Of 29 hematopoietic cell lines tested for susceptibility to human immunodeficiency virus (HIV)-1HTLV-IIIB infection, all CD4+ cell lines became infected. Continuous culturing of infected cell lines resulted in nine HIV-1 carrier cell lines, including, for the first time, an HIV-1 carrier megakaryoblastic cell line, MEG-01/HIV. The immunophenotypic profiles of a total of 17 HIV-1 carrier cell lines (nine newly and eight previously established cell lines) were compared with their respective parental noninfected cell lines. Except for total absence of CD4 expression, the expression of other antigens was variable among the 17 HIV-1 carrier cell lines. Persistent and consistent replication of infectious HIV-1 was detected in all of them in varying quantities. The great variability observed in both the altered marker expression, with respect to that of the noninfected parental cell lines, and in the quantities of persistently produced infectious HIV-1 was, nevertheless, specific to the individual cell lines. Furthermore, the present study demonstrates that there is no apparent correlation in the quantity of HIV-1 produced to either T cell, myelomonocytic cell, or megakaryocytic cell types. Instead, the results suggest that a particular interaction between HIV-1 and individual clonal cell lines may provide insight into the extremely complex immune dysregulation associated with the pathogenesis of acquired immune deficiency syndrome. Thus, the 17 HIV-1 carrier cell lines of diverse origin presented here provide valuable and unique models for further understanding acquired immune deficiency syndrome pathogenesis at the cellular and molecular levels. [P.S.E.B.M. 1993, Vol 202]
The enhancer-binding factor of human immunodeficiency virus (H1V)-1 was purified from human B cells by sequence-specific duplex oligonucleotide affinity chromatography.Gel retardation assay and footprint analysis showed that the purified factor bound specifically to the HIV-1 enhancer sequence, and protected both direct repeats in the HIV-1 enhancer.The purified factor consisted of four main polypeptides of the molecular weight of 36,000-42,000.At least three of them had enhancer-binding activity after elution from sodium dodecyl sulfate-polyacrylamide gel and renaturation.UV cross-linking analysis also showed that at least two of the polypeptides in purified fraction had a binding activity specific for the HIV-1 enhancer.The purified factor activated transcription from the HIV-1 promoter in uitro, confirming that it was indeed a transcription factor for HIV-1.The purified factor also recognized sequences in the immunoglobulin K gene enhancer and the major histocompatibility complex class I gene enhancer with almost the same affinity as the HIV-1 enhancer.These results suggested the existence of multiple proteins which recognize the &-related sequences.This regulatory factor should help in the study of the biochemical pathway underlying HIV production from latently infected cells.Transcription of the human immunodeficiency virus (HIV)-1' in latently infected T lymphocytes is induced by compounds such as phytohemaggutinin or phorbol esters, which activate the cells to secrete lymphokines (1,2).Induction of transcription by these compounds leads to the expression of virusencoded tram-acting factors specified by the tat and rev genes.
NSTI caused by E. coli monomicrobial infection is an extremely severe condition with high mortality. This report presented a case of monomicrobial NSTI caused by E. coli with septic shock in a patient with alcoholic liver cirrhosis and mentioned both pathogen virulence factors and host susceptibility factors.
The effects of human interferon-alpha (IFN-alpha) or maltose-stabilized IFN-alpha (MS-IFN-alpha) on IL-2 production by PHA- or anti-CD3 mAb-stimulated MOLT 16 cells, a human leukemic T cell line, were studied. MS-IFN-alpha is an IFN-alpha-containing powder in which maltose was used as an excipient, and has been shown to have a positive effect on human immunodeficiency virus (HIV)-infected patients. In this study, MS-IFN-alpha powder was dissolved in a culture medium and used for the experiments. IL-2 production by PHA- or anti-CD3 mAb-stimulated MOLT 16 cells was augmented by coculturing with IFN-alpha or MS-IFN-alpha. The augmentation of IL-2 production by IFN-alpha or MS-IFN-alpha was completely abrogated by rabbit anti-IFN-alpha antibody. We have previously shown that IL-2 production by PHA-stimulated MOLT 16 cells is augmented by coculturing with IL-1. Furthermore, IL-2 production by PHA-stimulated MOLT 16 cells was also augmented by human TNF-alpha in a dose-dependent manner. The TNF-alpha-induced augmentation was completely abrogated by rabbit anti-TNF-alpha antibody. Interestingly, both IFN-alpha and MS-IFN-alpha synergized with rIL-1 alpha or TNF-alpha resulting in IL-2 production being augmented far more effectively than either cytokine alone.(ABSTRACT TRUNCATED AT 250 WORDS)
We examined the responses of two Japanese monkeys with pollinosis to two major allergens (Cry j 1 and Cry j 2) of Japanese cedar pollen. The two monkeys (A and B) had specific IgE antibodies to the allergens and showed a strong positive reaction to both of them in the intradermal test. In the histamine release test with peripheral blood mononuclear cells (PBMC), monkey A showed a typical pattern similar to that seen in human patients, while monkey B released a low level of histamine. The proliferative response of PBMC to both allergens in monkey A was weak, but was typical in monkey B. From clinical as well as immunological points of view, these monkeys may be a suitable animal model for Japanese cedar pollinosis in humans.
Interleukin-18 (IL-18) induces apoptosis in human myelomonocytic KG-1 cells as determined by agarose gel electrophoresis, and flow cytometry after propidium iodide (PI) staining. Apoptosis was detected 20 hours from the start of culture at concentrations of 100 ng/ml of the cytokine. Although IL-18 induces the production of large amounts of interferon gamma (IFN-gamma) by KG-1 cells, conditioned media could not induce apoptosis of fresh cells. The protein expressions of p53 and Fas ligand by KG-1 cells, which constitutively express the Fas antigen (CD95), were found to increase after exposure to IL-18 for 20 hours. Both Fas ligand and its receptor were found to be functional by in vitro assays on Fas-expressing target cells and an agonist anti-Fas antibody, respectively. In conclusion, IL-18 enhances the expression of Fas ligand by Fas-expressing KG-1 cells and induces apoptosis in the cells through a mechanism probably involving the Fas pathway.
