Antibody-complement interactions with purified lymphocytic choriomeningitis virus

Immune complex formation and immune virolysis of the Armstrong strain of lymphocytic choriomeningitis virus (LCMV) were examined. LCMV, harvested from acutely infected BHK cells propagated in the absence of serum, was purified by methanol precipitation and sucrose density gradient centrifugation. The 31- and 23-S RNA species of LCMV were labeled under conditions of actinomycin D treatment of cells that prevented the labeling of cell ribosomes in the virion. The addition of guinea pig antibody (Ab) to LCMV lowered viral infectivity and enhanced the sedimentation rate but not the density of [U-³H]LCMV and ¹²⁵iodine-surface protein-labeled LCMV. This suggested that Ab aggregated the virions into faster sedimenting complexes. The addition of complement (C) to the LCMV-Ab complex further reduced the infectivity and increased both the sedimentation rate and density of [¹²⁵I]LCMV. When [U-³H]LCMV was reacted with Ab and C and subjected to rate zonal sedimentation, the RNA label remained at the top of the gradient rather than sedimenting with the ¹²⁵I-surface protein-membrane label. This observation, which indicated that Ab and C lysed the virus, was confirmed by electron microscopy showing first coating of the viral membrane with electron dense material, then swelling and rupture of the membrane and release of viral core material. Using sera deficient in specified C components, it was found that the C-mediated inactivation proceeded via the classical C pathway. Sera deficient in latter C components (beyond C3) augmented the inactivation of LCMV-Ab complexes, but this inactivation was far more extensive when a complete C source was used. Evidence suggesting that immune and persistently infected mice produce C-fixing Ab to the surface of the LCM virion was documented.     

Empyema due to Klebsiella pneumoniae

Three cases of post-pneumonic empyema due to infection with Klebsiella pneumoniae are reported. All were men considerably debilitated by complicating factors. The presence of persistent fistulae and of lung necrosis makes eradication of this infection very difficult and tedious, and in the management of these cases the objective is to secure adequate removal of necrotic tissue, effective drainage, and finally a satisfactory deroofing procedure to obliterate the empyema cavity.     

Preparation of Antisera Specific for Human B Cells by Immunization of Rabbits with Immune Complexes

Three rabbit antisera are described which are specific without absorption (titer 1:100) for separated human B cells, as measured by complement and non-complement fixing assays. The method of production of these sera involved injections of rabbits with precipitin lines formed between 10mul of three separate detergent solubilized membrane preparations and 4mul aliquots of rabbit antisera to human B cells. In addition to being B cell specific, the three sera block the MLC reaction, inhibit aggregated IgG binding to B cells, and show differential degrees of B cell lysis when tested on a panel of separated B and T cells. These and other properties suggest that the target specificities of the antibodies are the human equivalent of the murine Ia antigens.     

Intestinal disaccharidase activities in relation to age, race, and mucosal damage.

Studies were undertaken to determine the relationship of intestinal disaccharidase activity to age and race, and the relationship of mucosal damage to a primary low lactase activity. The first study consisted of data on 399 persons (339 whites, 53 blacks, and 7 American Indians) ages 1 month to 93 years, with normal intestinal histology. Among whites, all 117 children 5 years old or under had high lactase levels, whereas low levels were found only in subjects over 5 years of age. No low lactase levels were identified among the 11 black children 3 years old or under, but in comparison to coetaneous white children, their mean lactase activity was signficantly less. The majority of older blacks had low lactases. In whites and blacks alpha-disaccharidases did not participate in the age-related changes demonstrated with lactase. Of the 7 American Indians, none under 26 months old had low lactase levels, whereas the 4 over 10 years old had low activities. Heterozygotes for sucrase-isomaltase deficiency were identified only among whites. Low lactase levels developed during childhood in all races studied, however, many for unknown reasons maintained their lactose tolerance until adulthood. In the second study of 13 additional children with secondary disaccharidase deficiencies, emergence of a primary low lactase was related to age and race, rather than to mucosal damage. It appears that primary low intestinal lactase levels are absent or rare in whites under 5 and blacks under 3 years of age, and the deficiency is not related to mucosal damage.