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Journal of General Virology (1994),75, 2277-2284. Printed in Great Britain 2277
Cell-mediated immune responses to E7 peptides of human papillomavirus
(HPV) type 16 are dependent on the HPV type infecting the cervix
whereas serological reactivity is not type-specific
Anna S. Kadish, 1. Seymour L. Romney, 2 Richard Ledwidge, ~ Robert Tindle, 4 Germain J. P.
Fernando, 4 Sui Y. Zee, ~ Marc A. Van Ranst 3 and Robert D. Burk 3
Departments of 1 Pathology, 2 Obstetrics and Gynecology, and 3 Microbiology and Immunology, Albert Einstein College
of Medicine, 1300 Morris Park Avenue, Bronx, New York 10461, U.S.A, and 4Lions Human Immunology
Laboratories, Queensland University, Brisbane, Australia
Forty-two women attending a colposcopy clinic for
evaluation of abnormal cervical cytology and 13 normal
controls were studied for the presence of lymphocyte
proliferation (LP) cell-mediated immune (CMI) res-
ponses and serological reactivity to E7 peptides of
human papillomavirus type 16 (HPV-16). HPV was
typed by Southern blot hybridization of exfoliated
cervicovaginal cell DNA. Positive LP responses (stimu-
lation index /> 5-0) to one or more E7 peptides were
observed in 28.6% (12 of 42) of patients and 23.1%
(three of 13) of controls. Of patients infected with HPV-
16, -31 or -33, 63"6 % (seven of 11) showed a positive LP
response compared with 14.3 % (two of 14) of women
infected with other HPV types (P = 0.02), 17'6 % (three
of 17) negative for HPV (P = 0.02) and 23"1% (three of
13) of controls (HPV status unknown) (P = 0"05). C-
terminal peptide 109 (amino acids 72 to 97) elicited
positive LP responses in 45.4 % (five of 11) of patients
infected with HPV -16, -31 or -33 compared with 7"1%
(one of 14) patients infected with other HPVs (P = 0.04),
5"9 % (one of 17) of women negative for HPV (P = 0"02)
and 7"7% (one of 13) of controls (P = 0.05). HPV-16
group-specific LP responses of borderline significance
were also observed against E7 peptides 103,105 and 108
(17-37, 37-54 and 62-80) (P = 0.07). ELISA reactivity
(IgG) to E7 peptide 109 (72-97) was present in 7"7 %
(one of 13) of controls, 35.3 % (six of 17) of HPV-
negative patients, 42.9 % (six of 14) of patients infected
with other HPVs, and only 9.1% (one of 11) of patients
infected with HPV-16, -31 or -33. CMI responses to
C-terminal HPV-16 E7 peptide 109 (72-97) were thus
significantly related to ongoing cervical infection with
HPV-16 and closely related types, whereas serological
reactivity to E7 peptides was not HPV type-specific.
Introduction
Human papillomavirus (HPV) infection has been shown
to be the major risk factor for the development of both
premalignant disease and cancer of the uterine cervix
(Morrison et al., 1991; Koutsky et al., 1992; Reeves et
al., 1989). Of the HPV types known to infect the genital
tract, of which there are more than 20, several types
including HPV-16, -33 and -18 have been associated with
the development of high-grade precancerous disease and
cancer (Kadish et al., 1992; Lorincz et al., 1992). Of
women with squamous intraepithelial lesions (SILs), a
large proportion undergo regression, whereas others
have persistent disease and a small number progress to
invasive carcinoma (Schneider & Koutsky, 1992). Epi-
demiological studies demonstrating increased prevalence
and severity of HPV-induced lesions in immunosup-
pressed patients (Vermund et al., 1991; Kiviat et al.,
1990; Ho et al., 1994), in addition to histological studies
of regressing genital HPV-induced lesions (Rogozinski et
al., 1988) suggest that immune responses to HPV are
critical in mediating the regression of disease.
Studies of immune responses to HPV have been
hampered by the difficulty in obtaining sufficient quan-
tities of native HPV antigens. Bacterially expressed
fusion proteins and synthetic peptides corresponding to
the products of HPV open reading frames (ORFs) have
been used to demonstrate cell-mediated immune (CMI)
and humoral immune responses to HPV-encoded anti-
gens in both human and murine systems (Dillner, 1990;
Mtiller et al., 1990; Jenison et al., 1991; Jochmus-
Kudielka et al., 1989; Tindle et al., 1990, 1991). The
HPV-16-transforming proteins E6 and E7, which are
abundantly expressed in precancerous and malignant
cervical lesions (Stoler et al., 1992), have been shown to
be tumour rejection antigens in murine systems (Chen et
al., 1991, 1992). Human serological responses to HPV-16
E6 and E7 proteins have been reported to occur most
0001-2335 © 1994SGM