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[This corrects the article on p. 222 in vol. 18.].
Tanned red cell hemagglutination has been widely accepted for use in the detection of anti-thyroglobulin antibodies. The interpretation, however, especially when the hemagglutination was observed at a low titer of serum dilution, has remained equivocal. In order to separate specific and non-specific hemagglutination, we tried to concentrate serum IgG to compare the hemagglutination titer at various concentrations of IgG. If the hemagglutination is specific for the presence of antithyroglobulin antibodies, the hemagglutination titer would increase as the IgG concentration rises. On the contrary, when the hemagglutination is non-specific and irrelevant to the presence of anti-thyroglobulin antibodies, the hemagglutination titer is expected not to increase while the IgG concentration rises. Based on this hypothesis, sera which showed various hemagglutination titer for anti-thyroglobulin antibodies were studied to examine the parallelism between hemagglutination titer and IgG concentration. IgG was concentrated with the method of ammonium sulfate precipitation. The grade of concentrate was examined by the IgG determination with the method of immunodiffusion technique employing the kit distributed by Behringwerke. The hemagglutination test was performed with the Boyden's method using the kit distributed by the Wellcome Company. The results showed that 4 out of 15 sera whose original hemagglutination titer was 1:3 failed to show increase in hemagglutination titer even at the 2 to 4 fold concentration of IgG. On the contrary, only 2 out of 26 sera whose hemagglutination titer was more than 1:6, failed to increase the titer at the IgG concentrate to the same degree. Thus, it is possible to conclude that the hemagglutination observed at 1:3 dilution of the serum is highly non-specific, while that observed at a serum dilution of more than 1:6 is thought to be specific.
INTRODUCTION: M and N blood group antigens demonstrate inhibitory activity in inhibition reaction of viral hemagglutination with some influenza virus strains, with help of N-acetylneuraminic acid (sialic acid) which occurs in glycophorins on the red blood cells surface, and represent specific hemagglutunation receptors and substrate for action of influenza virus neuraminidase. MATERIAL AND METHODS: Reactivity of human O red blood cells with MM and NN phenotypes is established in inhibition reaction of viral hemagglutination by influenza virus A2 Singapore, with intention to fortify possibility of using human red blood cells in viral hemagglutination, to determine their reactivity in titration, retitration of hemagglutinins and inhibition reaction of hemagglutination. The aim of investigation was to describe destinations between different red blood cells in view of speed of reaction and receptor capacity. Material included 69 samples of sera from persons infected with influenza virus, among them 32 samples were positive with titres 1/80 and more. RESULTS: Reactivity of erythrocytes with MM and NN phenotypes in titration of hemagglutinins of influenza virus A2 Singapore in which base is viral hemagglutination is identical, because there are no statistically significant differences of average geomaterical levels of antibody titers. Enzymatically derived red cells by papain, which do not contain M and N blood group antigens, not cause viral hemagglutination phenomenon, because they sediment in all dilutions. Reactivity of red blood cells with MM and NN phenotypes in retitration of haemagglutinins and inhibition reaction of hemagglutination is identical, because there are no statistically significant differences in results with two kinds red blood cells. DISCUSSION: Results of investigation revealed that the reactivity of O human red blood cells different in MN phenotype is identical in regard to speed of reaction and receptor capacity in titration, retitration and inhibition reaction of viral hemagglutinatination and also showed that they demonstrate viral hemagglutination phenomenon in contrast with papainised red blood cells which do not contain M and N blood group antigens, which indirectly means that M and N blood group antigens contain receptors for influenza virus. CONCLUSIONS: Human red cells with MM and NN phenotypes cause viral hemagglutination phenomenon with influenza virus A2 Singapore, and could be used in routine virusological diagnostic procedures. O blood group red cells (MM and NN) in reaction of viral hemagglutination result identically in view of speed of reaction and receptor capacity, and have the same impact on result of this reaction. Enzymatically derived red cells by papain do not cause viral hemagglutination phenomenon, because they do not contain receptors for viral hemagglutinin on red cell membrane surface, which are hydrolazed by papain. Receptors for influenza virus on red cell membrane surface are a component part of M and N blood group antigens which are destroyed by papain.
Laboratory strains representing six numerical taxonomy clusters and fresh isolates of human Actinomyces viscosus and Actinomyces naeslundii were studied by standard flocculation slide tests for the ability to hemagglutinate erythrocytes (RBC) from various animal species. Human AB and horse RBC were agglutinated more frequently and rapidly than others; guinea pig RBC were agglutinated by only a few strains. Human AB RBC were selected for studies of hemagglutination mechanisms. Treatment of RBC with clostridial neuraminidase (NTRBC) greatly enhanced hemagglutination for almost all strains. In hapten inhibition experiments in which various concentrations of sugars were used, beta-galactosides were the most effective inhibitors of hemagglutination for both RBC and NTRBC; inhibition of NTRBC agglutination required higher concentrations. Soybean lectin agglutinated both RBC and NTRBC but not Actinomyces cells. NTRBC agglutinated at a 125-fold-lower concentration. Hemagglutination was sensitive to ethylenediaminetetraacetate for one strain tested. Hemagglutination reactions were reversible by addition of beta-galactosides. The ability of Actinomyces strains to "prime" RBC for hemagglutination by removing sialic acid to expose more penultimate beta-galactoside sites was studied by recycling Actinomyces-agglutinated RBC which were dispersed with a lactose solution and washed free of bacteria (primed RBC). Priming in this manner augmented subsequent hemagglutination by indicator Actinomyces strains and made the RBC more sensitive to agglutination by soybean lectin. The priming ability of Actinomyces strains generally correlated with the amount of sialic acid removed from primed RBC. Strains representing the numerical taxonomy clusters differed in both their hemagglutinating and priming activities. Cluster 5 strains (typical A. naeslundii) were good agglutinators of RBC, NTRBC, and primed RBC but were poor primers. Cluster 3 strains (atypical A. naeslundii) were the weakest hemagglutinators but could prime RBC adequately for subsequent agglutination by other strains. Together, these data indicate that Actinomyces hemagglutination proceeds via a two-step mechanism: (i) neuraminidase removal of terminal sialic acid and (ii) lectin-like binding to exposed beta-galactoside-associated sites on the RBC. Strains differ in the extent to which they can perform the two functions, and this specificity may relate to their taxonomic classification.
Procedures which make possible the enumeration of both infective and hemagglutinating influenza A virus particles have been developed and used in a quantitative investigation on the reproduction of the agent. Infective particles were found to be highly unstable and their half-life was only 147 minutes in allantoic fluid at 35 degrees C. both in vitro and in vivo. The instability of infective particles provides an explanation for the rapid accumulation of non-infective particles which retained the hemagglutinating property. The number of non-infective (N) particles was determined from the difference between the number of hemagglutinating (H) particles and the number of infective (I) particles as indicated by the relation: [N] = [H]- [1]. When the half-life of infective particles was taken into account, both infective and hemagglutinating particles were found to disappear from the allantoic fluid; i.e., were adsorbed by the allantoic membrane, at the same logarithmic rate after inoculation. Inoculation of any number of particles up to 3 x 10(7) was followed by a constant and progressive decrease in the proportion of unadsorbed particles from 0 to 4 hours. Approximately 20 per cent of particles were unadsorbed at 2 hours and about 5 per cent at 4 hours. Inoculation of 3 x 10(8) or more particles led to a larger proportion of unadsorbed particles at 4 hours. The maximum number of particles adsorbed was computed to be about 1.6 x 10(9). The concentration of both infective and hemagglutinating particles increased rapidly in the allantoic fluid after 4 hours when any number of infective particles up to 3 x 10(7) was inoculated. With such inocula, the rate of increase during the logarithmic period was constant and the time to double the concentration of infective or hemagglutinating particles was 46 minutes. With larger inocula, i.e. 3 x 10(8) particles, the concentrations of infective and hemagglutinating particles did not increase until after 8 hours and the rate of increase was much slower. The time to double the concentration of either then became 92 minutes. The number of infective particles was approximately equal to the number of hemagglutinating particles during the logarithmic increase period when any number of infective particles up to 3 x 10(6) was inoculated and no more than 10(6) non-infective particles were included in the inoculum. This finding was taken to indicate that all or almost all particles produced and released under these conditions were infective. That such particles became inactivated rapidly and led to the accumulation of an increasing number of non-infective particles after the logarithmic period can be explained by the short half-life of infective particles. The number of infective particles was no larger than one-tenth the number of hemagglutinating particles during the logarithmic increase period after 3 x 10(7) or more infective particles had been inoculated or when smaller inocula were used which also contained 3 x 10(7) or more non-infective particles. Non-infective particles prepared in vitro at 35 degrees or 22 degrees C. were as effective as those which accumulated in vivo in diminishing the proportion of infective particles in the yield. The extent of the reduction in the proportion of infective particles was directly related to the number of non-infective particles included in the inoculum. The yield of hemagglutinating particles was diminished when the inoculum contained 3 x 10(7) or more non-infective particles. The rate of increase was reduced so that the time to double the concentration became 92 minutes when the inoculum contained 3 x 10(8) non-infective particles. It appears from these findings that the single condition which will lead to the emergence of non-infective particles during the logarithmic period is a high initial particle-cell ratio. Because non-infective particles are equally as effective as infective particles in producing this result, it seems probable that the appearance of non-infective but hemagglutinating particles is not a necessary accompaniment of the reproductive process.
A total of 53 isolates of Bordetella bronchiseptica from dogs and pigs were tested for their ability to agglutinate chicken, horse, sheep, dog, pig, and guinea pig erythrocytes. No differences in hemagglutinating activity were attributed to the animal origin of the bordetella isolates. Horse and dog erythrocytes consistently resulted in the strongest hemagglutination reactions, whereas only 4% of the B. bronchiseptica isolates produced weak agglutination of chicken erythrocytes. A total of 85% of the isolates agglutinated horse, sheep, dog, pig, and guinea pig erythrocytes. One canine isolate with hemagglutinating activity, strain 110H, was examined to determine the nature of the hemagglutinin(s) involved. Hemagglutination was always accompanied by hemadsorption, as determined by dark-field or phase-contrast microscopy. Treatment of cells and cell extracts with heat or protease K inhibited the hemagglutination reaction. Sonicated bacterial cells had a greater hemagglutinating ability than did unsonicated live bacteria. The hemagglutination reaction was not inhibited by any of 17 sugars nor by N- acetylglucosamine or ethylene glycol-bis-(beta-aminoethyl ether)-N, N-tetraacetic acid. Hemagglutinins were not detected in sonic extracts nor in several bacterial subunit fractions, including isolated pili. Antigens in some of these preparations were, however, detectable by indirect hemagglutination with anti-B. bronchiseptica serum. Isolated pili could not be detected on the erythrocyte surface by electron microscopy; however, serial sections of erythrocytes agglutinated by the live Bordetella organisms showed that the bacterial outer membrane and the erythrocyte surface were separated by a space of approximately 20 nm. This study provided additional circumstantial evidence that B. bronchiseptica pili or at least heat-labile surface proteins which extend some distance from the bacterial surface are involved in hemagglutination. Multiple hemagglutinins are likely to exist within this species since one isolate lacking pili also agglutinated canine erthyrocytes. The hemagglutinins of B. bronchiseptica need to be isolated and characterized before the hemagglutination reaction can be applied to studies of attachment.
Our earlier studies demonstrated that clinical strains of Prevotella intermedia, isolated from human periodontal pockets, possess various types of fimbria (surface appendages) as determined ultrastructurally. These bacteria have the ability to agglutinate selected mammalian erythrocytes. Hemagglutinating activity exhibited by these cells may be attributable to these surface structures. Strain 17, which possess fimbriae of 8 nm in diameter and readily agglutinates human, monkey, sheep, rabbit, and mouse erythrocytes was selected to determine whether these fimbriae possessed the hemagglutinating activity. Fimbriae were mechanically sheared, concentrated by ammonium sulfate precipitation, solubilized in 10 mM Tris-HCl buffer containing 0.5% deoxycholate and partly purified by ultracentrifugation in a 10-50% linear sucrose gradient. Isolated fimbriae banded at a density of 1.20-1.15 g/ml, appeared fairly uniform ultrastructurally, and possessed hemagglutinating activity. The hemagglutinating activity of P. intermedia whole cells and isolated fimbriae was reduced by treatment with proteases and eliminated by treatment with heat at 80 degrees C for 10 min. The optimal pH for the hemagglutination was 7.0. In the process of hemagglutination, P. intermedia whole cells and isolated fimbriae bound to rabbit erythrocytes as observed by: (a) decrease in the hemagglutinating activity of bacterial whole cells and isolated fimbriae after incubation with rabbit erythrocytes, (b) increase in hemagglutinating activity of the red cells used for absorption, and (c) the presence of P. intermedia whole cells and fimbriae on red cells after absorption as revealed by immunoelectron microscopy. Both the immune immunoglobulin G of the rabbit polyclonal anti-fimbriae antibody and the immune immunoglobulin G and its Fab fragments of the murine monoclonal anti-fimbriae antibody were effective inhibitors of hemagglutination mediated by isolated fimbriae. Immunogold labeling showed that the monoclonal antibody bound specifically to P. intermedia fimbriae. These results collectively suggest that the hemagglutination exhibited by P. intermedia may be attributable to the fimbriae or the fimbrial-associated components.