Spontaneous in vitro secretion of antibody to cytomegalovirus (CMV) by human peripheral blood mononuclear cells: a new approach to studying the CMV-immune system interaction
Article Abstract:
Certain substances called antigens can trigger immune responses, including the production of specific antibodies, which are immune proteins directed against the antigen. After a person is exposed to antigens through a vaccine or during an infection, immune cells known as peripheral blood mononuclear cells (PBMC) release specific antibodies. When the PBMCs of an immunized person are removed from the body and grown in culture, or under laboratory conditions, the specific antibodies released by the PBMCs can be detected in the culture solution. This release is considered to be spontaneous because it is not in response to the addition of antigens to the culture medium. The release of specific antibodies from PBMCs is described as active. In addition, specific antibody release from PBMC that is detected 5 to 30 days following a booster shot is considered as transient. Cultured PBMCs from persons infected with the human immunodeficiency virus (HIV), which causes AIDS, were shown to release specific antibody directed against HIV. However, HIV antibody release was not transient but persistent, and could be detected throughout the duration of the disease. Persistent antibody secretion may result from continuous activation of the immune system by antigens of HIV. The secretion of antibodies directed against cytomegalovirus (CMV) has been detected in persons infected with CMV, and shown to be spontaneous and active. The secretion of CMV-specific antibodies from PBMCs of CMV-infected patients with or without HIV infection was assessed after culturing their PBMCs. HIV-infected persons commonly have a reduced number of immune T cells. CMV antibody release from cultured PBMCs was unaffected by the reduced number of immune T cells in HIV-infected persons. In fact, CMV antibodies accounted for 30 to 65 percent of all antibody production. The findings suggest that the persistent CMV antibody release may be related to the continuous stimulation of the immune system within the living host. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: Journal of Infectious Diseases
Subject: Health
ISSN: 0022-1899
Year: 1991
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Hypogammaglobulinemia associated with cytomegalovirus pneumonia
Article Abstract:
It is well known that cytomegalovirus (CMV) infection usually causes a slight decrease in CD4 (helper) T cells, that is, a class of white blood cells containing a surface molecule known as CD4. The effects of CMV infection on B cells, which are responsible for the production of antibodies, are unclear, however. A case is presented in which a 66-year-old woman, testing negative for HIV infection and suffering from CMV pneumonia, showed a decrease in immunoglobulins (antibodies) as well in CD4 cells. Analysis of her blood revealed that the level of CD4 cells was 14 percent - significantly reduced from the normal range of 24 percent to 32 percent. Since CD4 cells are known to induce B cells to produce immunoglobulins, this could explain why the levels of immunoglobulins were as low as they were. They continued to decrease throughout the illness. In this case the infection spontaneously remitted, with a consequent return to normal levels of immunoglobulins and T cells. The mechanism by which this case occurred, and remitted is unknown, but the case provides evidence of the effect that CMV can have on B cells. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: Journal of Infectious Diseases
Subject: Health
ISSN: 0022-1899
Year: 1991
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HIV-1 reactivation in resting peripheral blood mononuclear cells of infected adults upon in vitro CD4 cross-linking by ligands of the CDR2-loop in extracellular domain 1
Article Abstract:
HIV can be reactivated inside cells by binding to the CD4 receptor on T cells. When HIV infects T cells, it normally remains in an inactive state until it is activated. Once activated, it begins to reproduce and produce new virus particles. Researchers show that the inactive virus in the cell can stimulate the CD4 receptor, which in turn, activates the virus. The CDR2-loop in domain 1 (D1) of CD4 appears to play a major role in this activation.
Publication Name: Journal of Acquired Immune Deficiency Syndromes and Human Retrovirology
Subject: Health
ISSN: 1077-9450
Year: 1999
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