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At least 19 recordsLinked to original sources
PubMed1952

Experiments on the cause of the rabbit carcinomas derived from virus-induced papillomas. II. Loss by the Vx2 carcinoma of the power to immunize hosts against the papilloma virus.

Tests were made to learn whether an anaplastic, epidermal carcinoma, the Vx2, which had originated more than 8 years previously from a virus papilloma in a domestic rabbit, still rendered its hosts immune to the virus. It had done so in the first 22 successive groups of animals to which it was transferred during a period of 3(1/2) years, its growth regularly eliciting a blood antibody that neutralized the Shope virus and fixed complement in mixture with it; and on the assumption that this would continue to be the case no further observations were made for nearly 4(1/2) years more. Then direct inoculation of animals carrying the tumor in its 46th Generation showed them to be as susceptible to the virus as normal rabbits; and sera procured from hosts of the 46th, 47th, 48th, and 50th Generations failed to neutralize the virus or fix complement with it. Tests of this last sort, repeated at intervals since,-most recently with sera from animals carrying the tumor in its 73rd Generation,-have yielded consistently negative findings. Loss of the power to immunize against the papilloma virus was not attended by any perceptible change in the Vx2 carcinoma. Manifestly the antigen responsible for the immunity cannot, as such, have been the actuating cause of the tumor. Attempts were made to infect the cells providing 48th Generation cancers, by mixing them with a suspension of the papilloma virus at time of implantation, or by injecting this agent into the blood stream of rabbits in which the tumog had already begun to proliferate. Its morphology and rate of growth remained unaltered; but tests of the animals to which transfers were next made yielded what appeared to be evidence of some slight immunity to the virus.

Animals↗
PubMed1957

Fluorescent antibody detection of the antigens of the Shope papilloma virus in papillomas of the wild and domestic rabbit.

The results obtained by a fluorescent antibody study of the Shope papilloma virus in papillomas of the wild and domestic rabbit are presented. In the wild rabbit papillomas the viral antigens occurred exclusively in the nucleus and were present in the differentiating cells of the keratohyaline layers and in the keratinized layers. The antigens were not present in the deeper proliferating epithelial cells of the papillomas. The Shope viral antigens were present in very minute amounts in papillomas of the domestic rabbit, as compared with papillomas of the wild rabbit, and were only detected in the superficial keratinized layers. It is postulated that virus is present in the nuclei of the proliferating cells of the papillomas of the wild and domestic rabbit but exists there in an early stage of development, consisting mainly of nucleic acid and deficient in protein, therefore non-antigenic and not demonstrable by fluorescent antibody. The nucleic acid moiety of the virus may be infective, and the protein component may provide immunologic specificity and serve to preserve transmissibility. The protein-deficient virus can be referred to as masked virus.

Animals↗
PubMed1994

Association of Epstein-Barr virus, human papilloma virus, and cytomegalovirus with nine nasopharyngeal carcinoma cell lines.

BACKGROUND: Epstein-Barr virus (EBV) has been proposed to be closely associated with nasopharyngeal carcinoma (NPC). To evaluate the actual relationship, EBV was analyzed in nine established NPC cell lines and in four original NPC biopsy specimens. EXPERIMENTAL DESIGN: We used Southern blot analysis alone or after polymerase chain reaction to determine whether EBV was present in our NPC cell lines. We also used in situ nucleic acid hybridization and in situ polymerase chain reaction to identify EBV in 4 original biopsy specimens. For comparison, we investigated the cell lines for the presence of human papilloma virus type 16 (HPV-16) and human cytomegalovirus (HCMV). RESULTS: Southern blots alone for detection of 3 viruses in 9 cell lines were all negative. PCR plus Southern blotting revealed that 5 cell lines contained EBV in earlier passages, and all became negative in later passages. Some cell lines also contained HPV-16 and HCMV. At earlier passages, some cell lines contained EBV, HPV-16, and HCMV concurrently. Three out of four biopsy specimens contained EBV in certain tumor cells, lymphocytes, and glandular epithelia. CONCLUSIONS: These findings indicate that EBV, HPV-16, and HCMV may be present in certain NPC cell lines and in only a small fraction of each positive cell line, and that a cell line may contain these three viruses concurrently. EBV is present not only in a fraction of tumor cells, but also in some lymphocytes and glandular epithelia in biopsy specimens. It is present as an episomal form but not as an integrated form in the infected cells, suggesting that the carcinogenesis of non-EBV containing NPC tumor cells is not related to EBV infection.

Base Sequence↗
PubMed1959

Studies on the Shope rabbit papilloma virus. II. The location of infective virus in papillomas of the cottontail rabbit.

A method has been devised to determine the location of infective Shope virus in the papillomas of cottontail rabbits. Frozen sections of the growths were burned selectively with a microcautery to destroy either the keratinized or proliferating layer and the sections were then applied directly to the sensitized epidermis of domestic rabbits. No papillomas appeared when the keratohyaline and keratinized areas had been eliminated leaving the proliferating cell layer, whereas papillomas arose when the proliferating cell areas were destroyed leaving the keratohyaline and keratinized layers. The results indicate that infective Shope papilloma virus is situated mainly, perhaps entirely, in the keratohyaline and keratinized areas of cottontail papillomas. This is in accord with the previous disclosure by the fluorescence technique that virus antigen in demonstrable quantity is present only in these situations.

Animals↗
PubMed1992

Metal thiolate coordination in the E7 proteins of human papilloma virus 16 and cottontail rabbit papilloma virus as expressed in Escherichia coli.

The oncogenic E7 proteins of human papilloma virus (HPV 16) and of cottontail rabbit papilloma virus (CRPV) have been purified from an expression system in Escherichia coli. The proteins as purified from E. coli contain one tightly bound Zn(II) ion per molecule. The metal site shows facile exchange with either Cd(II) or Cu(I). The HPV 16 E7 maximally bound one Cd(II) or two Cu(I) ions, while the CRPV E7 bound two Cd(II) or three Cu(I) ions. The Cd(II) and Cu(I) E7 molecules exhibited optical transitions in the ultraviolet suggestive of metal:thiolate coordination. E7 proteins from HPV 16 and CRPV contain 7 and 8 cysteines/molecule, respectively. Reaction of the E7 proteins with the sulfhydryl reagent, dithiodipyridine, revealed that all the cysteinyl sulfurs are present in the reduced thiol state. Cu(I)-E7 molecules are luminescent with maximal emission at 570 nm. The observed emission at room temperature is indicative of metal coordination within a compact protein environment shielded from solvent interactions. The emission maxima occurs at the same wavelength (570 nm) as Cu(I)-cysteinyl sulfur clusters in Cu(I)-metallothioneins. The single Zn(II) atom in each protein can be removed from E7 in the presence of EDTA. The resulting apoE7 molecules remain soluble and can be partially reconstituted with Cd(II) to regain the ultraviolet charge transfer transitions.

Animals↗
PubMed1989

The human DNA tumor viruses: human papilloma virus and Epstein-Barr virus.

HPV and EBV are common infectious agents that persist after primary infection in a latent state with occasional shedding of virus. Therefore, one of the fundamental questions in the etiology of those cancers that are linked to infection with such ubiquitous viruses is why cancer develops in a few people when many are infected. Because only a small subset of infected people will develop specific cancers, it has been suggested that the presence of the viral genomes in the malignancies merely indicates a persistent or latent infection. However, if the viral infection was not an etiologic factor in the development of the specific cancers, then one would predict that the proportion of cancers that contained the viral genome would reflect the proportion of infected people and that the same cancers could develop in uninfected people. The sporadic detection from nonendemic areas of Burkitt's lymphoma without EBV initially suggested that EBV infection was not etiologic. However, the rate of incidence of BL in infected populations of children is disproportionately greater than the very low incidence in uninfected children, which suggests that EBV infection is an important contributing factor. Moreover, the development of EBV-induced lymphomas in the immunocompromised and the consistent detection of EBV in specific epithelial malignancies such as NPC suggest that EBV infection is essential in the induction of specific cancers. Similarly, the consistent detection of particular HPV types in certain types of cancer suggests that HPV is also an etiologic factor. There are several strikingly similar aspects of infection with HPV and EBV. In latent infection, both of the viral genomes persist as an extrachromosomal episome with an origin of replication that is activated by binding to a virally encoded polypeptide. The state of viral infection appears to be linked with the state of cellular differentiation such that latent infections are activated into a replicative state as the cells differentiate. Moreover, elevated levels of expression of the putative transforming genes are linked to transformation. However, perhaps most importantly, the malignancies are clonal with regard to the viral infection; HPV-associated malignancies have unique integrative events and EBV-associated malignancies have clonal episomal forms. This reveals that the specific cancers are clonal cellular proliferations that developed after viral infection. In vitro, the initially polyclonal cell lines produced by EBV infection rapidly evolve to oligoclonality or monoclonality. This could be due to a slightly faster rate of growth such that the progeny of one clone rapidly predominate.(ABSTRACT TRUNCATED AT 400 WORDS)

Burkitt Lymphoma↗
PubMedDate not supplied

The inter-relationship of herpes virus, papilloma 16/18 virus infection and Pap smear pathology in Israeli women.

A previous survey of the seroprevalence of the herpes virus type 2 (HSV-2) infection in Israel provided us with an opportunity to study a) the prevalence of human papillomavirus (HPV) 16/18 in selected groups of women; b) the correlation between the infection with HSV-2, HPV-16/18 and Papanicolaou (PAP) pathology; and c) to identify groups of women who might benefit from routine PAP screening. Four different population groups of women aged 17-60 years were studied: groups 1 and 2 comprised healthy women government employees and kibbutz and moshav residents, respectively, and groups 3 and 4 comprised Jewish and non-Jewish women with gynecological complaints. In women without gynecological problems the prevalence of HPV-16/18 was 1.8% in group 1 and 0% in group 2. The prevalence was several-fold higher in the Jewish and non-Jewish gynecological clinic groups, 9% and 12%, respectively. There was no correlation between the prevalence of HSV-2 antibodies and HPV-16/18 infection in women without gynecological problems. One of the 692 women studied had markers of both infections. The very few cases of cervical intraepithelial neoplasia (CIN) II and CIN III occurred in women who were negative for HSV-2 and HPV-16/18 infection. Thus from our limited study, it is not possible to define any group of healthy women who might benefit from continuous PAP smear screening for cervical cancer.

Adolescent↗
PubMed1988

Frequency of cervico-vaginal infections (Trichomonas vaginalis; Chlamydia trachomatis -CHL-; herpes simplex virus -HSV-; human papilloma virus -HPV-) in cervical intraepithelial neoplasia.

The Authors have carried out a cyto-hystologic study on 533 cervical intraepithelial neoplasias (CIN) devoted to identifying the association frequency between cervical dysplastic lesions and cervico-vaginal infections caused by Trichomonas vaginalis, Chlamydia Trachomatis, Herpes Simplex virus and Human Papilloma virus. HPV lesions have revealed the pathology found more frequently in CIN lesions (33.2%) compared to 0.19% in the normal population, while the other infections have not shown significant differences between dysplastic lesions and normal control. In patients with CIN, the assumption of the estro-progestinic pill does not seem to contribute to the increase of frequency of cervico-vaginal infections.

Adolescent↗
PubMed2001

Detection of herpes simplex virus and human papilloma virus in ophthalmic pterygium.

PURPOSE: To evaluate the presence of herpes simplex virus (HSV) and human papilloma virus (HPV) in pterygia and phenotypically normal conjunctiva and the possible relation between viral presence and clinical information. METHODS: Fifty pterygia and respective conjunctival specimens were obtained. A personal and family history was recorded for each patient. HSV and HPV detection and typing were accomplished by polymerase chain reaction amplification of viral sequences. Results were statistically analyzed. RESULTS: HSV (type 1) was detected in 11 (22%), HPV (type 18) in 12 (24%), and both HSV-1 and HPV-18 in 3 (6%) of pterygia. No conjunctival specimen displayed HSV, whereas HPV was detected in four (8%). Postoperative recurrence and history of conjunctivitis were significantly more common in patients with simultaneous detection of HSV and HPV. CONCLUSION: The fact that HSV was not detected in conjunctival specimens implies a more specific correlation with pterygium, as compared with HPV. The detection of potentially oncogenic viruses, such as HSV and HPV, supports the concept that pterygium can be considered a neoplastic condition. The correlation of postoperative recurrence and a history of conjunctivitis with the simultaneous detection of HPV and HSV, implies a possible viral cooperation affecting the clinical profile of pterygium.

Adult↗
PubMed1998

Identification of p53 and human papilloma virus in Schneiderian papillomas.

Schneiderian papilloma of the nose is an unusual neoplasm with the propensity for local tissue destruction, recurrence, and malignant degeneration. Human papilloma virus (HPV) is related to a subset of sinonasal papillomas and has been implicated in the pathogenesis of cancer by interaction with the host p53 protein. Detection of p53 and HPV could be clinically useful as tumor markers for lesions with oncogenic potential. Thirty specimens for p53 were studied and nine (30%) stained positive. HPV was detected in six (20%). In the presence of p53, an odds ratio for carcinoma was 1.19:1, or 19% higher than expected. In the presence of HPV the odds ratio for carcinoma was 11.5:1, or 11.5 times higher than expected. In the presence of HPV an odds ratio for finding an elevated amount of p53 was 2.2:1. The data support the hypothesis that HPV and p53 may interact in a novel manner and elevate the risk for neoplasia.

Biomarkers, Tumor↗
PubMedDate not supplied

[Interactions of Shope papilloma virus with SV40 in adult domestic rabbit cell lines derived from normal skin or from Shope papilloma virus infected skin (author's transl)].

Three cell lines from adult domestic rabbit are infected with SV40: LP 17 and LP 45 derived from normal skin and LP 42 PS derived from skin infected for 24 h with Shope papilloma virus. The fibroblastic morphology of the cultures is not changed. SV40 is not recovered and T antigen is only detected in LP 42 PS cell line after 29 passages. To know if Shope papilloma virus facilitates penetration of SV40, cultures of LP 45 are first infected with Shope papilloma virus for 2 h and for 24 h, then superinfected with SV40. There is no cellular alteration, and T antigen induced by SV40 is only detected in cells pretreated for 24 h with Shope papilloma virus, after 20 passages. When cultures LP 45 are infected with Shope papilloma virus neutralized with a high titer antiserum and superinfected with SV40, T antigen is not detected. Superinfected cells containing specific SV40 T antigen do not induce tumors either in new born hamsters or in rabbits but they are able to grow in colonies in soft agar. LP 42 PS cell line and LP 45 cells infected with Shope papilloma virus for 24 h containe Shope papilloma virus genome which is able to modify the permissivity of rabbit cells to SV40.

Animals↗
PubMed1982

Molecular cloning and characterization of human papilloma virus DNA derived from a laryngeal papilloma.

Papilloma virus DNA from a laryngeal papilloma was cloned in phage lambda L 47 and characterized after cleavage with different restriction enzymes. Hybridization with the DNAs of human papilloma virus types 1, 2, 3, 4, 5, and 8 showed no homology under stringent hybridization conditions. Human papilloma virus type 6 DNA, however, was partially identical to laryngeal papilloma virus DNA; different restriction enzyme fragments hybridizing with the other DNA were identified on each genome. The degree of homology was determined by reassociation kinetics to be 25%. According to the present nomenclature, laryngeal papilloma virus therefore represents a different type of human papilloma virus and is tentatively designated as human papilloma virus type 11. Sequences homologous to laryngeal papilloma virus DNA were also found in four of nine additional laryngeal papillomas. Attempt to detect homologous DNA in 12 carcinomas of the larynx were negative.

Adolescent↗