Abstract
Indirect immunofluorescence (IF) techniques were used to measure IgG and IgA antibodies to membrane antigens (anti‐MA) and IgA antibodies to virus capsid antigens (anti‐VCA) of herpes simplex type 2 (HSV‐2)‐infected cells in sera from patients with cervical dysplasia and neoplasia, controls who had been matched for ethnic origin, age and social class, patients with other malignancies and patients with genital herpes. IgA anti‐MA were detected significantly more frequently and at higher titres in patients with cervical dysplasia and neoplasia than among matched controls. A high proportion of patients whose cervical cancer had previously been treated by radiotherapy, patients with other squamous carcinomas and patients with genital herpes also had IgA anti‐MA and at higher titres than matched controls and patients with non‐squamous cancers. In contrast, IgG anti‐MA and IgA anti‐VCA did not distinguish patients from controls. The IgA anti‐MA response was more type‐specific than the IgG anti‐MA response. IgA anti‐MA appeared to persist in sera from patients with genital herpes for at least 17 months after clinical attack, while IgA anti‐VCA were usually detected for only 2‐3 months. The persistence of IgA anti‐MA may suggest a persisting antigenic stimulus among patients with genital herpes as well as patients with cervical dysplasia and neoplasia. HSV‐2‐specific antibodies measured by ELISA were also detected in a significantly higher proportion of patients with cervical neoplasia than in matched controls, although 32–48% of patients did not possess these antibodies. Furthermore, there was no consistent difference in the prevalence of HSV‐2‐specific antibodies when cohorts of patients with cervical neoplasia and controls born at the same time were compared. The possibility is discussed that IgA anti‐MA, which were detected in a high proportion of patients with other squamous carcinomas as well as in patients with squamous carcinoma of the cervix, are reacting with cross‐reacting antigens found both in human squamous carcinoma cells and in HSV‐infected cells.