Characterization of JC papovavirus adapted to growth in human embryonic kidney cells.

Human papovavirus JC virus was adapted to growth in human embryonic kidney (HEK) cells. After eight passages, the HEK-adapted JC virus produced high virus yields and was capable of forming plaques in HEK monolayer cultures. Eleven plaque-purified stocks were prepared and characterized. Biologically, the plaque-purified virus induced tumor and viral antigens in HEK cells earlier and in a higher percentage of cells than uncloned virus. Cytopathic changes were also evident sooner and were more extensive. The DNA from uncloned as well as plaque-purified isolates was analyzed by restriction endonuclease cleavage followed by gel electrophoresis. The DNA from uncloned HEK-adapted virus was heterogeneous. Plaque-purified virus isolates yielded DNA which, although much less heterogeneous than the uncloned stock, still consisted of two or more species of viral DNA.     

Three ent-secoaromadendrane-type sesquiterpene hemiacetals and a bicyclogermacrene from Plagiochila ovalifolia and Plagiochila yokogurensis

A new ent-secoaromadendrane-type sesquiterpene hemiacetal, plagiochiline G, was isolated from Plagiochila ovalifolia. Four new ent-sesquiterpene hemiacetals, plagiochiline H and I, and two pungent methoxyplagiochilines A₁, A₂ and non-pungent methoxyplagiochiline C were also isolated from P. yokogurensis. The methoxylated plagiochilines A₁, A₂ and C were derived from the plagiochilines A and C during the extraction procedure. A new germacrene, ent-3α-acetoxybicyclogermacrene, ent-maaliol and the previously known ent- aromadendrane-type sesquiterpenes have been obtained from P. yokogurensis. The structures of the new compounds were elucidated by ¹H NMR spectral data and by chemical correlation.     

Physical and Biochemical Properties of Progressive Pneumonia Virus

The physical and biochemical characteristics of progressive pneumonia virus were found to be remarkably similar to those of the ribonucleic acid (RNA) tumor viruses. Significant findings included the presence of a 60 to 70S RNA genome, RNA-dependent deoxyribonucleic acid polymerase activity, and common morphological properties. This information correlates with previously reported biological observations and supports the provisional inclusion of enveloped RNA-containing "slow viruses" within the RNA tumor virus group.     

The structure of syringomycins A1, E and G

By a combination of 1D and 2D 1H- and 13C-NMR, FAB-MS, and chemical and enzymatic reactions carried out at the milligram level, it has been demonstrated that syringomycin E, the major phytotoxic antibiotic produced by Pseudomonas syringae pv. syringae, is a new lipodepsipeptide. Its amino acid sequence is Ser-Ser-Dab-Dab-Arg-Phe-Dhb-4(Cl)Thr-3(OH)Asp with the beta-carboxy group of the C-terminal residue closing a macrocyclic ring on the OH group of the N-terminal Ser, which in turn is N-acylated by 3-hydroxydodecanoic acid. Syringomycins A1 and G, two other metabolites of the same bacterium, differ from syringomycin E only in their fatty acid moieties corresponding, respectively, to 3-hydroxydecanoic and 3-hydroxytetradecanoic acid.     

Analysis of T antigen and viral DNA in mouse cells transformed by K virus, a nononcogenic murine papovavirus

A tumorigenic line of mouse cells transformed by the nononcogenic murine K papovavirus was established and characterized. Tumor-bearing animals produced antibody specific for K virus-transformed cells; the K virus T antiserum did not react with polyomavirus-transformed cells. Immunoprecipitation of the T antigen in the transformed cells revealed large T antigen (molecular weight 84,000). About 10 to 15 copies of K virus DNA were found to be integrated in the cellular DNA.     

Induction of tumor cytotoxic immune cells using a protein from the bitter melon (Momordica charantia)

The fruit and seeds of the bitter melon (Momordica charantia) have been reported to have anti-leukemic and antiviral activities. This anti-leukemic and antiviral action was associated with an activation of murine lymphocytes. A partially purified protein factor from the bitter melon caused an infiltration and activation of peritoneal exudate cells in C57B1/6J, C3H/HeJ, and C3H/HeN mice. When the extract was injected twice a week at 8 micrograms of protein per ip injection for 0-4 weeks, the peritoneal exudate cells from the treated mice were cytotoxic in a long-term (18-hr) 51Cr-release assay against a range of labeled targets: L1210, P388, and MOLT-4 tumor cells. Cytotoxicity was also observed against YAC-1 targets in a short-term (4-hr) assay. Fractionation of the cytotoxic immune cells implicated a nonadherent cell population which was capable of killing an NK-sensitive cell line in a 4-hr 51Cr-release assay. Unit gravity sedimentation studies indicated that the cytotoxicity was due to either a neutrophil or a large lymphocyte. Antibody depletion experiments using antibody to asialo GM1, an NK cell-specific antibody, depleted cytotoxicity observed in nonadherent, Ficoll/Hypaque-separated PEC. This suggests that at least part of the anti-leukemic activity of the bitter melon extract is due to the activation of NK cells in the host mouse.     

Hyperreactivity of activated B cells to B cell growth factor in patients with systemic lupus erythematosus

Inasmuch as B cell function is in large part determined by lymphokine-derived accessory signals, we studied the effects of recombinant IL-2 and low-molecular-weight B cell growth factor (BCGF) on peripheral blood B cells activated with Staphylococcus aureus Cowan I to explain the B cell hyperfunction in patients with SLE. When S. aureus Cowan I-activated normal B cells were separated into Tac-antigen (Tac-Ag)+ and Tac-Ag- cells by employing a rosette technique, IL-2 induced only the Tac-Ag+ cells to proliferate, whereas both the Tac-Ag+ and Tac-Ag- cells responded to BCGF. The Tac-Ag+ and Tac-Ag- fractions of activated SLE B cells behaved like respective fractions of activated normal B cells for the pattern of response to these growth factors. It should be pointed out, however, that although the Tac-Ag+ B cells of SLE patients and those of normal controls responded to IL-2 to almost the same degree, both the Tac-Ag+ and Tac-Ag- B cells of SLE patients exhibited markedly enhanced proliferative responses to BCGF. The selectively enhanced responsiveness of a broader range of activated SLE B cells may lead to B cell hyperactivity in this disease.