Bourbon virus infection pathophysiology: Difference between revisions

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==Pathophysiology==
==Pathophysiology==
*Virus attaches to sialic acid receptor though GP protein and is endocytosed by clathrins in the host cell.
===Replication===
*Endosome acidification induces fusion of virus membrane with the vesicle membrane
*Virus attaches to the sialic acid receptors on the host cell through glycoprotein
*The virus gets endocytosed by clathrins into the host cell.
*Endosome acidification induces fusion of virus membrane with the vesicle membrane.
*Encapsidated RNA segments migrate to the nucleus.
*Encapsidated RNA segments migrate to the nucleus.
*Transcription of genomic segments by the viral polymerase produces mRNAs that are capped and polyadenylated by the viral polymerase.
*Transcription of genomic segments by the viral polymerase produces mRNAs that are capped and polyadenylated by the viral polymerase.

Revision as of 14:54, 13 July 2017

Bourbon virus infection Microchapters

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

Overview

Pathophysiology

Replication

  • Virus attaches to the sialic acid receptors on the host cell through glycoprotein
  • The virus gets endocytosed by clathrins into the host cell.
  • Endosome acidification induces fusion of virus membrane with the vesicle membrane.
  • Encapsidated RNA segments migrate to the nucleus.
  • Transcription of genomic segments by the viral polymerase produces mRNAs that are capped and polyadenylated by the viral polymerase.
  • Replication of genomic segments.
  • High level of M1 protein induces genomes segments export from nucleus by NEP protein.
  • Virus assembly and budding occurs at the plasma membrane.

References

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