Evidence from several sources has suggested that adeno-associated virus (AA
V) infection might protect against cervical cancer, in part, by interfering
with human papillomavirus (HPV)induced tumorigenesis. Detection of AAV typ
e 2 (AAV-2) DNA in cervical tissues has been reported. However, there have
been few in vivo studies of women with cervical HPV infection or neoplasia,
and these have reported inconsistent results. Therefore, we used polymeras
e chain reaction (PCR) assays targeted to the AAV-2 rep and cap genes to te
st tissue specimens from women in an epidemiological study of cervical neop
lasia in Jamaica. We tested 105 women with low-grade cervical intraepitheli
al neoplasia (CIN-1), 92 women with CIN-3/carcinoma in situ or invasive can
cer (CIN-3/CA), and 94 normal subjects. PCR amplification of human beta-glo
bin DNA was found in almost all cervical specimens, indicating that these m
aterials were adequate for PCR testing. The prevalence of HPV DNA, determin
ed by HPV L1 consensus primer PCR was, as expected, strongly associated wit
h presence and grade of neoplasia. Each of the AAV PCR assays detected as f
ew as 10 copies of the virus genome. However, none of the 291 cervical spec
imens from Jamaican subjects tested positive for AAV DNA. Negative AAV PCR
results were also obtained in tests of cervical samples from 79 university
students in the United States. Exposure to AAV was assessed further by sero
logy. Using a whole virus AAV-2 sandwich enzyme-linked immunosorbent assay,
we found no relationship between AAV antibodies and presence or grade of n
eoplasia in either the Jamaican study subjects or women enrolled in a U.S.
cervical cancer case (n = 74) -control (n = 77) study. Overall, the data pr
ovide no evidence that AAV infection plays a role in cervical tumorigenesis
or that AAV commonly infects cervical epithelial cells. (C) 1999 Wiley-Lis
s, Inc.