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Glycopeptides of murine leukemia viruses. I. Comparison of two ecotropic viruses

Journal of Virology
|July 1, 1979
PubMed

Insights

Murine leukemia virus (MuLV) glycopeptides were analyzed, revealing distinct size classes and glycosylation patterns. The large G(1) glycopeptide suggests MuLV infection may alter host cell glycosylation, but this is virus-specific.

Area of Science:

  • Virology
  • Glycobiology
  • Molecular Biology

Background:

  • Murine leukemia virus (MuLV) is a retrovirus known to cause various diseases in mice.
  • Glycopeptides are proteins with attached carbohydrate chains, crucial for viral structure and function.
  • Understanding viral glycopeptide composition is key to deciphering viral pathogenesis and developing interventions.

Purpose of the Study:

  • To characterize and compare glycopeptides from different MuLV strains.
  • To investigate the glycosylation patterns of MuLV-associated glycopeptides.
  • To determine if MuLV infection alters host cell glycosylation.

Main Methods:

  • Pronase digestion of MuLV virions.
  • Gel filtration chromatography to separate glycopeptides by size.
  • Analysis of sugar precursor incorporation.
  • Enzymatic digestion with endo-beta-N-acetylglucosaminidase H.
  • Comparison of glycopeptides from MuLV-infected and uninfected cells.

Main Results:

  • Four glycopeptide size classes (G(1)-G(4)) were identified in Rauscher MuLV virions.
  • G(1) and G(2) are complex (type I) glycopeptides, while G(3) and G(4) are mannose-rich (type II).
  • G(1) glycopeptides are significantly more sulfated than G(2), explaining differences in gp52 and gp70 sulfation.
  • No alterations in Sindbis virus glycopeptides were observed in MuLV-infected cells, indicating G(1) acquisition is virus-specific.

Conclusions:

  • MuLV glycopeptide composition varies by size and type.
  • The large size and high sulfation of G(1) suggest a unique role in MuLV structure or function.
  • The acquisition of specific glycopeptides like G(1) is dependent on the virus-coded polypeptide backbone, not host cell alterations.

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