Reference : Structural basis of hemadsorbing sites during the formation of syncytia in measles-infec...
Scientific congresses and symposiums : Paper published in a journal
Human health sciences : Immunology & infectious disease
Structural basis of hemadsorbing sites during the formation of syncytia in measles-infected cells
Rentier, Bernard mailto [Université de Liège - ULg > National Institutes of Health - NIH, Bethesda, MD, USA > Infectious Diseases Branch, Section on Electron Microscopy > > >]
Dubois-Dalcq, Monique [National Institutes of Health - NIH, Bethesda, MD, USA > Infectious Diseases Branch > Section on Electron Microscopy > >]
Journal of Cell Biology
Rockefeller University Press
396a - VI
Yes (verified by ORBi)
17e Meeting Annuel de la Société Américaine de Biologie Cellulaire
San Diego
[en] The surfaces of cells Infected with measles virus adsorb monkey red blood cells (RBC). In this study,
the structure and localization of viral hemadsorbing (HAD) sites and their relationship with antigenic
sites and with cell fusion were investigated in measles virus infected Vero cells. Transmission and
scanning electron microscopy were combined with immunolabeling, using human anti-measles IgG
(Ab) and protein A from Staph, aureus coupled to peroxidase.. In the early syncytia (50-100 2 in
diameter), HAD sites were clustered in the center but scattered at the periphery. In contrast, mature
giant cells (400 to 500 2) had all HAD sites in the central area which displayed scattered villi. The
periphery of the mature giant cells and the mononucleated cells did not hemadsorb but were covered
with numerous villi. In the central area, RBC were firmly attached to villi and ridges over nucleocapsids
but rarely to viral buds. Villi and ridges under the RBC were covered with antigenic sites which were
not detected at the periphery of the mature syncytia. When living cells were treated with Ab at 4°C,
complete inhibition of hemadsorption was only observed when RBC were applied to the cells in the
cold. In other experiments, cells reacted with Ab at 4°C were washed, brought to 37°C and treated
with RBC immediately or after 1-24 hrs. After 1-2 hrs, some HAD sites were present only at the
periphery of immature giant cells, suggesting that RBC receptors had already emerged in membrane
areas where fusion started again. After 24 hrs, the distribution of HAD and antigenic sites was the
same as on cells not exposed to Ab. It seems that when fusion begins, HAD sites appeared on the
periphery of the syncytia and then move spontaneously towards the center. With cessation of fusion,
HAD sites disappear from the periphery of the giant cell. Receptors for RBC are closely associated
with antigenic sites and correlated with viral induced fusion but not with virus production.

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