We investigated viral infections in the tonsils, pharynx and renal tis
sues of patients with IgA nephropathy using cell culture, polymerase c
hain reaction (PCR) and immuno-fluorescent techniques, and measured an
tibody titers against numerous types of viruses. Neutralization tests
found no significant inhibition of growth of adenovirus-1, 2, 3, 4, 5,
6, 7, 11 or 19, Coxsackie virus-A7, A9, A16, B1, B2, B3, B4, B5 or B6
, or RS virus. Swabs of the oral cavity of patients with IgA nephropat
hy were cultured with Hel cells, MDCK cells, FL cells, BHK-21 cells an
d RD-18S cells. No cytopathic effect was detected in any of these cell
cultures. We failed to detect the presence of herpes simplex virus-1
and -2, varicella-zoster virus, cyto-megalovirus and Epstein-Barr viru
s (EBV)-1 and -2 in tonsils, renal tissues and mouthwashings from pati
ents with IgA nephropathy. On the other hand, EBV alone was detected w
ith the PCR technique, in mouthwashings from 6 out of 14 patients with
IgA nephropathy (42%). Immunohistological and serological analyses we
re done to examine the relationship between EBV and IgA nephropathy. N
o evidence was obtained that EBV-infected B lymphocytes were producing
IgA. It seems unlikely that the viral infections examined in this stu
dy play a significant role in the pathogenesis of IgA nephropathy.