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
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.