Immune Response to Papillomavirus Infection

Spradbrow, P. B.

doi:10.1007/978-3-642-71097-1_12

Cited by 18 publications

(16 citation statements)

References 103 publications

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“…Other studies indicate, however, that there are no differences in the lymph node status, tumor recurrence, or survival between patients with HPV-positive and HPV-negative cervical cancer (16,18). It is possible that the immunological status of patients vis-a-vis their tumors contributes to the discrepancies between these findings since there is strong evidence that immune responses are involved in the control of HPVassociated cervical cancers (21,22,(28)(29)(30)31 (32).…”

Section: Resultscontrasting

confidence: 46%

Metastatic conversion of cells by expression of human papillomavirus type 16 E6 and E7 genes.

Chen

Ashe

Singhal

et al. 1993

Proc. Natl. Acad. Sci. U.S.A.

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The There is convincing epidemiological and experimental evidence linking specific types of human papillomavirus (HPV) with the etiology of cervical cancer (1, 2). HPV-16 and -18 are present in >70% of cervical dysplasias and carcinomas, whereas HPV-6 and -11 are usually found in benign genital condyloma acuminata (3, 4). The E6-E7 genes of HPV-16, which are expressed at high levels in cervical carcinomas, encode proteins that are capable of transcriptional regulation and cellular transformation through interactions with cellular proteins, such as the tumor suppressor gene products pRB and p53 (5). These functions suggest an important role of HPV-16 in the initiation of cervical cancers.The HPV-16 DNA is frequently found in metastases of cervical cancers in either local lymph nodes (6)(7)(8)(9)(10)(11)(12)(13)(14) or distant site (15). The same HPV DNA sequences are consistently detected in metastases and primary tumors from the same patients, suggesting the same origin of viral DNA, and in situ hybridization has demonstrated the HPV DNA within the nuclei of metastatic cells (9, 10). HPV-16 DNA can also be detected in histologically negative lymph nodes (8, 11), suggesting that it may provide a sensitive indicator for early metastases. It is not known, however, whether the expression of HPV genes influences the ability of a tumor to metastasize, and it is controversial whether human cervical cancers with HPV-16 DNA are more invasive than those associated with nononcogenic HPV types or HPV-negative cancers (16)(17)(18).To investigate the relationship between the expression of HPV-16 genes and tumor metastasis, we have assessed the ability of murine cell lines expressing the E6 and E7 genes from oncogenic HPV-16 or nononcogenic HPV-6b to formThe publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact. metastasis in a nude mouse model. We report here that the expression in mouse cell lines of the E6 and E7 genes from HPV-16, but not from HPV-6b, results in metastatic conversion. MATERIALS AND METHODSMice. Female BALB/c (nu/nu) mice, 4-8 weeks old, and C3H/HeN mice, 6-8 weeks old, were bought from HarlanSprague-Dawley.Cell Lines. NCTC2555 is a fibrosarcoma line of C3H/HeN mouse origin (19), and the NIH 3T3 fibroblast line is BALB/c mouse origin. The CaSki line was derived from a HPV-16-positive squamous cell carcinoma of human cervix. PA317 and t-2 are packaging cell lines for amphotropic or ecotropic retroviruses, respectively. YAC-1 is a natural killer (NK) cell-sensitive lymphoma line and EL-4 is a NK-resistant lymphoma line. All cells were purchased from American Type Culture Collection and were maintained at 37°C with Dulbecco's modified Eagle's medium (DMEM) containing 10% fetal calf serum (HyClone) in a humidified atmosphere of 5% C02/95% air.Gene Transfer by Recombinant Retroviruses. Retroviruses were prepared as described (20,21) at biosafety level 2....

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Section: Resultscontrasting

confidence: 46%

Metastatic conversion of cells by expression of human papillomavirus type 16 E6 and E7 genes.

Chen

Ashe

Singhal

et al. 1993

Proc. Natl. Acad. Sci. U.S.A.

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“…One possible explanation is the activation of a suppressor mechanism by these cell lines. Immunosuppression is known to be associated with papillomas and with the development of malignant papilloma virus lesions [20].…”

Section: Discussionmentioning

confidence: 99%

Generation of cell-mediated cytotoxicity against bovine-papilloma-virus-transformed primary mouse cell lines

Laatikainen

Karjalainen

Sarkkinen

et al. 1990

Cancer Immunol Immunother

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The immunogenicity and immunosensitivity of primary mouse cell lines transformed by bovine papilloma virus 1 (BPV1) DNA were studied in a syngeneic mouse model by determining cell-mediated cytotoxicity in the spleens of mice immunized with the transformed cells. One of the cell lines induced the generation of cell-line-specific Thy1.2-positive cytotoxic effector cells. However, most of the cell lines tested induced the generation of Thy1.2-positive effector cells, which in addition to BPV1-transformed cells were able to lyse a syngeneic cell line transformed by methylcholanthrene. The lysis of BPV1- and methylcholanthrene-transformed cell lines was mediated by recognition of the same antigenic determinants expressed on these cells, and all the BPV1-transformed cell lines were sensitive to lysis by these nonspecific effector cells of the lymphokine-activated killer (LAK) type.

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“…Antibodies to HPVs have been detected in human sera by a number of investigators using single or pooled antigen sources and a variety of methods, such as immunodiffusion, immune electron microscopy, complement fixation, ELISA, haemagglutination inhibition or radioimmunoprecipitation (for reviews, see Kirchner, 1986;Spradbrow, 1987). To date, two published reports have employed PV capsid proteins synthesized in E. coli for antibody detection in human sera using Western blots.…”

Section: Discussionmentioning

confidence: 99%

Expression in Escherichia coli of Seven DNA Fragments Comprising the Complete L1 and L2 Open Reading Frames of Human Papillomavirus Type 6b and Localization of the 'Common Antigen' Region

Strike

Bonnez

Rose

et al. 1989

Journal of General Virology

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SUMMARYMolecular cloning was used to express human papillomavirus type 6b (HPV-6b) antigens in Escherichia coli. Seven genomic DNA fragments of HPV-6b which together comprise the complete L1 and L2 open reading frames, known to code for capsid proteins, were cloned and expressed in E. coli as both fl-galactosidase and TrpE fusion proteins. Western blots of HPV-6b fl-galactosidase fusion proteins using 'genusspecific' antisera produced by immunization of rabbits with disrupted bovine papillomavirus type 1 (BPV-1) showed that polypeptides encoded by two DNA fragments from the mid portion of L1 of HPV-6b were cross-reactive. Only one of these two polypeptides reacted with antisera raised against disrupted HPV-1, directly demonstrating that this polypeptide contains the papillomavirus 'common antigen'. The cross-reactive region was confirmed by reversing antigen and antibody. Polyclonal antisera were raised against the seven HPV-6b/3-galactosidase fusion proteins and tested against BPV-1 virion proteins on Western blots. Only antiserum against the mid portion of L1 of HPV-6b reacted with the BPV-1 major capsid protein. HPV-6b fusion proteins were also used to test human sera for antibodies reactive in Western blots.

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Immune Response to Papillomavirus Infection

Cited by 18 publications

References 103 publications

Metastatic conversion of cells by expression of human papillomavirus type 16 E6 and E7 genes.

Metastatic conversion of cells by expression of human papillomavirus type 16 E6 and E7 genes.

Generation of cell-mediated cytotoxicity against bovine-papilloma-virus-transformed primary mouse cell lines

Expression in Escherichia coli of Seven DNA Fragments Comprising the Complete L1 and L2 Open Reading Frames of Human Papillomavirus Type 6b and Localization of the 'Common Antigen' Region

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