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In this work, the estrogenic effects of three classes of substances included in cosmetic formulations-parabens, ultraviolet (UV) screens, and musk fragrances-were studied. Their estrogenic activity was measured with the use of three reporter cell lines: HELN, HELN ERalpha, and HELN ERbeta. These three cell lines allowed for the measurement of estrogenic activity toward estrogen receptors alpha and beta (ERalpha and ERbeta, while taking nonspecific interactions into account. Eight of the 15 substances tested showed specific estrogenic activity with the following degree of potency on ERalpha butylparaben > propylparaben > homosalate = octyl-dimethyl-PABA = 4-methyl-benzylidenecamphor = octyl-methoxycinnamate > ethylparaben = galaxolide. Among these active substances, parabens activated ERalpha and ERbeta similarly, UV screens activated ERalpha moderately and had almost no effect on ERbeta, and fragrances did not activate ERbeta. Methylparaben, ethylparaben, musk moskene, celestolide, and cashmeran did not activate estrogenic responses up to 10(-5) M. Musk ketone and benzophenone-3 were not considered estrogenic at 10(-5) M.

A prospective study was carried out during 1 year in order to correlate intussusceptions in childhood with a viral infection. A virus was incriminated in 50% of the 64 patients in this survey. Adenovirus infections remain predominant as compared to rotavirus infections.

The Epstein-Barr virus (EBV) BamHI restriction endonuclease fragment K (B95-8 strain) was introduced into a polyoma virus expression vector and used to transfect murine NIH 3T3 cells. An EBV-associated nuclear antigen was detected in these cells in an indirect immunofluorescence test using anti-EBV nuclear antigen-positive human sera. These sera recognized a Mr 88,000 polypeptide in 3T3 cells transfected with the BamHI fragment K-containing polyoma virus plasmid by radioimmunoelectrophoresis. A Mr 88,000 polypeptide also was detected in a B-cell line latently infected with the B95-8 strain of EBV. Plasmids containing insertion and deletion mutations in BamHI fragment K directed the synthesis of truncated forms of the Mr 88,000 polypeptide in 3T3 cells. These data directly demonstrate that the polypeptide identified in EBV-infected lymphocyte lines by anti-EBV nuclear antigen-positive human sera is encoded by the viral genome.Infection of human B lymphocytes with Epstein-Barr virus (EBV) results in the establishment of permanent cell lines (1). These immortalized cells contain most, if not all, of this herpesvirus genome as a multicopy episome (2). B-cell lines that are EBV genome-positive may also be established from the blood of individuals who have had a prior EBV infection (infectious mononucleosis or inapparent infection; ref.3) and from tumor tissue in 90% of the cases of Burkitt's lymphoma in Africa (4). EBV remains in a latent state in most of these lymphoblastoid cell lines with 10% or less of the viral DNA expressed as cytoplasmic polyadenylylated RNA (5); only rare cell lines express late viral functions and produce infectious virus. Very little is known about the proteins encoded by the EBV genome in latently infected lymphocytes, but potential functions include immortalization of B lymphocytes, control of EBV gene expression, and maintenance of the viral genome as an episome.All EBV-infected cells contain a nuclear antigen (EBNA) that may be detected in an anti-complement immunofluorescence (ACIF) test using serum from individuals who have had a prior EBV infection (6). This antigen is not detected in EBV-negative lymphoblastoid cell lines using the same sera (6). DNA transfer experiments have demonstrated that the BamHI restriction endonuclease fragment K of EBV DNA is able to induce the expression of a new nuclear antigen in mouse fibroblasts that may be detected with EBNA antibody-positive but not EBNA antibody-negative human sera (7). In addition, anti-EBNA sera identified polypeptides varying between Mr 65,000 and Mr 73,000 in EBV-positive lymphoblastoid cell lines by radioimmunoelectrophoresis (RIE); these species were not detected in EBV-negative lines (8). It has been suggested that the BamHI fragment K contains at least part of the coding sequences for the antigen detected by RIE and that variation in the size of this protein between different EBV-infected cell lines is due to variation in the size of a repeated DNA sequence (internal repeat 3, IR3) contained within that fragment (9)...

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