Infection of human CD4+ rabbit cells with HIV-1 the possibility of the rabbit as a model for HIV-1 infection

Although human T cell surface glycoprotein CD4 is the cellular receptor for human immunodeficiency virus 1 (HIV-1), the introduction of the human CD4 gene into murine cells does not render them susceptible to HIV-1 infection. Here we have established rabbit transfectant cell lines expressing human CD4 on the cell surface and demonstrated that the CD4+ rabbit transfectants could be readily infected by HIV-1 by co-cultivating with a HIV-1-infected human MOLT-4 T cell line (MOLT-4/HIV). Avid syncytia formation was observed upon co-cultivation and the syncytia abundantly produced HIV-1 mature particles, as revealed by electron microscopy. A significant increase of HIV-1 p24 antigen was also detected in the culture supernatant. The syncytia formation was blocked by pretreating the transfectant with anti-human CD4 or by pretreating the MOLT-4/HIV with anti-HIV-1 serum obtained from an infected individual, indicating that the syncytia formed as a result of the interaction of human CD4 on the rabbit transfectant with the HIV-1 envelope protein expressed on MOLT-4/HIV. In contrast, only a very small proportion of the rabbit transfectants expressed HIV-1-specific antigens upon infection with an HIV-1 stock. This may indicate that, although rabbit cells have partially acquired susceptibility to HIV-1 by transfection of human CD4 gene, rabbit cells may further require such a molecule as might be provided by MOLT-4 to become fully susceptible to HIV-1 infection. The possibility of the rabbit as a model for HIV-1 infection is also discusse

Epidemiologic Studies on Venereal Diseases in Okayama District Report II. Statististical Observations on Venereal Diseases in 1955 and 1956

Consecutively from the first report, observations were made on venereal diseases, syphilis, gonorrhea, ulcus molle and lymphogranulomatosis venereum at Okayama Health Centre in 1955 and 1956. Syphilis gradually decrease since few years, whereas any decline could be found on gonorrhea and ulcus molle, and rather more acute gonorrhea have an increasing tendency

Critical Role of Smad and AP-1 Complexes in TGF-β-Dependent Apoptosis

Transforming growth factor-β1 (TGF-β1) induces not only cell growth inhibition but also apoptosis in hepatocytes, myeloid cells, and epithelial cells. Smad complexes (Smad2-Smad4 and Smad3-Smad4) are identified as key signaling molecules which transmit TGF-β1 signal for growth inhibition from the TGF-β receptors to the nucleus (1, 2). However, their roles are unclear in the induction of apoptosis. Our results show here that both Smad and AP-1 complexes play a critical role in TGF-β1 signaling for apoptosis.National Institutes of Health (U.S.) (Grant CA63260

New Mutants of Apolipoprotein E Associated with Atherosclerotic Diseases But Not to Type Ill Hyperlipoproteinemia

Abstract. We analyzed the heterogeneity of apo E in very low density lipoprotein from 58 hyperlipidemic subjects with or without atherosclerosis, 69 patients with ischemic heart disease, and 100 apparently healthy individuals. Apo E gene frequencies in the group of healthy individuals were comparable with those in German and American populations. The distribution of six common apo E phenotypes in the groups of hyperlipidemia and ischemic heart disease was similar to that in the healthy group. In addition to the three major isoforms of apolipoprotein E (apo E-4, E-3, and E-2) and the new one (apo E-5) which was recently found in this laboratory, we have discovered an additional series of components, which showed themselves as at least three bands on an isoelectric focusing gel in the region of E-VII through E-V, in four patients with hyperlipidemia and atherosclerosis. The new series of apo E components, named apo E-Suita, was identical with the ordinary apo E in its interaction with heparin-Sepharose gel and with antiapo E antibody. The most basic component of apo E-Suita (E-VII) was the unsialylated form and other components (E-VI and E-V), the sialylated forms. Family studies revealed that apo E-Suita was determined by inheritance of a new apo E allele located at the same locus as the hitherto known apo E components. Apo E-5 and apo E-Suita isoproteins had isoelectric points more basic than apo E-3, the parent type, by tw