α/β signaling in infected dendritic cells.…”

T Cell Responses to an HLA-B*07-Restricted Epitope on the Dengue NS3 Protein Correlate with Disease Severity

“…This is consistent with our report that cryopreserved PBMC obtained during or early after acute DV infection were unresponsive to in vitro stimulation and that IL-2 restored their responsiveness to Ag or mitogen stimulation (50). Other groups have found that PBMC collected during acute infections with measles virus or CMV showed reduced in vitro proliferation responses (51,52). Lechner et al (34) found that IFN-␥ ELISPOT assays significantly underestimated the frequency of hepatitis C virus-specific T cells in PBMC collected during the acute infection; however, they did not study the effect of incubation of PBMC with IL-2.…”

The status of CMV as a human pathogen

“…Accessory macrophages were reported to be responsible for this defect (Carney & Hirsch, 1981) and recently Rodgers et al (1985) described an inhibitor of interleukin 1 released by monocytes after exposure to CMV. However, the latter effect could not be reproduced using stocks of CMV free from contamination with mycoplasma (Scott & Sissons, 1987) and so it must be concluded that the inhibitory action on interleukin 1 was caused by mycoplasma.…”