Sendai virus utilizes specific sialyloligosaccharides as host cell receptor determinants.

Markwell, Mary Ann K.; Paulson, James C.

doi:10.1073/pnas.77.10.5693

Cited by 118 publications

(52 citation statements)

References 33 publications

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“…For this reason, the test system may not be sensitive enough to detect minor differences in receptor avidity. We postulated that such altered avidity can be revealed by the use of RBC partially depleted of cell surface receptors (5,16,24) and that the relationship between the degree of this depletion and the extent of HAD on the different HN-expressing cells would give a relative measure of receptor binding avidity. This modification would increase the sensitivity of the assay to differences in binding avidity.…”

Section: Infectivity Of Wt and Variant Viruses In The Presence Of 4-gmentioning

confidence: 99%

Mutations in Human Parainfluenza Virus Type 3 Hemagglutinin-Neuraminidase Causing Increased Receptor Binding Activity and Resistance to the Transition State Sialic Acid Analog 4-GU-DANA (Zanamivir)

Murrell

Porotto²,

Weber

et al. 2003

J Virol

103

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Entry and fusion of human parainfluenza virus type 3 (HPF3) require the interaction of the viral hemagglutinin-neuraminidase (HN) glycoprotein with its sialic acid receptor. 4-GU-DANA, a potent inhibitor of influenza virus neuraminidase, inhibits not only HPF3 neuraminidase but also the receptor binding activity of HPF3 HN and thus its ability to promote attachment and fusion. We previously generated a 4-GU-DANAresistant HPF3 virus variant (ZM1) with a markedly fusogenic plaque morphology that harbored two HN gene mutations resulting in amino acid alterations. The present study using cells that express the individual mutations of ZM1 HN shows that one of these mutations is responsible for the increases in receptor binding and neuraminidase activities as well as the diminished sensitivity of both activities to the inhibitory effect of 4-GU-DANA. To examine the hypothesis that increased receptor binding avidity underlies 4-GU-DANA resistance, parallel studies were carried out on the high-affinity HN variant virus C22 and cells expressing the C22 variant HN. This variant also exhibited reduced sensitivity to 4-GU-DANA in terms of receptor binding and infectivity but without concomitant changes in the neuraminidase activity of HN. Another high-affinity HN variant, C0, was not resistant in terms of infectivity; however, a small increase in the receptor binding activity of C0 HN and a partial resistance of this activity to 4-GU-DANA were revealed by sensitive methods that we developed. In each virus variant, one mutation in HN accounted for both increased receptor binding avidity and 4-GU-DANA resistance; the higher affinity for the receptor overcomes the inhibitory effect of 4-GU-DANA. Thus, in contrast to influenza viruses for which 4-GU-DANA escape variants include hemagglutinin mutants with decreased receptor binding avidity that promotes virion release, for HPF3, HN mutants with increased receptor binding avidity are those that can escape the growth inhibitory effect of 4-GU-DANA.

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Section: Infectivity Of Wt and Variant Viruses In The Presence Of 4-gmentioning

confidence: 99%

Mutations in Human Parainfluenza Virus Type 3 Hemagglutinin-Neuraminidase Causing Increased Receptor Binding Activity and Resistance to the Transition State Sialic Acid Analog 4-GU-DANA (Zanamivir)

Murrell

Porotto²,

Weber

et al. 2003

J Virol

103

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“…precursor (Lamb & Kolakofsky, 1996) into the active F " and F # subunits (lane 12). Treatment of 3T3 cells with Vibrio cholerae sialidase, which hydrolyses endogenous cell surface sialoglycoconjugates (Markwell & Paulson, 1980), renders the cells resistant to VLPHN + infection (lane 10). Sialidase-treated 1-7-1 cells, by contrast, can still be infected by VLPHN + (lane 11) indicating that there is an alternative route of entry for the particles via ASGP-R.…”

mentioning

confidence: 99%

Sendai virus-like particles devoid of haemagglutinin-neuraminidase protein infect cells via the human asialoglycoprotein receptor.

Leyrer

Bitzer

Lauer

et al. 1998

Journal of General Virology

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Virus-like particles with genetically defined envelope proteins were generated from cDNA in order to examine the requirement of Sendai virus haemagglutinin-neuraminidase (HN) protein for particle formation, and the role of fusion protein (F) in receptor binding and membrane fusion. Characterization of particles devoid of HN protein showed that particle formation was unimpaired by the absence of HN protein, indicating that HN protein is dispensable for virus assembly and budding. Infection studies further demonstrated that virus adsorption and penetration can be mediated solely by the F protein when the human asialoglycoprotein receptor is present at the surface of host cells.

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“…It was not surprising that the UV-SeV-pretreated T cells, from which the sialic acid residues had been dissociated, would be infected by SeV-EGFP during the culture periods, because it was assumed that the UV-SeV-pretreated T cells regained the specific receptor for SeV on T cells. 28 These findings suggest that the receptor of SeV might be expressed on the naive T cells.…”

Section: Entry Of the Sev Vector After Cell Surface Attachment Occumentioning

confidence: 92%

“…The following factors may have led to the observed difference in transduction efficiency between naive and activated T cells: (i) a difference in the expression of a specific receptor for SeV, 28 (ii) a difference in the expression of a putative coreceptor for membrane fusion, 16,17 (iii) a difference in the intracellular signal induced by T-cell activation, which could have affected the transcription of SeV after entry. 15 To explore these factors, we performed the following experiments using murine T cells, the experiments in which it was not necessary to separate naive T cells from activated/ memory T cells.…”

Section: Entry Of the Sev Vector After Cell Surface Attachment Occumentioning

confidence: 99%

Recombinant Sendai virus vectors for activated T lymphocytes

et al. 2003

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Sendai virus utilizes specific sialyloligosaccharides as host cell receptor determinants.

Cited by 118 publications

References 33 publications

Mutations in Human Parainfluenza Virus Type 3 Hemagglutinin-Neuraminidase Causing Increased Receptor Binding Activity and Resistance to the Transition State Sialic Acid Analog 4-GU-DANA (Zanamivir)

Mutations in Human Parainfluenza Virus Type 3 Hemagglutinin-Neuraminidase Causing Increased Receptor Binding Activity and Resistance to the Transition State Sialic Acid Analog 4-GU-DANA (Zanamivir)

Sendai virus-like particles devoid of haemagglutinin-neuraminidase protein infect cells via the human asialoglycoprotein receptor.

Recombinant Sendai virus vectors for activated T lymphocytes

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