SYSTEMIC MONOCYTE AND T-CELL ACTIVATION IN A PATIENT WITH HUMAN PARVOVIRUS B19 INFECTION

Citation
Ad. Wagner et al., SYSTEMIC MONOCYTE AND T-CELL ACTIVATION IN A PATIENT WITH HUMAN PARVOVIRUS B19 INFECTION, Mayo Clinic proceedings, 70(3), 1995, pp. 261-265
Citations number
17
Categorie Soggetti
Medicine, General & Internal
Journal title
ISSN journal
00256196
Volume
70
Issue
3
Year of publication
1995
Pages
261 - 265
Database
ISI
SICI code
0025-6196(1995)70:3<261:SMATAI>2.0.ZU;2-E
Abstract
Infection with human parvovirus B19 induces a biphasic disease. The in itial phase has been associated with viremia. During the second phase of the disease, a spectrum of clinical syndromes can manifest, includi ng erythema infectiosum, perinatal complications, and symmetric arthro pathy that resembles rheumatoid arthritis. Although investigators have suspected that some of the second-phase symptoms are related to immun e complex formation, the pathogenesis of parvovirus B19-induced clinic al manifestations is not understood. Herein me describe a 63-year-old woman with malaise, fever, and symmetric polyarthritis who had IgM ant ibodies specific for parvovirus B19. Messenger RNA (mRNA) specific for interleukin (IL) 1 beta, IL 6, and interferon-gamma (IFN-gamma) was d etected by polymerase chain reaction. Transcript concentrations were s emiquantified by serial dilution of cells and determination of the min imal number of cells that provided a positive signal. Concentrations o f IL 1 beta and IL 6 mRNA in peripheral blood mononuclear cells collec ted during acute disease were increased by the factor of 32 and 8, res pectively. IFN-gamma was detected at a 16-fold increased concentration . Two months later, after the patient had experienced complete recover y, production of monokines and IFN-gamma was almost normalized. These data raise the possibility that acute parvovirus B19 infection is char acterized by a widespread and systemic activation of monocytes, T cell s, and natural killer cells. The correlation of increased cytokine mRN A levels and clinical symptoms suggests a potential role of proinflamm atory monokines and lymphokines in disease manifestations.