Journal of Neuro-Oncology 4:389-396 (1987) © Martinus Nijhoff Publishers, Boston - Printed in the Netherlands 389 A cultured human oligodendroglioma cell line and herpes simplex virus- infected cells share antigenic determinants P.G.E. Kennedy 1, B.A. Watkins 2, N.B. LaThangue 3, G.B. Clements 4 and D.G.T. Thomas 5 1Department of Neurology, Institute of Neurology, London (present address)," 2.SGough-Cooper Department of Neurological Surgery, Institute of Neurology, London, 3ICRF Tumour Immunology Unit, Department of Zoology, University College; 4Institute of Virology, Church St., Glasgow, United Kingdom," 1Department of Neurology, Institute of Neurological Sciences, Southern General Hospital, Glasgow, United Kingdom (1addressfor offprints)," 3Department of Biochemistry, Cancer Research Campaign Eukaryotic Molecular Genetics Research Group, Imperial College of Science and Technology, London (present address) Keywords: oligodendroglioma, herpes simplex virus, monoclonal antibody Abstract Cell cultures derived from 60 different human brain tumors were screened for the presence of HSV infected cell antigens by indirect immunofluorescence using a polyclonal rabbit antiserum reacting with herpes sim- plex virus (HSV), 3 monoclonal antibodies recognising different HSV-specified proteins, and one monoclonal antibody TI81 reacting with a DNA binding protein present in HSV-infected cells. Only one tumor (IN/157), derived from an oligodendroglioma, stained with the polyclonal antiserum. TI81 but none of the other monoclonal antibodies used also specifically reacted with IN/157 cells. High levels of the TI81-defined pro- tein were detected using immunoblotting in HSV-1 infected BHK/21 cells but not in IN/157 cells. TI81 may react with either an epitope shared between two different molecules in HSV-1 infected and IN/157 ceils or a cell-specified polypeptide that is upregulated after HSV-1 infection. Introduction Although a number of viruses have been shown to induce brain tumors experimentally in animals, no aetiological association between a particular virus and any type of human brain tumor has been demonstrated (Reviewed in 1). A direct approach to the identification of a particular virus as having a possible role in the causation of a brain tumor is to attempt to isolate the virus from tissues obtained at biopsy or autopsy. In experimental models with DNA tumor viruses, transformed cells and tumors generally fail to produce infectious virus. However some cases of Burkitt's lymphoma produce infec- tious virus - indeed this is how Epstein Barr virus was first discovered. An alternative approach to the problem is to grow brain tumor biopsy-derived cell populations in vitro and screen for the presence of viral antigens. We have adopted this second strate- gy to look for herpes simplex virus (HSV) encoded antigens in 60 different brain tumor cell cultures. We chose HSV because a) HSV has the ability to re- main in latent form in human and animal nervous tissue perhaps by achieving a highly specific inter- action with neural cells [2]; b) there is an epidemio- logical association between human cervical cancer and previous infection with HSV, though a causal