Heterogeneous host DNA attached to the left end of mature bacteriophage Mu DNA.
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Base Composition↗
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Results for “host attachment”
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Recognition and invasion of human erythrocytes by malarial parasites: contribution of sialoglycoproteins to attachment and host specificity.
The receptivity of human erythrocytes to invasion by Plasmodium falciparum merozoites can be decreased by neuraminidase or trypsin treatment, an observation that supports a role for the erythrocyte sialoglycoproteins (glycophorins) in invasion. We have found that alpha 1-acid glycoprotein (AGP), added to in vitro cultures, can restore invasion of enzyme-treated human erythrocytes. AGP is structurally different from the glycophorins although it does carry 12% sialic acid. Its ability to restore receptivity to desialylated cells is dependent on its sialic acid complement, its concentration, and its binding to the erythrocyte surface. We present evidence that AGP forms a bridge between the merozoite and the enzyme-treated erythrocyte that allows the stronger and more complex interactions of invasion to proceed. We suggest that the glycophorins play the same role on the surface of the intact erythrocyte.
Erythrocytes↗
Peptide, peptidomimetic and small-molecule drug discovery targeting HIV-1 host-cell attachment and entry through gp120, gp41, CCR5 and CXCR4.
This review highlights selected examples of peptide, peptidomimetic and small-molecule drug discovery targeting HIV-1 to advance novel anti-HIV pharmaceuticals that inhibit initial stages of the viral cycle; namely, attachment and entry. Some of these approaches have culminated in the development of peptide-based drugs, while other have exploited peptides as enabling tools toward the identification of small-molecule lead compounds. Both of these conceptually different approaches have facilitated lead optimization of molecules with complementary and often surprising anti-HIV pharmacological properties, supporting their role in pharmaceutical development. Furthermore, such molecules enabled mechanistic elucidation of viral attachment and entry and provided additional insights toward achieving the desired drug profile.
Amino Acid Sequence↗
Consequences of microbial attachment: directing host cell functions with adhesins.
We take the view that adherence is not just a static process of holding hands but rather elicits a response in the targeted cell. From this point of view, adherence is an active process with an outcome. This outcome or fate is predictable only when several parameters of the host cell-adhesin interaction are known: is the adhesin acting alone or in series with other products, is the receptor up- or down-regulated at the time of ligation, which domain of the receptor is bound, and finally, which intracellular response circuits are connected to the receptor in the cell type targeted? Variations in these parameters are the basis for the ability of the adhesins of pathogens to orchestrate outcomes as disparate as simple address recognition versus actin nucleation, cytokine induction, activation of plasmin, derangement of leukocyte migration, or deposition of antibody on host cell membranes. The recognition of the relatedness of some eukaryotic and prokaryotic adhesive domains and the shared use of existing eukaryotic cell-cell interaction systems between host and pathogen suggest that the cellular interactions of interest in eukaryotic cell biology can be revealed by taking clues from the pathogens, which have studied and adapted to them the longest.
Animals↗
beta1-chain integrins are not essential for intimin-mediated host cell attachment and enteropathogenic Escherichia coli-induced actin condensation.
Intimin is a bacterial outer membrane protein required for intimate attachment of enterohemorrhagic and enteropathogenic Escherichia coli (EHEC and EPEC) to mammalian cells. beta1-chain integrins have been proposed as candidate receptors for intimin. We found that binding of mammalian cells to immobilized intimin was not detectable unless mammalian cells were preinfected with EPEC or EHEC. beta1-chain integrin antagonists or inactivation of the gene encoding the beta1-chain did not affect binding of preinfected mammalian cells to intimin or the actin condensation associated with the attachment of EPEC. The results indicate that beta1-chain integrins are not essential for intimin-mediated cell attachment or EPEC-mediated actin polymerization.
Actins↗
Nucleotide sequences involved in the neolysogenic insertion of filamentous phage Cf16-v1 into the Xanthomonas campestris pv. citri chromosome.
Following a protracted carrier state in the infected cell, filamentous bacteriophage Cf16-v1 neolysogenizes Xanthomonas campestris pv. citri by inserting the phage genome into the host chromosome. The integration region in the phage and the host chromosome, respectively, and the two junctions in the lysogen chromosome were isolated and their nucleotide sequence was determined. The phage and host attachment sites shared an identical 15-bp "core," 5'-TATACATTATGCGAA-3'. Located on either side of each core were two unique arm sequences. Each of the two phage-host junctions contained an intact core flanked by a hybrid combination of phage and host arm sequences. A 10-bp symmetrical sequence arranged as inverted repeats with 1-bp spacing straddled the core sequence. A 10-bp repeated sequence, 5'-GCGCTATGGC-3', was found distal to the core in opposite orientation at the phage attachment site, while an abbreviated form of this sequence was present in the host attachment site. These sequence characteristics indicate that neolysogenic insertion of Cf16-v1 was accomplished by a site-specific recombination mechanism similar to lambda integration. However, in contrast to lambda, the phage and the host attachment sites in the Cf16-v1 system contained a high G + C nucleotide bias (except for the core sequence itself).
Bacteriophages↗
Mechanism of C. trachomatis attachment to eukaryotic host cells.
A novel trimolecular mechanism of microbial attachment to mammalian host cells was characterized for the obligate intracellular pathogen Chlamydia trachomatis. Using purified glycosaminoglycans (GAGs) and specific GAG lyases, we demonstrated that a heparan sulfate-like GAG present on the surface of chlamydia organisms is required for attachment to host cells. These observations were supported by inhibition of attachment following binding of heparan sulfate receptor analogs to chlamydiae and by demonstrating that chlamydiae synthesize a unique heparan sulfate-like GAG. Furthermore, exogenous heparan sulfate, as an adhesin analog, restored attachment and infectivity to organisms that had lost these attributes following treatment with heparan sulfate lyase. These data suggest that a GAG adhesin ligand mediates attachment by bridging mutual GAG receptors on the host cell surface and on the chlamydial outer membrane surface.
Animals↗
Host-finding in Trichobilharzia ocellata cercariae: swimming and attachment to the host.
The cercaria of Trichobilharzia ocellata finds and identifies its duck host with a series of different behavioural phases. Dispersal and selection of the water surface as microhabitat is achieved by an intermittent swimming behaviour, which is governed by the interplay of passive dropping with forward and backward swimming movements and includes a positive phototactic and a geonegative orientation. Then the cercariae tend to cling to the water surface in an energy-saving resting position. A movement towards the duck feet as the site of entry occurs when shadows evoke forward swimming movements, which are directed away from the source of light, i.e. normally downwards. Forward swimming movements are also stimulated by touch, but only in free-swimming cercariae and not when these are in the resting position. Attachments occur only when a substrate is touched during forward swimming movements. Attachments are stimulated by warm substrates (1 degrees C temperature difference triggers a nearly maximal response) and by chemical components of duck-foot skin, and the readiness to attach is increased when the forward swimming movement is started by shadow stimuli.
Animals↗
Interchangeability of the adsorption proteins of bacteriophages Ff and IKe.
The wild-type adsorption protein (g3p) of filamentous phage IKe cannot be exchanged with its analogous protein in the related Ff (M13, fd, and f1) phage particles. Deletion mutants of the protein, however, are assembled into Ff phage particles. These hybrid Ff phage particles bearing deleted IKe g3p attach to N pili, thus conserving the host attachment property of the protein but not its infection-initiating function. This means that the attachment specificity is determined by IKe g3p independently of other phage components in contact with it. Infection initiation function, the process in which phage DNA is released into the host, in contrast seems to require either more complex structural features of the protein (for example, a certain oligomeric structure) provided only in the original particle, or a concerted action of g3p with another particle component, not replaceable by its homologous counterpart in the related phage.
Amino Acid Sequence↗
Characterization of phi8, a bacteriophage containing three double-stranded RNA genomic segments and distantly related to Phi6.
The three double-stranded RNA genomic segments of bacteriophage Phi8 were copied as cDNA, and their nucleotide sequences were determined. Although the organization of the genome is similar to that of Phi6, there is no similarity in either the nucleotide sequences or the amino acid sequences, with the exception of the motifs characteristic of viral RNA polymerases that are found in the presumptive polymerase sequence. Several features of the viral proteins differ markedly from those of Phi6. Although both phages are covered by a lipid-containing membrane, the protein compositions are very different. The most striking difference is that protein P8, which constitutes a shell around the procapsid in Phi6, is part of the membrane in Phi8. The host attachment protein consists of two peptides rather than one and the phage attaches directly to the lipopolysaccharide of the host rather than to a type IV pilus. The host range of Phi8 includes rough strains of Salmonella typhimurium and of pseudomonads
Amino Acid Motifs↗
A mechanism for inducing plant development: the genesis of a specific inhibitor.
Parasitic strategies are widely distributed in the plant kingdom and frequently involve coupling parasite organogenesis with cues from the host. In Striga asiatica, for example, the cues that initiate the development of the host attachment organ, the haustorium, originate in the host and trigger the transition from vegetative to parasitic mode in the root meristem. This system therefore offers a unique opportunity to study the signals and mechanisms that control plant cell morphogenesis. Here we establish that the biological activity of structural analogs of the natural inducer displays a marked dependence on redox potential and suggest the existence of a semiquinone intermediate. Building on chemistry that exploits the energetics of such an intermediate, cyclopropyl-p-benzoquinone (CPBQ) is shown to be a specific inhibitor of haustorial development. These data are consistent with a model where haustorial development is initiated by the completion of a redox circuit.
Journal Article↗
The effects of temperature, relative humidity and host factors on the attachment and survival of Boophilus decoloratus and Boophilus geigyi larvae to skin slices.
Attachment and survival of Boophilus decoloratus and B. geigyi larvae were examined using skin slices from cattle, sheep and goats. Results indicate that B. decoloratus has a wider range of temperature (24-40 degrees C) at which more than 50% of larvae would attach to bovine skin, while B. geigyi has a narrower range (24-30 degrees C). The larvae of both species had two peaks of attachment--the 4th and 20th hour, the value for the second peak being greater than the first. The influence of humidity on larval attachment was only apparent where the temperature was high, and in such cases more than 70% of B. decoloratus larvae attached, while less than 20% of B. geigyi larvae attached by the 20th hour. Less than 50% of larval attachment was recorded on both sheep and goats. The results are related to the geographical distribution of both species in Nigeria, and to the problems of tick water balance, stimuli for tick attachment and host specificity.
Animals↗
Integrins alpha(v)beta3 and alpha5beta1 mediate attachment of lyme disease spirochetes to human cells.
Borrelia burgdorferi (sensu lato), the agent of Lyme disease, is able to cause chronic, multisystemic infections in human and animal hosts. Attachment of the spirochete to host cells is likely to be important for the colonization of diverse tissues. The platelet-specific integrin alpha(IIb)beta3 was previously identified as a receptor for all three species of Lyme disease spirochetes (B. burgdorferi sensu stricto, B. garinii, and B. afzelii). Here we show that B. burgdorferi also recognizes the widely expressed integrins alpha(v)beta3 and alpha5beta1, known as the vitronectin and fibronectin receptors, respectively. Three representatives of each species of Lyme disease spirochete were tested for the ability to bind to purified alpha(v)beta3 and alpha5beta1. All of the strains tested bound to at least one integrin. Binding to one integrin was not always predictive of binding to other integrins, and several different integrin preference profiles were identified. Attachment of the infectious B. burgdorferi strain N40 to purified alpha(v)beta3 and alpha5beta1 was inhibited by RGD peptides and the appropriate receptor-specific antibodies. Binding to alpha(v)beta3 was also shown by using a transfected cell line that expresses this receptor but not alpha(IIb)beta3. Attachment of B. burgdorferi N40 to human erythroleukemia cells and to human saphenous vein endothelial cells was mediated by both alpha5beta1 and alpha(v)beta3. Our results show that multiple integrins mediate attachment of Lyme disease spirochetes to host cells.
Bacterial Adhesion↗
Attachment sites and frequency distribution of erythraeid mites, Leptus indianensis (Acari: Prostigmata), ectoparasitic on harvestmen, Leiobunum formosum (Opiliones).
Host attachment sites and frequency distribution of parasitism were investigated for the larval erythraeid mite Leptus indianensis parasitising a sample of 500 harvestmen. Leiobunum formosum in Tennessee, USA. A significant difference was found in the number of mites attached to different body segments of the harvestmen with the greatest number of mites attached to femurs I-IV. Scanning electron microscopy revealed that the mites attached to smooth areas of the host integument between rows of stout setae. The frequency distribution of mites parasitising the harvestman population was highly clumped (Coefficient of Dispersion = 3.34) with a relatively small number of hosts being parasitised by most of the mites.
Animals↗
Integrated regulatory responses of fimB to N-acetylneuraminic (sialic) acid and GlcNAc in Escherichia coli K-12.
Bacterial-host attachment by means of bacterial adhesins is a key step in host colonization. Phase variation (reversible on-off switching) of the type 1 fimbrial adhesin of Escherichia coli involves a DNA inversion catalyzed by FimB (switching in either direction) or FimE (mainly on-to-off switching). fimB is separated from the divergent yjhATS operon by a large (1.4 kbp) intergenic region. Short ( approximately 28 bp) cis-active elements (regions 1 and 2) close to yjhA stimulate fimB expression and are required for sialic acid (Neu(5)Ac) sensitivity of its expression [El-Labany, S., Sohanpal, B. K., Lahooti, M., Akerman, R. & Blomfield, I. C. (2003) Mol. Microbiol. 49, 1109-1118]. Here, we show that whereas NanR, a sialic acid-response regulator, binds to region 1, NagC, a GlcNAc-6P-responsive protein, binds to region 2 instead. The NanR- and NagC-binding sites lie adjacent to deoxyadenosine methylase (Dam) methylation sites (5'-GATC) that are protected from modification, and the two regulators are shown to be required for methylation protection at regions 1 and 2, respectively. Mutations in nanR and nagC diminish fimB expression, and both fimB expression and FimB recombination are inhibited by GlcNAc (3- and >35-fold, respectively). Sialic acid catabolism generates GlcNAc-6-P, and whereas GlcNAc disrupts methylation protection by NagC alone, Neu(5)Ac inhibits the protection mediated by both NanR and NagC as expected. Type 1 fimbriae are proinflammatory, and host defenses enhance the release of both Neu(5)Ac and GlcNAc by a variety of mechanisms. Inhibition of type 1 fimbriation by these amino sugars may thus help balance the interaction between E. coli and its hosts.
Acetylglucosamine↗
Pleiotropic costs of niche expansion in the RNA bacteriophage phi 6.
Natural and experimental systems have failed to universally demonstrate a trade-off between generalism and specialism. When a trade-off does occur it is difficult to attribute its cause to antagonistic pleiotropy without dissecting the genetic basis of adaptation, and few previous experiments provide these genetic data. Here we investigate the evolution of expanded host range (generalism) in the RNA virus phi6, an experimental model system allowing adaptive mutations to be readily identified. We isolated 10 spontaneous host range mutants on each of three novel Pseudomonas hosts and determined whether these mutations imposed fitness costs on the standard laboratory host. Sequencing revealed that each mutant had one of nine nonsynonymous mutations in the phi6 gene P3, important in host attachment. Seven of these nine mutations were costly on the original host, confirming the existence of antagonistic pleiotropy. In addition to this genetically imposed cost, we identified an epigenetic cost of generalism that occurs when phage transition between host types. Our results confirm the existence in phi6 of two costs of generalism, genetic and environmental, but they also indicate that the cost is not always large. The possibility for cost-free niche expansion implies that varied ecological conditions may favor host shifts in RNA viruses.
Adaptation, Physiological↗
Attachment of Toxoplasma gondii to host cells involves major surface protein, SAG-1 (P30).
Previous observations have demonstrated that monoclonal and polyclonal antibodies directed at SAG-1, the major surface protein of Toxoplasma gondii, decreased the number of T. gondii that infected fibroblast monolayers. Direct evaluation of parasite-host cell attachment using glutaraldehyde-fixed human fibroblasts and live tachyzoites was performed to determine whether SAG-1 was a ligand for the host cell receptor. The interaction between the fixed cells and T. gondii was specific and saturable as determined by a radioisotope competitive binding assay. Moreover, the specificity of this interaction was confirmed by comparison to another member of the Apicomplexa, Besnoitia jellisoni. Treatment of fresh extracellular T. gondii with rabbit polyclonal anti-SAG-1 serum inhibited parasite attachment to host cells by 71%. A monoclonal antibody (6A8) directed at SAG-1 was able to inhibit parasite binding to fixed host cells by 65%. Other mAb's directed at SAG-1 failed to inhibit parasite attachment in this assay. Fab derived from 6A8 mAb showed dose-dependent inhibition of parasite attachment. At an Fab concentration of 25 micrograms/ml, 47% inhibition was observed. Attachment assays using mutant parasites with defective SAG-1 (PTgA and PTgC) showed significantly reduced binding (26 and 39%) when compared to wild-type (SAG-1+) parentals. Taken together, these observations suggest that SAG-1 is an important parasite ligand that binds to the host cell in the process of T. gondii invasion.
Animals↗
A role for host phosphoinositide 3-kinase and cytoskeletal remodeling during Cryptosporidium parvum infection.
Cryptosporidium parvum preferentially infects epithelial cells lining the intestinal mucosa of mammalian hosts. Parasite development and propagation occurs within a unique intracellular but extracytoplasmic parasitophorous vacuole at the apical surface of infected cells. Parasite-induced host cell signaling events and subsequent cytoskeletal remodeling were investigated by using cultured bovine fallopian tube epithelial (BFTE) cells inoculated with C. parvum sporozoites. Indirect-immunofluorescence microscopy detected host tyrosine phosphorylation within 30 s of inoculation. At >30 min postinoculation, actin aggregates were detected at the site of parasite attachment by fluorescein isothiocyanate-conjugated phalloidin staining as well as by indirect immunolabeling with monoclonal anti-actin. The actin-binding protein villin was also detected in focal aggregates at the site of attachment. Host cytoskeletal rearrangement persisted for the duration of the parasitophorous vacuole and contributed to the formation of long, branched microvilli clustered around the cryptosporidial vacuole. The phosphoinositide 3-kinase inhibitor wortmannin significantly inhibited (P < 0.05) C. parvum infection when BFTE cells were pretreated for 60 min at 37 degreesC prior to inoculation. Similarly, treatment of BFTE cells with the protein kinase inhibitors genistein and staurosporine and the cytoskeletally acting compounds 1-(5-iodonaphthalene-1-sulfonyl)-1H-hexahydro-1,4-diazapine, cytochalasin D, and 2,3-butanedione monoxime significantly inhibited (P < 0.05) in vitro infection at 24 h postinoculation. These findings demonstrate a prominent role for phosphoinositide 3-kinase activity during the early C. parvum infection process and suggest that manipulation of host signaling pathways results in actin rearrangement at the site of sporozoite attachment.
Animals↗