vendredi 24 avril 2009
par   G. Grégori

Alderete JF (1988) Alternating phenotypic expression of two classes of Trichomonas vaginalis surface markers. Rev Infect Dis 10 Suppl 2 :S408-412


The antigenic heterogeneity of Trichomonas vaginalis is due in part to the membrane disposition of immunogens (repertoire A) among some but not all isolates and among subpopulations of trichomonads of certain isolates. Heterogeneous T. vaginalis isolates undergo phenotypic variation for the A repertoire of immunogens. The presence of immunogens on (A+ phenotype) or the absence of them from (A- phenotype) trichomonal surfaces clearly influences the virulence traits of the pathogenic human trichomonads. A- parasites, for example, possess an enhanced ability to cause cytadherence-dependent killing of HeLa cells as compared with A+ parasites. A relation between phenotype of repertoire A and adherence was further substantiated by fractionating parasites of a parent T. vaginalis isolate, yielding adherent and nonadherent subpopulations. Trichomonad proteins were identified as putative adhesin candidates (repertoire B) ; adhesins were synthesized only by adherent (B+ parasites). Flow cytofluorometry of B+ and B- (nonadherent) subpopulations with antibody to proteins of the A repertoire demonstrated corresponding A- B+ and A+ B- phenotypes, respectively. Data support the hypothesis that trichomonads of some isolates of T. vaginalis undergo alternating expression of at least two classes of surface markers.

Balber AE, Frommel TO (1988) Trypanosoma brucei gambiense and T. b. rhodesiense : concanavalin A binding to the membrane and flagellar pocket of bloodstream and procyclic forms. J Protozool 35 :214-219


We have measured binding of fluorescein-conjugated succinyl-concanavalin A (Fl-s-Con A) to bloodstream and procyclic forms of Trypanosoma brucei gambiense and to bloodstream forms of T. b. rhodesiense by flow cytofluorimetry. Bloodstream forms bound an order of magnitude less lectin than procyclic forms. Trypsin-treating cells enhanced binding of Fl-s-Con A to bloodstream forms 3-16-fold depending on the strain and the length of trypsinization but had little effect on Fl-s-Con A binding by procyclics. The trypsinization protocol used did not remove major common glycoproteins detected on lectin blots of either life cycle form but removed greater than 95% of the variant specific glycoprotein and fragments derived from this protein of bloodstream forms. Microscopically detectable Fl-s-Con A binding to bloodstream forms was confined to the flagellar pocket. Trypsinized bloodstream forms and procyclics bound Fl-s-Con A in the flagellar pocket, on the flagellum, and on the cell surface. Lectin remained cell associated but appeared to redistribute towards the flagellum and pocket when cells that had bound lectin on ice were subsequently incubated at physiological temperatures. The Fl-s-Con A binding had specificity characteristic of the interaction between the lectin and oligosaccharides. These results are consistent with the hypothesis that the variant specific surface glycoprotein blocks binding of the lectin to surface glycoproteins of bloodstream forms and suggest that concanavalin A-binding glycoproteins are abundant in the flagellar pocket of both life cycle forms.

Banas JA, Loesche WJ, Nace GW (1988) Possible mechanisms responsible for the reduced intestinal flora in hibernating leopard frogs (Rana pipiens). Appl Environ Microbiol 54 :2311-2317


Mechanisms and factors that normally control the large intestinal flora were investigated to determine whether changes in these parameters could account for the decreased bacterial concentration and facultative nature of the flora found in hibernating frogs. It appeared that low temperatures and limited nutrients were the main factors responsible for the decrease in the bacterial concentration and may also have been responsible for the increase in the proportions of facultative organisms, since no change in the redox potential was seen. The hibernating frogs were extremely sluggish in the removal of India ink particles from the circulatory system by the Kupffer cells of the liver compared with nonhibernating frogs. They were unable to mount an antibody response to bovine serum albumin, but their serum did exhibit killing of Pseudomonas paucimobilis, suggesting opsonization by preformed antibody and complement. The role of these host factors in protecting the hibernating frog against this indigenous flora is discussed.

Bruschi CV, Chuba PJ (1988) Nonselective enrichment for yeast adenine mutants by flow cytometry. Cytometry 9 :60-67


The expression of certain adenine biosynthetic mutations in the yeast Saccharomyces cerevisiae results in a red colony color. This phenomenon has historically provided an ideal genetic marker for the study of mutation, recombination, and aneuploidy in lower eukaryotes by classical genetic analysis. In this paper, it is reported that cells carrying ade1 and/or ade2 mutations exhibit primary fluorescence. Based on this observation, the nonselective enrichment of yeast cultures for viable adenine mutants by using the fluorescence-activated cell sorter has been achieved. The advantages of this approach over conventional genetic analysis of mutation, recombination, and mitotic chromosomal stability include speed and accuracy in acquiring data for large numbers of clones. By using appropriate strains, the cell sorter has been used for the isolation of both forward mutations and chromosomal loss events in S. cerevisiae. The resolving power of this system and its noninvasiveness can easily be extended to more complex organisms, including mammalian cells, in which analogous metabolic mutants are available.

Chaffin WL, Ringler L, Larsen HS (1988) Interactions of monospecific antisera with cell surface determinants of Candida albicans. Infect Immun 56 :3294-3296


Flow cytometric analysis of indirect immunofluorescence showed that surface determinants recognized by antisera (Candida Check ; Iatron Laboratories, Tokyo, Japan) for factors 1, 4, 5, and 6 were expressed to the same extent by all cells of Candida albicans under each growth condition and for each morphology examined. Fluorescence intensity increased with increasing cell size.

Donnelly CW, Baigent GJ, Briggs EH (1988) Flow cytometry for automated analysis of milk containing Listeria monocytogenes. J Assoc Off Anal Chem 71 :655-658


This paper describes the application of flow cytometry to the analysis of milk for the presence of Listeria monocytogenes. A total of 939 raw milk samples from 54 farms were analyzed for the presence of L. monocytogenes by cold enrichment vs flow cytometry, which incorporated a selective enrichment step. Analyzed samples consisted of milk from individual farm bulk tanks ; string samples which represented milk from 25 to 40 cows ; and combination samples representing milk from 200 cows. Raw milk samples were directly enriched for 24 h at 37 degrees C and analyzed by flow cytometry following fluorescence labeling of bacterial populations, or were cold enriched for 1 month at 4 degrees C. Following cold enrichment, samples were streaked to McBride’s Listeria agar, and suspect colonies were biochemically identified as L. monocytogenes. L. monocytogenes was isolated from only 15 of the analyzed samples, all of which were common to one farm. Results of flow cytometry analysis yielded a 5.86% false positive rate and a 0.53% false negative rate when compared with culture procedures.

Elmendorf S, McSharry J, Laffin J, Fogleman D, Lehman JM (1988) Detection of an early cytomegalovirus antigen with two-color quantitative flow cytometry. Cytometry 9 :254-260


An early cytomegalovirus (CMV) antigen was detected with a monoclonal antibody by two-color fluorescent flow cytometry. With the aid of a human diploid fibroblast cell strain, FLOW 2000, infected with the AD169 strain of CMV, the viral antigen and the DNA content of infected or uninfected cells were measured. There was no evidence of change in the cell-cycle distribution of the infected cells. The viral antigen was detected within 30 minutes following virus adsorption at 0.1 and 1.0 plaque-forming units/cells ; and the percentage of positive cells increased with time and viral dosage. All stages of the cell cycle were susceptible to viral infection and the average fluorescence was greater than the background fluorescence. Flow cytometry detected the viral antigen earlier than conventional immunofluorescent microscopy and cell culture for CMV cytopathological effect (CPE). Ten bronchoalveolar lavages assayed by flow cytometry and conventional diagnostic procedures demonstrated that flow cytometry might be useful in early diagnosis for CMV infection.

Evans DL, Jaso-Friedmann L, Smith EE, Jr., St John A, Koren HS, Harris DT (1988) Identification of a putative antigen receptor on fish nonspecific cytotoxic cells with monoclonal antibodies. J Immunol 141 :324-332


In the present study mAb were derived against flow cytometry (FCM) purified fish (Ictalurus punctatus) nonspecific cytotoxic cells (NCC). mAb 5C6.10.4 and 6D3.2.10 produced 60 to 65% inhibition of lysis of NC-37 target cells (a human B-lymphoblastoid cell line) by unfractionated NCC. mAb 2B2.4.9 and 6D3.4.4 were noninhibitors of cytotoxicity. All mAb were the same isotype (IgM) and were cloned by limiting dilution (2x). Inhibitory activity was specific for the effector cells because the mAb had no effect on NCC cytotoxicity when only the target cells were treated. Inhibition could be produced by preincubation of the mAb with NCC or by no preincubation, and inhibition was not reversible. Killing by FCM-sorted NCC of NC-37 target cells was inhibited almost 100% by mAb 5C6.10.4. Inhibitor mAb also significantly reduced NCC killing of MOLT-4, K562, P815, U937, Daudi, YAC-1, and HL-60 cells. Experiments also were conducted to determine at which stage of the lytic cycle the mAb acted. Both inhibitor mAb significantly inhibited conjugate formation between effector and NC-37 target cells. The technique of FCM was combined with competitive binding experiments to determine that the Ag recognized by both inhibitor and noninhibitor mAb was found on the membranes of the same cells. These results were confirmed by demonstrating (by using FCM) that FITC-labeled inhibitor and biotinylated noninhibitor mAb bound to the same cells. FCM also was next used to determine mAb binding to various effector cell populations. Inhibitor and noninhibitor mAb bound to approximately 25% (5C6.10.4) and 39% (6D3.4.4) of fish anterior kidney cells ; to 42% (5C6.10.4) and 54% (6D3.4.4) of fish spleen cells ; and to 2.5% (5C6.10.4 and 6D3.4.4) of fish peripheral blood. mAb were used to purify the target cell binding structure found on NCC. Con A-Sepharose purified mAb were used as the fixed ligand for Affi-Gel-10 affinity chromatography experiments. FCM-purified NCC were solubilized and the receptor was purified by using this technique. Analysis of the NCC-purified receptor by 12% SDS-PAGE indicated that the mAb purified structure may be composed of a dimeric molecule consisting of 41 kDa and 38 kDa proteins. The same dimer was purified by using either inhibitory (6D3.2.10) or noninhibitory (6D3.4.4) mAb. Similar results were obtained with immunoprecipitation experiments by using mAb 5C6.10.4. These studies demonstrate that the Ag-binding receptor structure on fish NCC may be comprised of a dimeric complex.

Furuta I (1988) [Bacterial infection]. Rinsho Byori 36 :431-433


Goolsby C, Gay H, Docherty JJ, Todd P (1988) Flow cytometric detection of herpes simplex virus type 2 infected and transformed cells by immunoenzymatic and by indirect immunofluorescence staining. Cytometry 9 :126-130


The glucose oxidase antiglucose oxidase (GAG) immunoenzymatic staining procedure has been used to detect herpes simplex virus (HSV) antigens microscopically. In this study, the GAG procedure was adapted to cells in suspension, and its potential usefulness in flow cytometry was examined. HSV-2 infected monkey kidney and HSV-2 transformed mouse cells were stained using antisera to HSV-2 or to an HSV-2 specific protein with a molecular weight of 38 Kd, respectively, with the GAG procedure. Flow cytometric analysis of the GAG stained cells was then performed by the measurement of scattered light intensity in the angular intervals 1 degree-2 degrees, 2.5 degrees-19 degrees, and 3 degrees-6 degrees. The greatest scattered light intensity decrement caused by staining occurred in the 3 degrees-6 degrees angular interval, as predicted by previous work. In infected cells, which stain intensely by immunofluorescence, the difference between positively and negatively stained cells was adequate for detecting infected cells using the GAG method ; however, this was not the case for the lightly staining transformed cells. The indirect immunofluorescence method of analysis of the same populations was superior to the scattered light method of analysis of the GAG stained infected and transformed cells.

Jaso-Friedmann L, Evans DL, Grant CC, St John A, Harris DT, Koren HS (1988) Characterization by monoclonal antibodies of a target cell antigen complex recognized by nonspecific cytotoxic cells. J Immunol 141 :2861-2868


Fish nonspecific cytotoxic cells (NCC)3 recognize and lyse a large variety of human and mouse transformed cells. In an effort to determine the Ag recognized by NCC on these targets, mAb were raised against NC-37 target cells. Four anti-NC-37 mAb were chosen for further characterization based on their effects on NCC lysis of target cells. Purified mAb 18C2 and 1E7 (IgM isotype) inhibited NCC killing of the following targets : U937, MOLT-4, K562, HL-60, DAUDI, NC-37, P815, and YAC-1. The dose-dependent inhibitory activity occurred at the target cell level and ranged from 50 to 70% at a concentration of 50 micrograms/well when compared to noninhibitory mAb 7C6 and 1D4 (IgG isotype). Similarly, mAb 18C2 protected the fish parasite Tetrahymena pyriformis from lysis by NCC when compared to mAb 7C6. Adsorption experiments demonstrated that the inhibitory effect on NC-37 lysis by NCC could be removed in a titratable fashion by incubation of mAb 1E7 with any one of the other target cell lines, but it could not be removed by incubation with effector cells. The inhibitory activity of mAb 1E7 and 18C2 was shown to be caused by the inhibition of conjugate formation between effector and NC-37 target cells. The relative membrane concentration of the antigenic determinants recognized by these mAb on the target cells was studied by flow cytometry using FITC-labeled mAb. These experiments showed that all four mAb bound to the surface of the cells tested. Biochemical analysis with Western blots and immunoprecipitation showed that mAb 18C2 and 1E7 recognize two Ag in NC-37 lysates : a larger protein of around 80 kDa and a smaller one of 42 kDa.

Jung V, Jones C, Rashidbaigi A, Geyer DD, Morse HG, Wright RB, Pestka S (1988) Chromosome mapping of biological pathways by fluorescence-activated cell sorting and cell fusion : human interferon gamma receptor as a model system. Somat Cell Mol Genet 14 :583-592


Human chromosome 6 encodes both the interferon gamma receptor as well as the class I major histocompatibility complex antigens, HLA-A, -B, and -C. However, the presence of chromosome 6 in somatic cell hybrids is insufficient to confer sensitivity to human interferon gamma (Hu-IFN-gamma) as assayed by class I HLA induction ; it is necessary for both human chromosomes 6 and 21 to reside in the hybrid to generate a response to Hu-IFN-gamma. Treatment of such a hamster-human hybrid, Q72-18, with Hu-IFN-gamma induces the class I HLA antigens. Q72-18 cells selected by fluorescence-activated cell sorting for the loss of class I HLA induction also lost human chromosome 21. Fusions of such cells to a hybrid that contains only human chromosome 21 reconstitutes HLA antigen induction by Hu-IFN-gamma. Furthermore, fusions of hybrids containing a translocated human chromosome 6q and the HLA-B7 gene to a line containing only human chromosome 21 or a translocated 21q also reconstitutes HLA-B7 mRNA and antigen induction by Hu-IFN-gamma. Thus the segregation of cells on the basis of a biological effect by fluorescence-activated cell sorting and reconstitution by hybrid fusion provides a strategy by which some biological pathways can be mapped at a chromosomal level.

Kalo A, Segal E, Sahar E, Dayan D (1988) Interaction of Candida albicans with genital mucosal surfaces : involvement of fibronectin in adherence. J Infect Dis 157 :1253-1256


Kaufman SJ, Foster RF (1988) Replicating myoblasts express a muscle-specific phenotype. Proc Natl Acad Sci U S A 85 :9606-9610


During the terminal stage of skeletal myogenesis, myoblasts stop replicating, fuse to form multinucleate fibers, and express the genes that encode the proteins that convey contractile capacity. Because of this dramatic shift in proliferative state, morphology, and gene expression, it has been possible to readily identify and quantitate terminally differentiating myoblasts. In contrast, it is not clear whether the proliferating cells that give rise to postmitotic myoblasts are equally distinct in their phenotype and in fact whether distinct stages in skeletal myogenesis precede the onset of terminal differentiation. To address these questions, monoclonal antibodies and immunofluorescence microscopy were used to determine that replicating myoblasts from newborn rats do express a muscle-specific phenotype. To identify replicating cells, incorporation of 5-bromo-2’-deoxyuridine (BrdUrd) into DNA was assayed by using anti-BrdUrd antibody. The developmentally regulated, muscle-specific, integral membrane protein H36 and the intermediate-filament protein desmin were scored as markers of the myogenic phenotype. The percentage of BrdUrd+ (i.e., proliferative) cells among H36+ and desmin+ myoblasts was equal to the percentage of BrdUrd+ cells in the entire population, indicating that the expression of H36 and desmin is uniformly characteristic of replicating myoblasts. Inhibition of protein synthesis before and during growth in BrdUrd did not alter the frequency of desmin and H36 immunofluorescence in BrdUrd+ cells. Thus, desmin and H36 were present in the replicating myoblasts prior to the onset of growth in BrdUrd. These results were confirmed using H36+ cells selected by flow cytometry : these purified H36+ myoblasts replicate, express desmin, and differentiate. Similar results were obtained with mouse myoblasts. Desmin expression in these mammalian cells differs from that in chicken embryo myoblasts : only a small proportion of replicating chicken embryo myoblasts express desmin. That replicating mammalian myoblasts have a muscle-specific phenotype serves to define a distinct stage in myogenic development and a specific cell in the myogenic lineage. Further, it implies that there is a regulatory event activated during myogenesis that precedes terminal differentiation and that is required for expression of those genes whose products distinguish the replicating myoblast.

Kawaguchi S (1988) Reactivity of mouse antibodies against bromelain-treated mouse erythrocytes with various mouse cells before and after protease treatment. Int Arch Allergy Appl Immunol 86 :458-461


A mouse monoclonal antibody against bromelain-treated mouse erythrocytes (BrMRBC) was conjugated with fluorescein isothiocyanate. Various cells from the blood and lymphoid tissues of mice were stained before and after protease treatment with the fluorescent antibody. Without protease treatment, only the platelets were specifically, though dully, fluorescent. Protease treatment made all the erythrocytes, the majority of platelets, thymus and bone marrow cells and a small part of the spleen cells brightly fluorescent. The reactivity of the antibody with cells depended on the temperature, being stronger at 0 than at 37 degrees C. The present findings demonstrate that various mouse cells besides erythrocytes bear the epitopes for anti-BrMRBC antibodies in exposed or hidden form.

Maslow AS, Davis CH, Choong J, Wyrick PB (1988) Estrogen enhances attachment of Chlamydia trachomatis to human endometrial epithelial cells in vitro. Am J Obstet Gynecol 159 :1006-1014


Ultraviolet light-inactivated elementary bodies of Chlamydia trachomatis serovar E were fluorescently tagged with rhodamine isothiocyanate (5 micrograms/ml) and added to primary cultures of human endometrial gland epithelial cells. The elementary bodies, at a multiplicity of infection of 600:1, were allowed to adsorb to the cell monolayers for 1 hour at 35 degrees C in an atmosphere of 5% carbon dioxide. The monolayers were disaggregated by trypsinization and the individual cells were processed in the fluorescent activated cell sorter for chlamydial attachment. This method of analysis revealed attachment of C. trachomatis to approximately 50% of human endometrial gland epithelial cells. Addition of estrogen (10(-10) mol/L) to the culture medium enhanced chlamydial attachment to human endometrial gland epithelial cells to approximately 80% (p less than or equal to 0.005), and progesterone in combination with estrogen reduced chlamydial attachment in a dose-dependent fashion : 1 ng/ml progesterone, approximately 50% ; 5 ng/ml, about 30% ; 10 ng/ml, about 18%, respectively (p less than or equal to 0.025).

Minas W, Sahar E, Gutnick D (1988) Flow cytometric screening and isolation of Escherichia coli clones which express surface antigens of the oil-degrading microorganism Acinetobacter calcoaceticus RAG-1. Arch Microbiol 150 :432-437


Flow cytometry (FCM) in conjunction with immunocytochemical-labeling was used to analyze and screen a population of Escherichia coli clones containing a genomic library from the oil-degrading microorganism Acinetobacter calcoaceticus RAG-1 surface antigens. Reconstruction experiments using mixed populations indicated that RAG-1 cells could be clearly distinguished at a ratio of one RAG-1 cell to 500 Escherichia coli cells. Using this technique two clones, WM143 and WM191, were isolated and shown by restriction endonuclease cleavage and Southern hybridization to contain plasmids carrying inserts of RAG-1 DNA of 9.4 and 9.8 kb respectively.

Rose LM, Jackevicius SL, Clark EA (1988) Expression of leukocyte antigens on an oligodendroglial cell line. Ann N Y Acad Sci 540 :455-458


Smith MM, Stirling VB (1988) Histone H3 and H4 gene deletions in Saccharomyces cerevisiae. J Cell Biol 106 :557-566


The genome of haploid Saccharomyces cerevisiae contains two nonallelic sets of histone H3 and H4 genes. Strains with deletions of each of these loci were constructed by gene replacement techniques. Mutants containing deletions of either gene set were viable, however meiotic segregants lacking both histone H3 and H4 gene loci were inviable. In haploid cells no phenotypic expression of the histone gene deletions was observed ; deletion mutants had wild-type growth rates, were not temperature sensitive for growth, and mated normally. However, diploids homozygous for the H3-H4 gene deletions were slightly defective in their growth and cell cycle progression. The generation times of the diploid mutants were longer than wild-type cells, the size distributions of cells from exponentially growing cultures were skewed towards larger cell volumes, and the G1 period of the mutant cells was longer than that of the wild-type diploid. The homozygous deletion of the copy-II set of H3-H4 genes in diploids also increased the frequency of mitotic chromosome loss as measured using a circular plasmid minichromosome assay.

Tertti R, Eerola E, Granfors K, Lahesmaa-Rantala R, Pekkola-Heino K, Toivanen A (1988) Role of antibodies in the opsonization of Yersinia spp. Infect Immun 56 :1295-1300


We have determined the opsonic capacity of specific antibodies in patient sera obtained after Yersinia infection. The results indicate that Yersinia antibodies lead to complement activation through the classical pathway, thus overcoming the inhibition of complement-mediated opsonization in the absence of specific antibodies provided by the virulence plasmid in Yersinia enterocolitica and Yersinia pseudotuberculosis. Further, antibodies against plasmid-encoded structures, the Yersinia outer membrane proteins (YOPs), are not necessary in this effect. This is indicated by two facts. (i) Monoclonal antibodies directed against the O polysaccharide of Y. enterocolitica O:3 are capable of opsonizing the plasmid-containing bacteria through C1q binding. (ii) Rabbit antisera show opsonic activity when obtained by immunization both with plasmid-containing Y. enterocolitica expressing the YOPs and a plasmid-cured variant not expressing these proteins.

Toth TE, Veit H, Gross WB, Siegel PB (1988) Cellular defense of the avian respiratory system : protection against Escherichia coli airsacculitis by Pasteurella multocida-activated respiratory phagocytes. Avian Dis 32 :681-687


The concept of nonspecific cellular defense of the respiratory system of poultry against respiratory pathogens by "preventive activation" of avian respiratory phagocytes (ARPs) was tested in an in vivo protection trial. Chickens were stimulated intratracheally by Pasteurella multocida Choloral vaccine strain. Seven hours later, these and mock-inoculated control chickens were challenged with pathogenic Escherichia coli via the air-sac route. Stimulated chickens had a 25-fold-elevated number of ARPs compared with mock-inoculated control chickens. The proportion of active phagocytes and the phagocytic capacity of these cells was higher in the ARP populations of stimulated chickens than in the ARP populations of control chickens. In vivo protection against E. coli air-sac infection was demonstrated by reduction of morbidity and mortality rates, diminished weight loss, and lower scores of gross and histopathological lesions of P. multocida-stimulated chickens compared with mock-inoculated controls.

van Strijp JA, van Kessel KP, Miltenburg LA, Fluit AC, Verhoef J (1988) Attachment of human polymorphonuclear leukocytes to herpes simplex virus-infected fibroblasts mediated by antibody-independent complement activation. J Virol 62 :847-850


Herpes simplex virus (HSV)-infected cells can activate the human complement system without interference of specific anti-HSV antibodies. Analysis by flow cytometry showed that C3-like molecules were deposited on the membrane of the infected cell when incubated with human serum without specific antibodies. Depletion of calcium to block the classical pathway of the complement system had no effect on fluorescence intensity. The complement activation could be blocked by chelating both calcium and magnesium or by heating the serum. Furthermore, in the fluid phase C3 was converted to C3b by infected cells and not by uninfected cells. The antibody-independent activation did not lead to lysis of the virus-infected fibroblasts, indicating that the complement cascade is abrogated before formation of the membrane attack complex. This was also confirmed by measurement of the 50% hemolytic complement activities for total and alternative pathways. Polymorphonuclear leukocytes attached to infected fibroblasts after incubation of these fibroblasts with intact complement. This is most probably mediated by complement receptor binding of C3b and C3bi which is deposited on the membrane of the HSV-infected cell. Both type 1 and type 2 HSVs showed the same characteristics in complement activation and thereby mediated polymorphonuclear leukocyte adherence.