Isolation of a human melanoma adapted Newcastle disease virus mutant with highly selective replication patterns.

The apathogenic Newcastle disease virus (NDV) strain Ulster has been used successfully as an adjuvant component for active specific immunotherapy of malignant mouse lymphoma, and in nude mice it was shown to be able to lead to retardation of the s.c. growth of xenotransplanted human melanoma cells. In order to improve in vivo effectiveness of virotherapy of human tumors without significantly increasing the risk of unspecific viral replication in host cells, we adapted the virus for growth in a human melanoma line (MeWo M). For this purpose NDV Ulster was mutagenized and a variant was selected which could replicate and reinfect the tumor line. The mutant (NDV 1E 10) performed late lysis on the melanoma line. Replication was found to be at least 100 times more efficient in MeWo M than in 6 of 8 other human tumor cell lines of different tissue origin. In 10 of 11 murine cell lines, NDV 1E 10 did not replicate via multicycles. Chick embryonic fibroblasts were permissive for nonlytic replication. Neither the virulent wild-type NDV Italian nor the avirulent strain NDV Ulster shared these specific replication properties with the new variant. We also established MeWo melanoma sublines with different metastatic capacities and tested them as targets for NDV 1E 10 infection. The MeWo subpopulations exhibited comparatively small differences in permissivity for multicyclic replication, but the more metastatic MeWo Met, like allogeneic melanoma lines, was more resistant to lysis. NDV Italian, in contrast, showed no differences in replication and lysis on any of the tested melanoma lines. Trypsin-activation experiments suggested an incomplete cleavage of mutant envelope glycoprotein F by the permissive cell line and, thus, mechanisms of specific infection and replication not requiring fully activated envelope glycoproteins.

[1]  P. Hersey,et al.  Evidence that treatment with vaccinia melanoma cell lysates (VMCL) may improve survival of patients with stage II melanoma , 1987, Cancer Immunology, Immunotherapy.

[2]  E. Atkinson,et al.  Virus-augmented delayed hypersensitivity skin tests in gynecological malignancies , 2004, Cancer Immunology Immunotherapy.

[3]  E. Macher,et al.  Expression of surface antigens and its relation to parameters of malignancy in human malignant melanoma , 1981, Cancer Immunology, Immunotherapy.

[4]  H. Schild,et al.  Modification of tumor cells by a low dose of Newcastle disease virus , 2004, Cancer Immunology, Immunotherapy.

[5]  V. Schirrmacher,et al.  Modification of tumor cells by a low dose of Newcastle Disease Virus. , 1988, European journal of immunology.

[6]  P. Schlag,et al.  Active Specific Immunotherapy with Autologous Tumor Cell Vaccines Modified by Newcastle Disease Virus: Experimental and Clinical Studies , 1989 .

[7]  R. Heicappell,et al.  Prevention of metastatic spread by postoperative immunotherapy with virally modified autologous tumor cells. I. Parameters for optimal therapeutic effects , 1986, International journal of cancer.

[8]  D. Murray,et al.  Malignant melanoma. Inflammatory mononuclear cell infiltrates in cerebral metastases during concurrent therapy with viral oncolysate , 1986, Cancer.

[9]  H. Wanebo,et al.  A southeastern cancer study group phase I/II trial with vaccinia melanoma oncolysates , 1986, Cancer.

[10]  M. Hanna,et al.  Delayed cutaneous hypersensitivity to autologous tumor cells in colorectal cancer patients immunized with an autologous tumor cell: Bacillus Calmette-Guérin vaccine. , 1984, Cancer research.

[11]  R. Kerbel,et al.  A model of human cancer metastasis: extensive spontaneous and artificial metastasis of a human pigmented melanoma and derived variant sublines in nude mice. , 1984, Journal of the National Cancer Institute.

[12]  D. Murray,et al.  A phase II study on the postsurgical management of stage II malignant melanoma with a Newcastle disease virus oncolysate , 1983, Cancer.

[13]  I. Hellstrom,et al.  Cell Surface Antigens of Human Melanoma , 1983 .

[14]  H. Kobayashi Modification of tumor cell antigen. , 1983, Progress in clinical and biological research.

[15]  T. Martin,et al.  Calcitonin induction of a persistent activated state of adenylate cyclase in human breast cancer cells (T 47D). , 1981, The Journal of biological chemistry.

[16]  H. Klenk,et al.  Mutational changes of the protease susceptibility of glycoprotein F of Newcastle disease virus: effects on pathogenicity. , 1980, The Journal of general virology.

[17]  H. Klenk,et al.  The spread of a pathogenic and an apathogenic strain of Newcastle disease virus in the chick embryo as depending on the protease sensitivity of the virus glycoproteins. , 1979, The Journal of general virology.

[18]  C. Boone,et al.  Virus augmentation of the antigenicity of tumor cell extracts. , 1979, Advances in cancer research.

[19]  D. Murray,et al.  Viral oncolysate in the management of malignant melanoma. II. Clinical studies. , 1977, Cancer.

[20]  R. Webster,et al.  IMMUNOTHERAPY OF OSTEOSARCOMA PATIENTS WITH VIRUS‐MODIFIED TUMOR CELLS * , 1976, Annals of the New York Academy of Sciences.

[21]  P. Ralph,et al.  Lysozyme synthesis by established human and murine histiocytic lymphoma cell lines , 1976, The Journal of experimental medicine.

[22]  H. Klenk,et al.  Studies on the assembly of the envelope of Newcastle disease virus. , 1976, Virology.

[23]  A. Scheid,et al.  Protease activation mutants of sendai virus. Activation of biological properties by specific proteases. , 1976, Virology.

[24]  G. Klein,et al.  SURFACE MARKERS ON HUMAN B AND T LYMPHOCYTES , 1973, The Journal of experimental medicine.

[25]  A. Long,et al.  A human cell line from a pleural effusion derived from a breast carcinoma. , 1973, Journal of the National Cancer Institute.

[26]  R. Lowenthal,et al.  Immune responses in mice to tumour challenge after immunization with newcastle disease virus‐infected or X‐irradiated tumour cells or cell fractions , 1973, International journal of cancer.

[27]  R. J. Harris Immunological Aspects of Viral Oncolysis , 1967 .

[28]  W. Cassel,et al.  Newcastle disease virus as an antineoplastic agent , 1965, Cancer.

[29]  R. Bablanian,et al.  STUDIES ON THE MECHANISM OF POLIOVIRUS-INDUCED CELL DAMAGE. I. THE RELATION BETWEEN POLIOVIRUS,-INDUCED METABOLIC AND MORPHOLOGICAL ALTERATIONS IN CULTURED CELLS. , 1965, Virology.

[30]  J. Littlefield Three Degrees of Guanylic Acid — Inosinic Acid Pyrophosphorylase Deficiency in Mouse Fibroblasts , 1964, Nature.

[31]  H. Koprowski,et al.  Enhancement of susceptibility to viruses in neoplastic tissues. , 1957, Texas reports on biology and medicine.

[32]  A. E. Moore Effects of viruses on tumors. , 1954, Annual review of microbiology.

[33]  A. E. Moore VIRUSES WITH ONCOLYTIC PROPERTIES AND THEIR ADAPTATION TO TUMORS , 1952, Annals of the New York Academy of Sciences.