Relevant bibliographies by topics / Neuraminidase

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
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Academic literature on the topic 'Neuraminidase'

Author: Grafiati
Published: 4 June 2021
Last updated: 6 September 2023

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Journal articles on the topic "Neuraminidase"

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Hammond, Alexandria J., Ulrike Binsker, Surya D. Aggarwal, Mila Brum Ortigoza, Cynthia Loomis, and Jeffrey N. Weiser. "Neuraminidase B controls neuraminidase A-dependent mucus production and evasion." PLOS Pathogens 17, no. 4 (April 5, 2021): e1009158. http://dx.doi.org/10.1371/journal.ppat.1009158.

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Binding of Streptococcus pneumoniae (Spn) to nasal mucus leads to entrapment and clearance via mucociliary activity during colonization. To identify Spn factors allowing for evasion of mucus binding, we used a solid-phase adherence assay with immobilized mucus of human and murine origin. Spn bound large mucus particles through interactions with carbohydrate moieties. Mutants lacking neuraminidase A (nanA) or neuraminidase B (nanB) showed increased mucus binding that correlated with diminished removal of terminal sialic acid residues on bound mucus. The non-additive activity of the two enzymes raised the question why Spn expresses two neuraminidases and suggested they function in the same pathway. Transcriptional analysis demonstrated expression of nanA depends on the enzymatic function of NanB. As transcription of nanA is increased in the presence of sialic acid, our findings suggest that sialic acid liberated from host glycoconjugates by the secreted enzyme NanB induces the expression of the cell-associated enzyme NanA. The absence of detectable mucus desialylation in the nanA mutant, in which NanB is still expressed, suggests that NanA is responsible for the bulk of the modification of host glycoconjugates. Thus, our studies describe a functional role for NanB in sialic acid sensing in the host. The contribution of the neuraminidases in vivo was then assessed in a murine model of colonization. Although mucus-binding mutants showed an early advantage, this was only observed in a competitive infection, suggesting a complex role of neuraminidases. Histologic examination of the upper respiratory tract demonstrated that Spn stimulates mucus production in a neuraminidase-dependent manner. Thus, an increase production of mucus containing secretions appears to be balanced, in vivo, by decreased mucus binding. We postulate that through the combined activity of its neuraminidases, Spn evades mucus binding and mucociliary clearance, which is needed to counter neuraminidase-mediated stimulation of mucus secretions.
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Jost, B. H., J. G. Songer, and S. J. Billington. "Cloning, Expression, and Characterization of a Neuraminidase Gene from Arcanobacterium pyogenes." Infection and Immunity 69, no. 7 (July 1, 2001): 4430–37. http://dx.doi.org/10.1128/iai.69.7.4430-4437.2001.

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ABSTRACT Arcanobacterium pyogenes is an opportunistic pathogen, associated with suppurative infections in domestic animals. In addition to pyolysin, a pore-forming, cholesterol-binding toxin,A. pyogenes expresses a number of putative virulence factors, including several proteases and neuraminidase activity. A 3,009-bp gene, nanH, was cloned and sequenced and conferred neuraminidase activity on an Escherichia colihost strain. The predicted 107-kDa NanH protein displayed similarity to a number of bacterial neuraminidases and contained the RIP/RLP motif and five copies of the Asp box motif found in all bacterial neuraminidases. Recombinant His-tagged NanH was found to have pH and temperature optima of 5.5 to 6.0 and 55°C, respectively. Insertional deletion of the nanH gene resulted in the reduction, but not absence, of neuraminidase activity, indicating the presence of a second neuraminidase gene in A. pyogenes. NanH was localized to the A. pyogenes cell wall. A. pyogenes adhered to HeLa, CHO, and MDBK cells in a washing-resistant manner. However, the nanH mutant was not defective for adherence to epithelial cells. The role of NanH in host epithelial cell adherence may be masked by the presence of a second neuraminidase in A. pyogenes.
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Manco, Sonia, Fidelma Hernon, Hasan Yesilkaya, James C. Paton, Peter W. Andrew, and Aras Kadioglu. "Pneumococcal Neuraminidases A and B Both Have Essential Roles during Infection of the Respiratory Tract and Sepsis." Infection and Immunity 74, no. 7 (July 2006): 4014–20. http://dx.doi.org/10.1128/iai.01237-05.

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ABSTRACT We examined the role of the neuraminidases NanA and NanB in colonization and infection in the upper and lower respiratory tract by Streptococcus pneumoniae, as well as the role of these neuraminidases in the onset and development of septicemia following both intranasal and intravenous infection. We demonstrated for the first time using outbred MF1 mouse models of infection that both NanA and NanB were essential for the successful colonization and infection of the upper and lower respiratory tract, respectively, as well as pneumococcal survival in nonmucosal sites, such as the blood. Our studies have shown that in vivo a neuraminidase A mutant is cleared from the nasopharynx, trachea, and lungs within 12 h postinfection, while a neuraminidase B mutant persists but does not increase in either the nasopharynx, trachea, or lungs. We also demonstrated both neuraminidase mutants were unable to cause sepsis following intranasal infections. When administered intravenously, however, both mutants survived initially but were unable to persist in the blood beyond 48 h postinfection and were progressively cleared. The work presented here demonstrates the importance of pneumococcal neuraminidase A and for the first time neuraminidase B in the development of upper and lower respiratory tract infection and sepsis.
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Jost, B. Helen, J. Glenn Songer, and Stephen J. Billington. "Identification of a Second Arcanobacterium pyogenes Neuraminidase and Involvement of Neuraminidase Activity in Host Cell Adhesion." Infection and Immunity 70, no. 3 (March 2002): 1106–12. http://dx.doi.org/10.1128/iai.70.3.1106-1112.2002.

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ABSTRACT Arcanobacterium pyogenes, a common inhabitant of the upper respiratory and urogenital tracts of economically important animals, such as cattle and swine, is also an opportunistic pathogen associated with suppurative infections in these animals. A. pyogenes expresses neuraminidase activity encoded by the nanH gene, and previously, construction of a nanH mutant of A. pyogenes BBR1 indicated that a second neuraminidase is present in this strain. A 5,112-bp gene, nanP, was cloned and sequenced, and this gene conferred neuraminidase activity on an Escherichia coli host strain. The predicted 186.8-kDa NanP protein exhibited similarity to a number of bacterial neuraminidases and contained the RIP/RLP motif and five copies of the Asp box motif found in all bacterial neuraminidases. As expected, insertional inactivation of the nanP gene in A. pyogenes BBR1 resulted in a mutant with reduced neuraminidase activity. However, insertional inactivation of the nanP gene in the nanH mutant strain resulted in a complete lack of neuraminidase activity. Like NanH, NanP was localized to the A. pyogenes cell wall. However, unlike the nanH gene, which was present in 100% of the strains examined, nanP was present in only 64.2% of the isolates (n = 53). A. pyogenes adheres to HeLa cells, and a nanP mutant displayed a wild-type adhesion phenotype with these cells. In contrast, the ability of a nanH nanP double mutant to bind to HeLa cells was reduced by 53%. The wild-type adhesion phenotype was restored by providing nanP in trans. These data indicate that the neuraminidases of A. pyogenes play a role in adhesion of this organism to host epithelial cells.
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Teuton, Jeremy R., and Curtis R. Brandt. "Sialic Acid on Herpes Simplex Virus Type 1 Envelope Glycoproteins Is Required for Efficient Infection of Cells." Journal of Virology 81, no. 8 (January 17, 2007): 3731–39. http://dx.doi.org/10.1128/jvi.02250-06.

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ABSTRACT Herpes simplex virus type 1 (HSV-1) envelope proteins are posttranslationally modified by the addition of sialic acids to the termini of the glycan side chains. Although gC, gD, and gH are sialylated, it is not known whether sialic acids on these envelope proteins are functionally important. Digestion of sucrose gradient purified virions for 4 h with neuraminidases that remove both α2,3 and α2,6 linked sialic acids reduced titers by 1,000-fold. Digestion with a α2,3-specific neuraminidase had no effect, suggesting that α2,6-linked sialic acids are required for infection. Lectins specific for either α2,3 or α2,6 linkages blocked attachment and infection to the same extent. In addition, the mobility of gH, gB, and gD in sodium dodecyl sulfate-polyacrylamide gel electrophoresis gels was altered by digestion with either α2,3 specific neuraminidase or nonspecific neuraminidases, indicating the presence of both linkages on these proteins. The infectivity of a gC-1-null virus, ΔgC2-3, was reduced to the same extent as wild-type virus after neuraminidase digestion, and attachment was not altered. Neuraminidase digestion of virions resulted in reduced VP16 translocation to the nucleus, suggesting that the block occurred between attachment and entry. These results show for the first time that sialic acids on HSV-1 virions play an important role in infection and suggest that targeting virion sialic acids may be a valid antiviral drug development strategy.
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Baeza-Kallee, Nathalie, Raphaël Bergès, Victoria Hein, Stéphanie Cabaret, Jeremy Garcia, Abigaëlle Gros, Emeline Tabouret, Aurélie Tchoghandjian, Carole Colin, and Dominique Figarella-Branger. "Deciphering the Action of Neuraminidase in Glioblastoma Models." International Journal of Molecular Sciences 24, no. 14 (July 19, 2023): 11645. http://dx.doi.org/10.3390/ijms241411645.

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Glioblastoma (GBM) contains cancer stem cells (CSC) that are resistant to treatment. GBM CSC expresses glycolipids recognized by the A2B5 antibody. A2B5, induced by the enzyme ST8 alpha-N-acetyl-neuraminide alpha-2,8-sialyl transferase 3 (ST8Sia3), plays a crucial role in the proliferation, migration, clonogenicity and tumorigenesis of GBM CSC. Our aim was to characterize the resulting effects of neuraminidase that removes A2B5 in order to target GBM CSC. To this end, we set up a GBM organotypic slice model; quantified A2B5 expression by flow cytometry in U87-MG, U87-ST8Sia3 and GBM CSC lines, treated or not by neuraminidase; performed RNAseq and DNA methylation profiling; and analyzed the ganglioside expression by liquid chromatography–mass spectrometry in these cell lines, treated or not with neuraminidase. Results demonstrated that neuraminidase decreased A2B5 expression, tumor size and regrowth after surgical removal in the organotypic slice model but did not induce a distinct transcriptomic or epigenetic signature in GBM CSC lines. RNAseq analysis revealed that OLIG2, CHI3L1, TIMP3, TNFAIP2, and TNFAIP6 transcripts were significantly overexpressed in U87-ST8Sia3 compared to U87-MG. RT-qPCR confirmed these results and demonstrated that neuraminidase decreased gene expression in GBM CSC lines. Moreover, neuraminidase drastically reduced ganglioside expression in GBM CSC lines. Neuraminidase, by its pleiotropic action, is an attractive local treatment against GBM.
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Stadlbauer, Daniel, Xueyong Zhu, Meagan McMahon, Jackson S. Turner, Teddy J. Wohlbold, Aaron J. Schmitz, Shirin Strohmeier, et al. "Broadly protective human antibodies that target the active site of influenza virus neuraminidase." Science 366, no. 6464 (October 24, 2019): 499–504. http://dx.doi.org/10.1126/science.aay0678.

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Better vaccines against influenza virus are urgently needed to provide broader protection against diverse strains, subtypes, and types. Such efforts are assisted by the identification of novel broadly neutralizing epitopes targeted by protective antibodies. Influenza vaccine development has largely focused on the hemagglutinin, but the other major surface antigen, the neuraminidase, has reemerged as a potential target for universal vaccines. We describe three human monoclonal antibodies isolated from an H3N2-infected donor that bind with exceptional breadth to multiple different influenza A and B virus neuraminidases. These antibodies neutralize the virus, mediate effector functions, are broadly protective in vivo, and inhibit neuraminidase activity by directly binding to the active site. Structural and functional characterization of these antibodies will inform the development of neuraminidase-based universal vaccines against influenza virus.
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Mohan, Sankar, and B. Mario Pinto. "Exploration of the 150 cavity and the role of serendipity in the discovery of inhibitors of influenza virus A neuraminidase." Canadian Journal of Chemistry 96, no. 2 (February 2018): 91–101. http://dx.doi.org/10.1139/cjc-2017-0343.

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Influenza pandemics are an ongoing threat for the human population, as the avian influenza viruses H5N1 and H7N9 continue to circulate in the bird population and the chance of avian to human transmission increases. Neuraminidase, a glycoprotein located on the surface of the influenza virus, plays a crucial role in the viral replication process and, hence, has proven to be a useful target enzyme for the treatment of influenza infections. The discovery that certain subtypes of influenza neuraminidase have an additional cavity, the 150 cavity, near the substrate binding site has triggered considerable interest in the design of influenza inhibitors that exploit this feature. Currently available antiviral drugs, neuraminidase inhibitors oseltamivir and zanamivir, were designed using crystal structures predating this discovery by some years. This mini review is aimed at summarizing our group’s efforts, together with related work from other groups, on neuraminidase inhibitors that are designed to exploit both the catalytic site and the 150 cavity. The design of a parent scaffold that yields a potent inhibitor that is active in cell culture assays and retains activity against several neuraminidases from mutant strains is also described. Finally, the role of serendipity in the discovery of a new class of potent neuraminidase inhibitors with a novel spirolactam scaffold is also highlighted.
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Zhang, Jun-Yuan, Qian-Qian Chen, Jia Li, Lei Zhang, and Lian-Wen Qi. "Neuraminidase 1 and its Inhibitors from Chinese Herbal Medicines: An Emerging Role for Cardiovascular Diseases." American Journal of Chinese Medicine 49, no. 04 (January 2021): 843–62. http://dx.doi.org/10.1142/s0192415x21500403.

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Neuraminidase, also known as sialidase, is ubiquitous in animals and microorganisms. It is predominantly distributed in the cell membrane, cytoplasmic vesicles, and lysosomes. Neuraminidase generally recognizes the sialic acid glycosidic bonds at the ends of glycoproteins or glycolipids and enzymatically removes sialic acid. There are four types of neuraminidases, named as Neu1, Neu2, Neu3, and Neu4. Among them, Neu1 is the most abundant in mammals. Recent studies have revealed the involvement of Neu1 in several diseases, including cardiovascular diseases, diabetes, cancers, and neurological disorders. In this review, we center the attention to the role of Neu1 in cardiovascular diseases, including atherosclerosis, ischemic myocardial injury, cerebrovascular disease, congenital heart disease, and pulmonary embolism. We also summarize inhibitors from Chinese herbal medicines (CHMs) in inhibiting virus neuraminidase or human Neu1. Many Chinese herbs and Chinese herb preparations, such as Lonicerae Japonicae Flos, Scutellariae Radix, Yupingfeng San, and Huanglian Jiedu Decoction, have neuraminidase inhibitory activity. We hope to highlight the emerging role of Neu1 in humans and potentially titillate interest for further studies in this area.
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Hall, B. F., P. Webster, A. K. Ma, K. A. Joiner, and N. W. Andrews. "Desialylation of lysosomal membrane glycoproteins by Trypanosoma cruzi: a role for the surface neuraminidase in facilitating parasite entry into the host cell cytoplasm." Journal of Experimental Medicine 176, no. 2 (August 1, 1992): 313–25. http://dx.doi.org/10.1084/jem.176.2.313.

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Trypanosoma cruzi enters host cells via formation of an acidic vacuole which is subsequently disrupted, allowing the parasite access to the cytoplasm. We show that in an acid environment, release of the parasite surface neuraminidase is enhanced, and this release is likely mediated by a phosphatidylinositol-specific phospholipase C (PIPLC), since antibodies to a carbohydrate epitope (CRD) revealed in glycosylphosphatidylinositol (GPI)-anchored proteins after PIPLC cleavage remove the great majority of the soluble neuraminidase activity from culture supernatants. The neuraminidase is active at acidic pH, and is capable of desialylating known vacuolar constituents, i.e., lysosomal membrane glycoproteins. Parasite escape into the cytoplasm is significantly facilitated in terminal sialylation-defective mutant Lec 2 cells, and enzymatically desialylated membranes are more susceptible to lysis by a parasite hemolysin previously implicated in vacuole membrane rupture. These findings provide evidence that terminal sialylation on carbohydrate moieties contributes to maintaining lysosomal membrane integrity, and indicate a role for a protozoan-derived neuraminidase in facilitating parasite entry into host cells. These observations raise the possibility that other microbial neuraminidases may serve a similar function in acidic intracellular compartments.
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Dissertations / Theses on the topic "Neuraminidase"

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Wheatley, Nicola. "Mapping the haemagglutinin and neuraminidase functions of the human parainfluenza virus type 3 haemagglutinin-neuraminidase protein." Thesis, University of Ottawa (Canada), 1991. http://hdl.handle.net/10393/7739.

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The haemagglutinin-neuraminidase protein (HN) of human parainfluenza virus type 3 is a bifunctional protein. To map the functions to the protein, three truncations of the gene were constructed by digesting the HN gene with the restriction endonucleases Hind III, Bgl II or Xbo I and inserting a stop codon. An internal deletion using Rsa I was also constructed. The four mutants were expressed in the recombinant vaccinia virus system. The expression of the mutant proteins was analysed by both Western Blot and immunoprecipitation. The products of the three truncations migrated at the molecular weights predicted for the truncated proteins. The product of the internal deletion migrated more quickly than predicted and upon sequencing revealed a frame shift mutation and, therefore, a fourth truncation. The migration of the gene product was consistent with the molecular weight predicted for this truncation. The full length HN was functional in both haemagglutination and neuraminidase assays. The four mutants were active only in the neuraminidase assay, none of them haemagglutinated Guinea pig erythrocytes. This allows us to predict that the haemagglutination region is near the carboxy-terminus of the protein while the neuraminidase region is amino-terminal of amino acid 212.
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Driguez, Pierre-Alexandre. "Synthèse d'inhibiteurs de la neuraminidase grippale." Lyon 1, 1993. http://www.theses.fr/1993LYO10191.

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Les neuraminidases sont des enzymes (glycosidases) impliquees dans certaines pathologies d'origine bacterienne ou virale. En particulier, il est bien etabli que l'activite de la neuraminidase situee a la surface du virus de la grippe est indispensable a sa proliferation dans l'organisme infecte. Par ailleurs, elle pourrait etre a l'origine du declenchement d'une maladie auto-immune, la polyarthrite rhumatoide. Dans la mesure ou son site actif ne subit que peu ou pas de variations pendant les mutations du virus, des inhibiteurs selectifs de cette enzyme pourraient donc etre des medicaments potentiels pour ces maladies. Au cours de notre travail, nous avons synthetise plusieurs molecules inhibitrices de la neuraminidase grippale appartenant a deux familles d'inhibiteurs; des inhibiteurs de type etat de transition et des inhibiteurs suicides. Les inhibiteurs du premier type sont des analogues d'inhibiteurs connus des neuraminidases qui comportent une double liaison intracyclique. Celle-ci oblige la molecule a adopter une conformation proche de celle d'un intermediaire carbocationique de la reaction enzymo-catalysee, ce qui devrait leur conferer une grande affinite pour le site actif de cette enzyme. Nous avons prepare quatre molecules de ce type a partir de la n-acetylmannosamine ou du l-arabinose mais leurs activites inhibitrices se sont averees modestes ou moyennes. Deux inhibiteurs du deuxieme type ont ete synthetises a partir de l'acide n-acetylneuraminique commercial. Par analogie avec des inhibiteurs suicides recemment decrits dans la litterature pour des glucosidases, les molecules que nous avons preparees sont des substrats de l'enzyme cible qui generent, apres hydrolyse catalysee par la neuraminidase, une fluoroorthoquinone susceptible de desactiver l'enzyme par creation d'une liaison covalente avec un site nucleophile de cette derniere. Apres avoir determine que ces molecules sont bien des inhibiteurs de neuraminidases, leurs activites sur la proliferation du virus in vitro sont actuellement examinees. Des sequences d'acces a d'autres inhibiteurs potentiels de type etat de transition ou analogue du produit de la reaction ont egalement ete explorees. L'une d'entre elle devrait permettre d'obtenir prochainement la structure cible
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Horst, Gijsbertus Theodorus Johannes van der. "Identification and characterization of lysosomal neuraminidase." [S.l.] : Rotterdam : [The Author] ; Erasmus University [Host], 1993. http://hdl.handle.net/1765/13741.

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Wohlbold, Teddy John. "The Influenza Virus Neuraminidase as a Vaccine Antigen and the Potential of Neuraminidase Antibodies to Protect Against Infection." Thesis, Icahn School of Medicine at Mount Sinai, 2018. http://pqdtopen.proquest.com/#viewpdf?dispub=10746696.

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The influenza virus continues to cause significant morbidity and mortality in humans, resulting in up to 50,000 deaths per year in the United States. Annual vaccination remains the recommended prophylaxis for influenza. However, vaccines must be reformulated to account for antigenic drift and, even when vaccines contain strains that antigenically match circulating strains, they display suboptimal efficacies. Two glycoproteins coat the surface of the influenza virus – the more abundant and immunodominant hemagglutinin (HA), which serves as the receptor-binding protein, and the neuraminidase (NA), an enzyme that functions to free budding viruses from infected cells. Current influenza virus vaccine strategies aim to elicit neutralizing antibodies against the HA, but past studies have demonstrated that neuraminidase inhibition titers are correlated with reduced illness and viral shedding in humans. Despite the accumulated evidence that an anti-NA immune response is beneficial, the NA content in vaccines is not standardized.

Here, the potential breadth of protection afforded by NA antibodies was investigated by studying the use of NA as a vaccine antigen and by characterizing broadly cross-reactive murine monoclonal antibodies against the NA. Using baculovirus-expressed, purified protein, it was demonstrated that vaccination with adjuvanted NA was sufficient to induce protection against lethal influenza virus challenge in mice. In the same study, the N1 NA content of inactivated influenza virus vaccines from different companies was found to be highly variable. Furthermore, in humans vaccinated with standard inactivated influenza virus vaccine, the induction of serum NA titers was significantly lower than that of HA titers. In the second part of this dissertation, panels of monoclonal antibodies were generated against the N8 NA of an emerging H10N8 influenza virus strain and against the NA of influenza B virus. Monoclonal antibodies against the influenza B virus NA displayed in vivo prophylactic and therapeutic protection in mice, robustly activated antibody-dependent cellular cytotoxicity (ADCC) in vitro, and displayed neuraminidase inhibition against an oseltamivir-resistant influenza B virus. As a whole, our data strongly suggest that targeting the influenza virus NA may be beneficial when designing novel influenza virus vaccines or antibody-based therapeutics.

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da, Silveira Vieira da Silva Diogo. "Influenza neuraminidase assembly : Evolution of domain cooperativity." Doctoral thesis, Stockholms universitet, Institutionen för biokemi och biofysik, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-134470.

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Influenza A virus (IAV) is one of the most common viruses circulating in the human population and is responsible for seasonal epidemics that affect millions of individuals worldwide. The need to develop new drugs and vaccines against IAVs led scientists to study the main IAV surface antigens hemagglutinin (HA) and neuraminidase (NA). In contrast to HA, which facilitates cell binding and entry of IAVs, NA plays a critical role in the release and spreading of the viral particles. The aim of this thesis was to study how the enzymatic head domain, the stalk and transmembrane domains have evolved to facilitate NA assembly into an enzymatically active homotetramer, and to determine how these regions have evolved together over time. Initially, we observed that the NA transmembrane domain (TMD) assists in the assembly of the head domain by tethering the stalk to the membrane in a tetrameric conformation. Upon examination of the available sequences for NA, we found that the subtype 1 (N1) TMDs have become more polar since 1918 while the subtype 2 (N2) TMDs have consistently retained the expected hydrophobicity of a TMD. Further analysis of the amino-acid sequences revealed a characteristic indicative of an amphipathic assembly for the N1 TMDs that were absent in the TMDs from N2. The function of the amphipathic assembly was examined by creating two viral chimeras, where the original TMD was replaced by another more polar or an engineered hydrophobic TMD. In both cases the viruses carrying the NA TMD chimeras showed reduced growth indicating that the TMD changes created an incompatibility with the head domain of NA. After prolonged passaging of these viruses, natural occurring mutations were observed in the TMD that were able to rescue the defects in viral growth, head domain folding and budding by creating a TMD with the appropriate polar or hydrophobic assembly properties. Interestingly, we observed that N1 and N2 have a great difference in the localization and length of amino-acid deletions occurring in the stalk region. In line with this observation, our data suggests that N1 supports large stalk deletions due to its strong TMD association, whereas N2 requires the presence of a strong oligomerizing stalk region to compensate for its weak TMD interaction. These results have demonstrated how important the NA TMD is for viral infectivity and how the three different domains have evolved in a cooperative manner to promote proper NA assembly
Influensa är en av de mest smittsamma sjukdomarna som drabbar människor och de flesta kan räkna med att bli infekterade många gånger under sin livstid. Influensaviruset attackerar främst luftvägarna, men kan även leda till t.ex. lunginflammation. De enskilda viruspartiklarna (virionerna) kan komma i olika former, men den vanligaste formen som används för att beskriva viruset är den sfäriska. På en virions yta så finns det två olika typer av membranproteiner, som kan liknas med två olika sorters spikar som sticker ut från viruset. Den ena ”spiken” kallas neuraminidas, eller bara kort för NA, och den andra för hemagglutinin (HA). När man har andats in ett influensavirus så kan viruset ta sig till de övre luftvägarna och vidare ner i luftstrupen för att där använda sig av HA för att ta sig in i en cell. Viruset använder sig sedan av cellen för att skapa många nya virioner, som tar sig ut ur cellen för att infektera fler celler. NA är det protein som virionerna använder sig av för att klyva sig loss från modercellen. Målet för avhandlingen var att studera NA och beskriva hur proteinet måste vara ihopsatt för att vara aktivt. NA har en uppbyggnad liknande en trädklunga, där fyra stycken identiska träd (med tillhörande rötter, stammar och trädkronor) går ihop och bildar en enda aktiv enhet, en s.k. tetramer. ”Rötterna” hos NA är den transmembrana domänen (TMD), den del av proteinet som sitter fast i influenaviruskroppen. ”Stammen”, eller stjälkdelen av NA, binder samman TMD med den största delen, huvuddomänen som motsvarar ”trädkronan”. Det är just huvuddomänen som är ansvarig för att klyva loss viruspartiklar från en modercell. Vi har i våra studier sett att det kan vara väldigt viktigt att TMD-domänerna går ihop i grupper om fyra för att hela NA ska kunna gå ihop i en tetramer och aktivt kunna klyva loss viruspartiklarna. När vi studerade TMD från olika influensavirus så märkte vi att vissa egenskaper hos TMD krävs för att de skulle kunna gå ihop, men också att dessa egenskaper inte fanns hos alla influensavirus. Virusen har evolverat över lång tid och har anpassat sig efter värdorganismerna (inklusive människan) och har hittat olika lösningar på problemet med att behöva bilda en tetramer. När vi gjorde ändringar i en TMD som vanligtvis gick ihop till en tetramer, och därmed förhindrade detta, så noterade vi att huvuddomänens funktion påverkades vilket ledde till att influensaviruset hade svårt att spridas. Vidare så har våra pågående studier på stjälkdelen visat att även denna del kan ha stor betydelse för tetrameriseringen av NA, speciellt i de fall där TM-domänen saknar egenskaper för att gå ihop. Avhandlingen tillför inte bara ny och viktig information till influensaforskningen, utan även potentiellt för framställandet av nya influensavacciner/-mediciner.

At the time of the doctoral defense, the following paper was unpublished and had a status as follows: Paper 4: Manuscript.

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Rizzato, Vanessa Rodrigues. "Envolvimento da neuraminidase-1 na atrofia muscular." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/5/5138/tde-01122014-094857/.

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Sialidose é uma doença neurossomática causada pela deficiência congênita da neuraminidase-1 (Neu1), enzima envolvida na regulação do catabolismo de sialoglicoconjugados nos lisossomos. Com o acúmulo de sialoglicoconjugados, ocorre comprometimento sistêmico e neurológico. Achados histológicos musculares incluem expansão da matriz extracelular (MEC) devido à proliferação anormal de fibroblastos, invasão das fibras musculares por componentes da MEC, fragmentação do citoplasma, formação vacuolar e atrofia das fibras musculares. Entretanto o mecanismo da atrofia muscular na deficiência de Neu1 não está completamente esclarecido, sendo o objetivo desse estudo. Desnervou-se o músculo gastrocnêmio direito de camundongos com deficiência de Neu1 (Neu1 -/-) e de controles Neu1 +/+. Os animais foram eutanasiados 0, 3, 7, 14 e 21 dias pós desnervação. Os músculos desnervados e contralaterais foram submetidos às seguintes análises: 1) histologia geral e medida da área transversa das fibras; 2) autofagia, através da avaliação da presença de vacúolos autofágicos por estudo ultraestrutural e da análise da expressão da proteína LC3; 3) ativação do sistema lisossomal, por reação de fosfatase ácida e análise da expressão proteica de catepsina L e lamp1; 4) deposição de colágeno e infiltração de tecido conjuntivo no tecido muscular; 5) níveis das proteínas Akt e GSK3b; 6) expressão dos atrogenes MuRF1 e Atrogina-1; 7) níveis da proteína MyoD, relacionada à diferenciação muscular; e 8) expressão dos genes Neu1, Neu2, Neu3 e Neu4. Os animais Neu1-/- apresentaram menor peso corporal e muscular compararando-se com animais Neu1 +/+. Houve redução progressiva da área das fibras dos músculos desnervados em relação aos músculos contralaterais. Os animais Neu1-/- apresentaram atrofia muscular basal, com aumento acentuado dos espaços endomisiais e perimisiais. Ocorreu formação de vacúolos autofágicos a partir de 14 dias de desnervação tanto em animais Neu1+/+ quanto em Neu1-/-. Os níveis de expressão proteica de catepsina L e de lamp1 aumentaram a partir de 14 dias de desnervação, mais notadamente em músculos desnervados de camundongos Neu1-/-. A expressão proteica de colágeno III mostrou-se aumentada em animais Neu1-/-, principalmente após desnervação. A expressão proteica da forma fosforilada do Akt (forma ativada) diminuiu após 21 dias de desnervação principalmente em músculos desnervados de animais Neu1+/+. Os níveis de PGSK3 b, forma inativa de GSK3b, diminuíram após a desnervação, em animais Neu1+/+ e animais Neu1-/-. Houve aumento na expressão gênica de Atrogina-1 e MuRF1 após 3 e 7 dias de desnervação, respectivamente; a expressão gênica de Atrogina-1 nos camundongos Neu1-/- teve um aumento atrasado, mostrando diferença significante após 7 dias de desnervação. Não houve diferença significativa entre níveis proteicos de MyoD. A expressão gênica de Neu1 mostrou-se elevada em músculos desnervados de animais Neu1+/+. Conclui-se, portanto, que a Neu1 parece atuar na regulação da massa muscular principalmente controlando o processo de ativação do sistema lisossomal, porém aparentemente sem afetar a autofagia
Sialidosis, a severe neurosomatic disease, results from congenital neuraminidase-1 (Neu1) deficiency. This enzyme regulates the catabolism of sialoglycoconjugates in the lysosomes. Systemic and neurologic manifestations occur due to the sialoglycoconjugates accumulation. In the mouse model for Neu1 deficiency, the muscle histologic findings include extracellular matrix (ECM) expansion, due to abnormal fibroblast proliferation, muscle fibers invasion by ECM components, cytoplasm fragmentation, vacuolar formation and muscle atrophy. Nevertheless the mechanisms of muscle atrophy in Neu1 deficiency are not completely known. This study was designed to investigate Neu1 involvement in muscle atrophy process. Denervation of gastrocnemius muscle was performed by sectioning sciatic nerve from Neu1 deficient mice (Neu1 -/-) and from normal control Neu1 +/+; the animals were euthanized 0, 3, 7, 14 and 21 days after denervation. Denervated and control muscles were collected and submitted to several analysis: 1) histological; 2) autophagic vacuoles formation, performed by ultrastructural analysis and LC3 protein expression; 3) acid phosphatase reaction, lamp1 and cathepsin L protein expression, to analyze lysosomal activation; 4) collagen deposition and fibrous formation; 5) proteins involved with muscle trophism, Akt and GSK3b; 6) MuRF1 and Atrogin-1 gene expression; 7) MyoD protein expression; 8) Neu1, Neu2, Neu3 and Neu4 genes expression. Neu1 -/- mice presented decreased body and muscle weight comparing to Neu1 +/+ animals. Muscle fiber cross-sectional area was reduced in denervated muscles comparing to contralateral muscles. Neu1 -/- mice muscles presented basal atrophy and increase of endomisial and perimisial spaces, which became more evident after denervation. After 14 days of denervation, autophagosome formation was noticed on Neu1 +/+ and Neu1-/- animals. Cathepsin L protein levels were increased after 14 and 21 days of denervation, especially in denervated muscles from Neu1 -/- mice. Lamp1 protein expression was increased in Neu1-/- animals. Type III collagen protein levels were increased in Neu1-/- animals. There were no significant differences between MyoD protein levels. P-Akt, active form of Akt protein levels, decreased after 21 days of denervation, especially in denervated muscles from control group animals, indicating that protein synthesis is decreased. P-GSK3b, inactive form of GSK3b decreased in denervated muscles from Neu1 -/- and Neu1 +/+ animals, which indicates that this protein remained activated during muscle atrophy process. There were significant differences in Atrogin-1 and MuRF1 gene expression levels after 3 and 7 days of denervation. Neu1 -/- animals muscles presented a delayed Atrogin-1 response. Neu1 gene expression was increased in denervated muscles from Neu1 +/+ mice. These findings suggest that Neu1 seems to act in the regulation of muscle mass mainly by controlling the process of lysosomal system activation, but apparently without affecting autophagy
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Neves, Juliana de Carvalho. "Envolvimento da neuraminidase-1 na regeneração muscular." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/5/5138/tde-06052014-091743/.

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A neuraminidase-1 (Neu1) participa da regulação do catabolismo de sialoglicoconjugados nos lisossomos. A deficiência congênita da Neu1 é a base da sialidose, doença neurossomática grave associada a deformidades osteoesqueléticas, hipotonia e fraqueza muscular. Camundongos com deficiência de Neu1 (Neu1-/-) desenvolvem uma forma atípica de degeneração muscular caracterizada por expansão da matriz extracelular (MEC), invasão das fibras musculares por fibroblastos, fragmentação do citoplasma, formação vacuolar e atrofia muscular. Apesar de a degeneração muscular estar bem caracterizada nestes animais, a miogênese ainda não havia sido estudada. O objetivo desta pesquisa foi avaliar o envolvimento da Neu1 no processo de regeneração muscular, após aplicação de cardiotoxina (CTX) em camundongos Neu1-/-, em comparação com controles normais. A CTX foi administrada no músculo tibial anterior direito e os animais foram eutanasiados por deslocamento cervical 1, 3, 5, 7, 10, 14, 21 e 28 dias após a lesão. Os músculos foram analisados através de histologia; medição da área transversa das fibras musculares centronucleadas; verificação do potencial proliferativo celular por quantificação de marcação de BrdU; imunoistoquímica para inflamação, fibras regenerativas e fibrose; e expressão gênica e proteica de fatores de transcrição musculares. Os dados foram comparados estatisticamente e as variações significativas devem apresentar p <= 0,05. Nos animais com deficiência de Neu1, o processo inflamatório (especialmente a reação macrofágica) e o potencial proliferativo estavam aumentados nas fases iniciais, acompanhados da hiperexpressão de Pax7. Observamos atraso na maturação muscular caracterizado por maior expressão de miosina embrionária em estágios mais tardios da regeneração. Os genes MyoD e MyoG estavam com expressão aumentada no período de 5 a 10 dia após a lesão, embora a expressão destas proteínas estivesse reduzida. Ao final da regeneração, houve maior deposição de reticulina na MEC, indicando processo fibrótico. A Neu1 parece atuar em todos os estágios da regeneração muscular, desde a fase aguda da lesão através do controle da proliferação celular, até a maturação muscular e estágios finais em que regularia a deposição de componentes da MEC
Neuraminidase-1 (Neu1) participates in sialoglycoconjugates catabolism in lysosomes. Congenital Neu1 deficiency is the basis of sialidosis, a severe neurosomatic disorder associated with osteoskeletal deformities, hypotonia and muscle weakness. Mice with Neu1 deficiency (Neu1-/-) develop an atypical form of muscle degeneration characterized by abnormal fibroblast proliferation and expanded extracellular matrix (ECM), invasion of muscle fibers by fibroblast, cytosolic fragmentation, vacuolar formation and muscle atrophy. Despite muscle degeneration is well characterized in these animals, myogenesis has not been studied so far. The aim of this study was to evaluate the involvement of Neu1 in muscle regeneration process after cardiotoxin (CTX) injection in Neu1-/- mice and normal controls. CTX was applied in the right tibialis anterior muscle, and the animals were euthanized by cervical dislocation 1, 3, 5, 7, 10, 14, 21 and 28 days after injury. The muscles were analyzed through histology; cross-sectional area of regenerative muscle fibers; quantification of BrdU labeling; immunohistochemistry labelling for inflammation, regenerative fibers, and fibrosis; and gene and protein expression of muscle transcription factors. The data were compared and variances considered statistically significant in case p <= 0.05. In animals with Neu1 deficiency, both inflammatory process (mainly macrophagic response) and proliferative potential were increased in the initial stages, accompanied by overexpression of Pax7. We observed delay in muscle maturation characterized by higher expression of embryonic myosin later in muscle regeneration. MyoD and MyoG genes were overexpressed from 5 to 10 days after injury, though the expression of these proteins was reduced. At the end of muscle regeneration, reticulin deposition in ECM was increased, indicating fibrotic process. Neu1 seems to participate in all stages of muscle regeneration, since acute injury phase through the control of cell proliferation, towards muscle maturation, and at the final stages when it would regulate the deposition of ECM components
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Mamuya, Nellie. "Synthesis and NMR studies of neuraminidase inhibitors." Thesis, The University of Arizona, 1996. http://hdl.handle.net/10150/291545.

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Influenza is an enveloped virus, consisting of two surface glycoproteins, neuraminidase and hemagglutinin. The viral receptor is a glycoconjugate on which sialic acid is the terminal sugar. Neuraminidase catalyses the cleavage of the terminal sialic acid from the adjoining carbohydrate moiety, thereby assisting the virus to spread, and infect new cells. Thus development of neuraminidase inhibitors has been of great interest. Our studies are based on synthesis of new potential neuraminidase inhibitors. The synthetic strategy that was adopted for the preparation of the potential inhibitors, required the introduction of glycine ethyl ester at C1 of 1,4-lactone derivatives of N-acetylneuraminic acid. Furthermore, the rate of the ring opening of the 1,4-lactones was studied via proton NMR. Structural determination of the lactones are reported using specialized NMR techniques (Inverse Detected Single Quantum Filtered Long Range Spectroscopy). Conformational studies of the lactones were also determined with computational models.
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Barrere, Béatrice. "Inhibiteurs de synthèse des sialidases : études de leurs activités inhibitrices envers les sialidases d'origine bactérienne et virale et de leurs effets sur la multiplication des virus influenza." Lyon 1, 1995. http://www.theses.fr/1995LYO1T065.

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Wang, Qinning. "Erysipelothrix rhusiopathiae : epidemiology, virulence factors and neuraminidase studies." University of Western Australia. Microbiology Discipline Group, 2003. http://theses.library.uwa.edu.au/adt-WU2004.0043.

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Erysipelothrix rhusiopathiae, a Gram-positive bacillus, has long been an important pathogen in veterinary medicine as well as a cause of serious disease in humans. Infections caused by this organism have economic impact on animal industries, causing erysipelas in swine and morbidities in other farmed animals. Human infections are commonly erysipeloid (skin cellulitis) and occasionally septicaemia or endocarditis. Little is known of the diagnosis, epidemiology and pathogenesis of such infections in Western Australia. The aims of this thesis were to establish new diagnostic techniques for the detection and recovery of E. rhusiopathiae, to describe the epidemiology of Erysipelothrix infection in Western Australia in humans and animals, and to characterize virulence-associated characteristics, especially focusing on the neuraminidase produced by the organism. A protocol using 48 h Brain Heart Infusion enrichment followed by subculture to selective agar containing antibiotics achieved the highest recovery rate of 37% in a seafood survey. Twentyone isolates of Erysipelothrix spp., of which 19 were identified as E. rhusiopathiae, were obtained. Two published PCR assays for differentiating E. rhusiopathiae and other Erysipelothrix species were evaluated and the best PCR detection rate achieved was 67% following selective enrichment. The PCR method was 50% more sensitive than the culture method. Epidemiological surveys using the above methods showed that E. rhusiopathiae infection is present in farmed animals in Western Australia. The PCR positive frequencies (3.3-3.7%) and isolate recovery rate (2.8-3.3%) in samples from pig and sheep abattoirs and carcass washings indicate a potential threat to the economy of the farmed animal industry as well as a public health concern with the occurrence of E. rhusiopathiae in meat for consumption. Positive PCR results (1.1%) from human skin swabs of patients with cellulitis and wounds may suggest the existence of Erysipelothrix colonization in the general population. Genetic relatedness of 92 isolates of Erysipelothrix species from various sources was analyzed and a total of 64 distinct PFGE patterns identified. Isolates were further classified into 20 clonal groups based on pattern similarities, and most E. rhusiopathiae were clustered into six groups. A few patterns of other Erysipelothrix species were clustered into separate groups from E. rhusiopathiae but shared greater than 70% similarity with E. rhusiopathiae. The genetic relatedness of colonial variants was well demonstrated using this method. PFGE typing promises to be a useful tool for epidemiological and taxonomic studies of Erysipelothrix. Several virulence-associated factors were characterized in 86 isolates of Erysipelothrix spp. A rapid and sensitive peanut lectin hemagglutination assay for neuraminidase was developed and the influence of media, incubation conditions and pH on the production of the enzyme was investigated. All 61 isolates of E. rhusiopathiae produced neuraminidase in cooked meat broth with titres between 1:10 and 1:320, with no significant difference in titre among isolates from different sources. The enzyme activity was not detected in non-pathogenic Erysipelothrix spp. Capsule was produced by 78.7% of isolates of E. rhusiopathiae but not by other species, while both hyaluronidase and haemolysin were produced by non-pathogenic Erysipelothrix spp. It was concluded that neuraminidase and capsule are most likely to be virulence factors of E. rhusiopathiae. The gene encoding neuraminidase was cloned from the type strain E. rhusiopathiae ATCC 19414. The cloned fragment was a functional partial nanH gene with a mol% G+C of 39.7. The predicted amino acid sequence displayed homology with many microbial neuraminidases and contained conserved sequences found in most bacterial neuraminidases. Southern hybridization experiments demonstrated that the gene was present as a single copy on the bacterial genomic DNA. A neuraminidasenegative mutant vector was constructed by insertional inactivation using a tetM cassette. This has provided starting material for developing a neuraminidase-deficient E. rhusiopathiae mutant, which will permit the study of the role of neuraminidase in pathogenesis. Based on the cloned sequence, a sensitive neuraminidase-specific nested PCR technique was designed and optimized. The specificity was tested in 61 isolates of E. rhusiopathiae, 25 Erysipelothrix species, and 62 other species of neuraminidaseproducing and non-producing bacteria. All isolates of E. rhusiopathiae were PCR positive and all other bacteria were negative; thus this PCR is a highly specific method suitable for application in clinical investigations of Erysipelothrix infection. In conclusion, the present study has contributed new knowledge of the biology of Erysipelothrix spp. and current occurrence of Erysipelothrix infections in Western Australia, as well as to the understanding of pathogenesis of E. rhusiopathiae. Development of several new cultural and molecular approaches in combination with other established techniques will facilitate future studies of the epidemiology, taxonomy and pathogenesis of this bacterial species.
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Books on the topic "Neuraminidase"

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Collins, Kay R. Variation in the haemagglutinin-neuraminidase gene of human parainfluenza 3 virus. [s.l.]: typescript, 1994.

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D'Agrosa, Raffaele Michael. The gbs galactosidase-neuraminidase-protective protein complex and associated lysosomal storage disorders. Ottawa: National Library of Canada, 1990.

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King, Samantha Jane. Epidemiology and evolution of pneumococcal neuraminidases. [s.l.]: typescript, 1999.

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Sedlacek, H. H. Tumor Therapy with Tumor Cells and Neuraminidase. S. Karger AG, 1987. http://dx.doi.org/10.1159/isbn.978-3-318-03410-3.

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Tumor Therapy With Tumor Cells and Neuraminidase (Contributions to Oncology, Vol 27). S. Karger AG (Switzerland), 1987.

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Bodnaruk, Tetyana Daria Evhenia. Neuraminidase-1, a subunit of the elastin receptor, alters mitogenic growth factor receptors and down-regulates proliferation of arterial smooth muscle cells. 2006.

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Influenza Virus Sialidase A Drug Discovery Target. Birkhauser, 2010.

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Federico, Antonio, and Silvia Palmeri. Oligosaccharidoses. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0057.

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Oligosaccharidoses are a group of lysosomal diseases, also called glycoproteinoses, biochemically characterized by storage of protein-bound oligosaccharides within lysosomes and excretion with urine of corresponding sugars. Storage of oligosaccharides results from absence or defective function of a specific lysosomal enzyme. Classification includes α‎ and β‎ mannosidosis, fucosidosis, sialidosis types I and II, Schindler disease, and aspartylglycosaminuria. Galactosialidosis characterized by deficiency of β‎-galactosidase and α‎-neuraminidase with presence in patient urine of oligosaccharides has been included among oligosaccharidoses but may be better classified as a lysosomal enzyme protection defect disease in relation to its primary defect of cathepsine A-protective protein. The clinical spectrum of the diseases vary widely, as is common in lysosomal storage disorders. Patients frequently have neurological symptoms, but in rare cases presenting in adulthood symptoms may be very subtle. Psychiatric presentations have been described in adults. For adult cases, no treatments are available except for supportive care.
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Alexander, D. J., N. Phin, and M. Zuckerman. Influenza. Edited by I. H. Brown. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0037.

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Influenza is a highly infectious, acute illness which has affected humans and animals since ancient times. Influenza viruses form the Orthomyxoviridae family and are grouped into types A, B, and C on the basis of the antigenic nature of the internal nucleocapsid or the matrix protein. Infl uenza A viruses infect a large variety of animal species, including humans, pigs, horses, sea mammals, and birds, occasionally producing devastating pandemics in humans, such as in 1918 when it has been estimated that between 50–100 million deaths occurred worldwide.There are two important viral surface glycoproteins, the haemagglutinin (HA) and neuraminidase (NA). The HA binds to sialic acid receptors on the membrane of host cells and is the primary antigen against which a host’s antibody response is targeted. The NA cleaves the sialic acid bond attaching new viral particles to the cell membrane of host cells allowing their release. The NA is also the target of the neuraminidase inhibitor class of antiviral agents that include oseltamivir and zanamivir and newer agents such as peramivir. Both these glycoproteins are important antigens for inducing protective immunity in the host and therefore show the greatest variation.Influenza A viruses are classified into 16 antigenically distinct HA (H1–16) and 9 NA subtypes (N1–9). Although viruses of relatively few subtype combinations have been isolated from mammalian species, all subtypes, in most combinations, have been isolated from birds. Each virus possesses one HA and one NA subtype.Last century, the sudden emergence of antigenically different strains in humans, termed antigenic shift, occurred on three occasions, 1918 (H1N1), 1957 (H2N2) and 1968 (H3N2), resulting in pandemics. The frequent epidemics that occur between the pandemics are as a result of gradual antigenic change in the prevalent virus, termed antigenic drift. Epidemics throughout the world occur in the human population due to infection with influenza A viruses, such as H1N1 and H3N2 subtypes, or with influenza B virus. Phylogenetic studies have led to the suggestion that aquatic birds that show no signs of disease could be the source of many influenza A viruses in other species. The 1918 H1N1 pandemic strain is thought to have arisen as a result of spontaneous mutations within an avian H1N1 virus. However, most pandemic strains, such as the 1957 H2N2, 1968 H3N2 and 2009 pandemic H1N1, are considered to have emerged by genetic re-assortment of the segmented RNA genome of the virus, with the avian and human influenza A viruses infecting the same host.Influenza viruses do not pass readily between humans and birds but transmission between humans and other animals has been demonstrated. This has led to the suggestion that the proposed reassortment of human and avian influenza viruses takes place in an intermediate animal with subsequent infection of the human population. Pigs have been considered the leading contender for the role of intermediary because they may serve as hosts for productive infections of both avian and human viruses, and there is good evidence that they have been involved in interspecies transmission of influenza viruses; particularly the spread of H1N1 viruses to humans. Apart from public health measures related to the rapid identification of cases and isolation. The main control measures for influenza virus infections in human populations involves immunization and antiviral prophylaxis or treatment.
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Noris, Marina, and Tim Goodship. The patient with haemolytic uraemic syndrome/thrombotic thrombocytopenic purpura. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0174.

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The patient who presents with microangiopathic haemolytic anaemia, thrombocytopenia, and evidence of acute kidney injury presents a diagnostic and management challenge. Haemolytic uraemic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP) are two of the conditions that frequently present with this triad. They are characterized by low platelet count with normal or near-normal coagulation tests, anaemia, and signs of intravascular red cell fragmentation on blood films, and high LDH levels.HUS associated with shiga-like toxins produced usually by E.coli (typically O157 strains) may occur in outbreaks or sporadically, with geographical variations in incidence. It is predominantly a disease of young children in which painful blood diarrhoea in a minority of infected patients is succeeded by microangiopathy and acute kidney injury. Management is supportive and recovery is usual, although permanent renal damage may lead to later deterioration. Older patients may be affected and tend to have worse outcomes. Neuraminidase-producing Streptococcus pneumoniae infections (usually pneumonia) very rarely cause a similar HUS.Atypical HUS occurs sporadically and is increasingly associated with defects in the regulation of the complement pathway, either genetic or autoimmune-caused. It may respond to plasma exchange for fresh frozen plasma. Recurrences are common, including after transplantation.TTP is associated with more neurological disease and less renal involvement, but HUS and TTP overlap substantially in their manifestations. The underlying problem is in von Willebrand factor (vWF) cleavage. The plasma metalloprotease ADAMTS13 is responsible for cleaving vWF multimers, a process that is important to prevent thrombosis in the microvasculature. Autoantibodies or rarely genetic deficiency may impair this process. Plasma exchange may remove antibodies and replenish the protease.
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Book chapters on the topic "Neuraminidase"

1

Sewell, A. C. "Neuraminidase." In Lexikon der Medizinischen Laboratoriumsdiagnostik, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-49054-9_2246-1.

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Colman, P. M. "Neuraminidase." In The Influenza Viruses, 175–218. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0811-9_4.

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Sewell, A. C. "Neuraminidase." In Springer Reference Medizin, 1741. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_2246.

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Pedersen, Janice C. "Neuraminidase-Inhibition Assay for the Identification of Influenza A Virus Neuraminidase Subtype or Neuraminidase Antibody Specificity." In Avian Influenza Virus, 67–75. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-279-3_9.

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Aruksakunwong, Ornjira, Thanyada Rungrotmongkol, Nadtanet Nunthaboot, and Supot Hannongbua. "Influenza Neuraminidase – Computational Studies." In Encyclopedia of Biophysics, 1044–48. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-16712-6_239.

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Pedersen, Janice C. "Neuraminidase-Inhibition Assay for the Identification of Influenza A Virus Neuraminidase Virus Subtype or Neuraminidase Antibody Specificity." In Methods in Molecular Biology, 27–36. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-0758-8_3.

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Van Epps, Stacy. "Carboxylic-Acid-Based Neuraminidase Inhibitors." In Bioactive Carboxylic Compound Classes: Pharmaceuticals and Agrochemicals, 133–48. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2016. http://dx.doi.org/10.1002/9783527693931.ch10.

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Colman, P. M. "Drugs Targeting Influenza Virus Neuraminidase." In Structure-Based Drug Design, 87–93. Dordrecht: Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-015-9028-0_8.

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Russell, Rupert J., Steven J. Gamblin, and John J. Skehel. "Influenza glycoproteins: Hemagglutinin and neuraminidase." In Textbook of Influenza, 67–100. Oxford, UK: John Wiley & Sons, Ltd, 2013. http://dx.doi.org/10.1002/9781118636817.ch5.

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Sriwilaijaroen, Nongluk, Christopher J. Vavricka, Hiromasa Kiyota, and Yasuo Suzuki. "Influenza A Virus Neuraminidase Inhibitors." In Methods in Molecular Biology, 321–53. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2635-1_21.

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Conference papers on the topic "Neuraminidase"

1

LI, X., H. JANKOWSKI, S. BOONPATCHARANON, V. TRAN, X. WANG, and J. M. HEFFERNAN. "CLUSTERING NEURAMINIDASE INFLUENZA PROTEIN SEQUENCES." In 15th International Symposium on Mathematical and Computational Biology. WORLD SCIENTIFIC, 2016. http://dx.doi.org/10.1142/9789813141919_0014.

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Yan, Shaomin, and Guang Wu. "Description of evolution of neuraminidase from influenza A virus." In 2nd International Conference on Computer Vision, Image and Deep Learning, edited by Fengjie Cen and Badrul Hisham bin Ahmad. SPIE, 2021. http://dx.doi.org/10.1117/12.2604572.

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Yan, Shaomin, and Guang Wu. "Description of evolution of neuraminidase from influenza A virus." In 2nd International Conference on Computer Vision, Image and Deep Learning, edited by Fengjie Cen and Badrul Hisham bin Ahmad. SPIE, 2021. http://dx.doi.org/10.1117/12.2604572.

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Дешева, Юлия Андреевна, and Надежда Николаевна Петкова. "STUDY OF NEURAMINIDASE ANTIBODIES TO A(Н3N2) INFLUENZA VIRUS." In Психология. Спорт. Здравоохранение: сборник избранных статей по материалам Международной научной конференции (Санкт-Петербург, Декабрь 2021). Crossref, 2022. http://dx.doi.org/10.37539/psm300.2021.44.58.003.

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В реакции ингибирования нейраминидазной активности (РИНА) изучен коллективный иммунитет в группах пациентов различного возраста к эпидемическому вирусу гриппа A/Гонконг/4801/2014 Изучены сывороточные антитела к антигенам вируса А/H3N2 у лиц, привитых трехвалентной живой гриппозной вакциной (ЖГВ). Показано, что антитела к NA могут служить дополнительным критерием оценки иммуногенности гриппозных вакцин. In the enzyme linked lectin assay (ELLA), the collective immunity to the A/Hong Kong/4801/2014 (H3N2) influenza virus was evaluated among different age groups of patients. Serum antibodies to antigens of the A/H3N2 virus were studied in individuals vaccinated with trivalent live influenza vaccine (LAIV). It has been shown that antibodies to NA can serve as an additional criterion for assessing the immunogenicity of influenza vaccines.
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Yoo, G., S. H. Kim, I.-W. Choi, and S. Y. Choi. "Diarylheptanoids isolated from Alpinia officinarum as novel influenza neuraminidase inhibitors." In GA – 70th Annual Meeting 2022. Georg Thieme Verlag KG, 2022. http://dx.doi.org/10.1055/s-0042-1759270.

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Ruban, M., N. Chamberlain, Z. Mark, S. Bruno, A. Kumar, R. Chandrasekaran, D. Souza De Lima, and V. Anathy. "Redox Regulation of Influenza Neuraminidase by Protein Disulfide Isomerase A3." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a3982.

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Matos, Aline, Thiago Sousa, Thiago Souza, Paola Resende, Milene Miranda, Maria Oliveira, Braulia Caetano, Cristiana Garcia, Fernando Motta, and Marilda Siqueira. "Ten years of consecutive influenza surveillance to neuraminidase inhibitors resistance Brazil." In IV International Symposium on Immunobiologicals & VII Seminário Anual Científico e Tecnológico. Instituto de Tecnologia em Imunobiológicos, 2019. http://dx.doi.org/10.35259/isi.sact.2019_32855.

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Singh, Dadabhai T., Rahul Trehan, Pradeep Ray, and Bertil Schmidt. "Phylogenetic Analysis of Neuraminidase Genes of H5N1 Isolates using HPC Technologies." In 2007 9th International Conference on e-Health Networking, Application and Services. IEEE, 2007. http://dx.doi.org/10.1109/health.2007.381652.

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Tindal, David J., Jeffrey C. Dyason, Robin J. Thomson, and Mark von Itzstein. "A GRID STUDY OF THE HAEMAGGLUTININ-NEURAMINIDASE OF NEWCASTLE DISEASE VIRUS." In XXIst International Carbohydrate Symposium 2002. TheScientificWorld Ltd, 2002. http://dx.doi.org/10.1100/tsw.2002.566.

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Krüger, L., S. Handtke, K. Jahn, P. T. Kohler, J. Wesche, S. Hammerschmidt, and A. Greinacher. "Role of Neuraminidase A of S. pneumoniae on platelet-bacteria-interaction." In GTH Congress 2023 – 67th Annual Meeting of the Society of Thrombosis and Haemostasis Research – The patient as a benchmark. Georg Thieme Verlag, 2023. http://dx.doi.org/10.1055/s-0042-1760604.

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Reports on the topic "Neuraminidase"

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Perk, Shimon, Maricarmen Garcia, Alexander Panshin, Caroline Banet-Noach, Irina Gissin, Mark W. Jackwood, and David Stallknecht. Avian Influenza Virus H9N2: Characterization and Control Strategies. United States Department of Agriculture, June 2007. http://dx.doi.org/10.32747/2007.7709882.bard.

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Control of Avian Influenza (AI) infection is a highly topical subject of major economicimportance for the worldwide poultry industry at the national level and for international trade.H9N2 viruses are endemic in poultry throughout Asia and the Middle East, causing major losses inproduction. Moreover, these viruses pose wider threats since they have been isolated from bothswine and humans. At the same time, study of the AI viruses affords an opportunity to explore anumber of problems of intriguing scientific interest. The overall goal of this project was to developa sound control strategy for avian influenza subtype H9N2 viruses (AI H9N2) in commercialpoultry in Israel. The one-year feasibility study focused on two main goals, namely: to study themolecular characteristics of AI H9N2 circulating during the last seven years in Israel and todevelop tools enabling differentiation between the immune response to vaccination and infectionwith H9N2.Genetic and phylogenetic characterization of 29 selected AI H9N2 isolates (2000-2006)was performed by complete sequencing of hemagglutinin (HA), neuraminidase (NA), and all sixinternal genes [nucleoprotein (NP), polymerase basic 1 (PB1), polymerase basic 2 (PB2),polymerase acid (PA), matrix (M), and nonstructural (NS) genes]; comparative phylogenetic andgenetic analyses of these sequences; and comparative genetic analyses of deduced amino acidsequences of the HA, NA, NS1, and NS2 proteins. The major conclusions of the molecularanalyses were: (1) Israeli isolates, together with other H9N2 viruses isolated in Middle Eastcountries, comprise a single regional sublineage related to the G1-lineage. In addition, Israeliisolates subdivided into three different subgroups. Genetic analysis of these viruses suggests thatthey underwent divergent evolution paths.
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