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A mutant of sindbis virus with a host-dependent defect in maturation associated with hyperglycosylation of E2

Virology
|June 1, 1984
PubMed

Insights

A Sindbis virus (SV) mutant showed temperature sensitivity and poor replication in vertebrate cells due to abnormal glycoprotein modifications. This suggests host-specific glycosylation impacts viral host range and assembly.

Area of Science:

  • Virology
  • Molecular Biology
  • Cell Biology

Background:

  • Sindbis virus (SV) is an arbovirus with a broad host range.
  • Understanding viral adaptation to different hosts is crucial for controlling infectious diseases.

Purpose of the Study:

  • To investigate the molecular basis of host-specific replication defects in a Sindbis virus mutant.
  • To explore the role of viral glycoprotein modifications in host adaptation.

Main Methods:

  • Serial passage of Sindbis virus in mosquito cells to isolate mutants.
  • Replication studies in different cell types (mosquito, chick, BHK) at varying temperatures.
  • Complementation tests to assign mutants to complementation groups.
  • Analysis of viral glycoproteins (PE2, E2) using techniques like glycosylation analysis.

Main Results:

  • A mutant, SVap15/21, exhibited temperature sensitivity and poor replication in vertebrate cells but not mosquito cells.
  • The mutant was assigned to complementation group E, with a replication block at nucleocapsid envelopment.
  • SVap15/21 displayed hyperglycosylation of PE2 and E2 glycoproteins compared to the parent virus.
  • Analysis of revertants indicated a link between glycoprotein hyperglycosylation and host-specific maturation defects.

Conclusions:

  • Hyperglycosylation of Sindbis virus PE2 and E2 glycoproteins is associated with a host-specific defect in virion maturation.
  • Host-specific glycosylation patterns may play a significant role in determining the viral host range.

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