Activation of Epstein-Barr virus in hybrid cells.

Human-primate hybrid cell lines were established by fusion of African green monkey kidney cells (VERO) with lymphoblastoid cells from patients with infectious mononucleosis (IM)(IMK101) and from Burkitt's lymphoma culture (HR1K). Both Epstein-Barr virus (EBV)-specific antigens and EBV particle-containing cells increased in the hybrid lines (IMK1-1/VERO,HR1K/VERO). Treatment of the hybrids with 5-bromodeoxyuridine induced more antigen-positive and more virus-containing cells. EBV could be activated from IM lymphoblastoid cells by fusion of the lymphoblastoid cells with the VERO cells. The increase of viral antigens and virus particles may have been due to the cellular interaction between VERO cells and the lymphoblastoid cells or to a possible derepressor supplied by the VERO component of the hybrid. Virus derived from the HR1K cell line was replicated in the human-primate hybrid, but further investigation may be necessary to determine if it was identical to the EBV derived from the human cell line.

The effect of cortisol on glycogen and fructose-1,6-bisphosphatase in baby hamster kidney cells infected with Chlamydia trachomatis.

This study was designed to assay changes in glycogen synthesis which may occur as a result of cortisol treatment of chlamydial-infected cells. Monolayers of baby hamster kidney (BHK) cells, unlabeled and prelabeled with [6-14C]glucose, were treated with various concentrations of cortisol before (pretreated) or during (post-treated) infection with Chlamydia trachomatis. At designated times after absorption, the cells were harvested and assayed for total glycogen and 14C accumulation in glycogen. The total amount of glycogen accumulated in cells during the period of greatest chlamydial glycogen synthesis (36 h) was not affected by cortisol treatment. Cortisol treatment appeared to have retarded the accumulation of glycogen in treated infected cells until 30 h after infection. Treated infected cells prelabeled with [6-14C]glucose accumulated a greater amount of 14C in glycogen than untreated infected cells. All cortisol-treated, infected cells exhibited elevated levels of fructose-1,6-bisphosphatase activity, whereas untreated infected cells did not. The hypothesis that cortisol affects chlamydia multiplication by altering the intracellular environment of the host cell is compatible with the results obtained.

The use of frozen intravenous crystalloid solutions as the refrigerant for shipping blood.

The authors studied whether cooled sterile intravenous crystalloid solutions could be used to refrigerate red cells during shipment. Six 1000-ml bags of 0.9 percent normal saline and lactated Ringers (RL) solutions were supercooled and tested separately at temperatures ranging from 1 to -78 degrees C, with either 5 or 30 units of packed red cells (PRBCs). The PRBCs were shipped in a standard military container that permitted separation of the supercooled solutions from the PRBCs. Cooling RL solutions to 6 degrees C and to -22 degrees C maintained acceptable storage temperatures of the PRBC for 36 and 50 hours, respectively, and did not cause visible damage to the units. No significant changes were observed in various biochemical measurements of the cells and plasma. Cooling the RL solution to -78 degrees C caused a significant (p less than 0.05) increase in plasma potassium concentration. The effectiveness of the crystalloid solutions in refrigerating blood varied with the ratio of the number of PRBCs to the volume of cooled solutions and with the ambient temperature surrounding the container. The results of this study suggest that cooled intravenous crystalloid solutions can be used as refrigerants for PRBCs during shipment.