TRAN Mong Ky Guy*, KIRKIACHARIAN S.**
University Paris V, Corresp. : 31 Av. du Bois, 92290
** University Paris XI, Faculty of Pharmacy,92 296 Cedex,
Chatenay Malabry, FRANCE.
HIV patients, progressive multifocal leucoencephalopathy (PML) is
characterized by an intense gliosis and caused by a
polyomavirus (PV).Brain glioma are induced in newborn
hamsters by PV. OHGAKI H (1998) found PV with a
high frequency in human glioma. More
worrying is the anti-poliomyelitis vaccine contamination by
SV 40 in the 1950s., because authentic SV 40 was found in
childhood brain tumors. An increase in neural tumors was
reported in children born from mothers receiving this
vaccine during pregnancy. PV large T (= Tumor) antigen also
binds to anti-oncogens p53 and Rb.
Method: We compared, by amino acid sequences
alignment, PV t
antigens (which in transgenic mice induced glioma ) to
Growth Factors (GF): Epidermal GF,
Fibroblast GF, Platelet-derived GF, sis oncogene of
Simian Sarcoma Virus (SSV), because glioma have
amplification of EGF Receptor in 40% cases and also of the
other GFs and their receptors. Insulin like GF-1 antisense
therapy blocked glioma formation in animals. SSV inoculation
in marmosets induced astrocytomas.
1°) PV ( JCV, BKV , SV 4O) are
homologous to EGF active site, Notch 4 and
2°) to bFGF, FGF-7, FHF-4 :
active site (79-81) ( R K K is read in normal sense, IFKK
& IVP in antisense because of the 3 dimensional
structure) matched with BKV and JC.
4°) IGF 1 is homologous to mouse PV.
sequence LRMLNGGTGFQV (NL is read in antisense) to the
proto-oncogene Notch (EGF family) LRCLNGGTCRQTand heregulin.
Conclusion: Polyomavirus t antigen contains
the same growth factors (EGF, FGF, PDGF, IGF 1)which are
amplified, with their receptors, in glioma.This is coherent
with a viral etiology (SV4O, polyomavirus; SSV) of glioma
& possible antiviral drug trial (Ara-C, cidofovir;
antiretroviral). The long term safety (cancers) of
SV4O-contaminated antipoliomyelitis vaccine may also be