Repulsion of superinfecting virions: A mechanism for rapid virus spread (Science, 2010, 327:873-876)

報告日期: 2010/10/12
報告時間: 17:10/18:00
報告學生: 王莉萩
講評老師: 王貞仁
附件下載:

http://basicmed.med.ncku.edu.tw/admin/up_img/991012-3.pdf

Repulsion of superinfecting virions: A mechanism for rapid virus spread

Virginie Doceul et al.  Science (2010) 327: 873-876

 

Student: Li-Chiu Wang (王莉萩)

Commentator: Dr. Jen-Ren Wang (王貞仁)

Time: 2010-10-12, 17:10-18:00

Room: 602

 

A plaque is described as an area of cells destroyed by virus, which is initially formed from a single cell in a monolayer infected with a single virus and followed by the destruction of surrounding cells by newly produced virions. The size of a plaque is determined by the replication kinetics or spread rate of a given virus. However, in the present study, the authors examined carefully into the plaque formed by vaccinia virus and found that it spread rapidly than its replication kinetics would allow. Vaccinia virus is a DNA virus belongs to the Orthopoxvirus genus within Poxviridae family. It is named “vaccinia” because it is used for vaccination against smallpox. In the present study, the authors found that vaccinia virus spread across a single cell every 1.2 hr in a speed faster than its replication kinetics, in which new virions are produced 5 to 6 hours after infection. Vaccinia virus is known to spread directed via (1) virus-induced actin tails formed on infected cells that propel virions away and (2) virus-triggered cell motility. Yet, both phenomena occurred only 5 to 6 hours after infection, and migration of infected cells was restricted in plaques. According to their observations, these two mechanisms are unlikely involved in the rapid spread of vaccinia virus and imply the involvement of another mechanism. Using EGFP-tagged virus, the authors discovered that actin tails were formed in cells before new virions were produced, and each actin tail was tipped with a single virion. The early formation of actin projections required expressions of two viral genes, A33 and A36. The plaque size and distance of virus spread were significantly reduced in mutant strains with deletion of A33 or A36. Similar results were observed in recombinant virus with the expression of A33 or A36 driven only by a  late promoter. In conclusion, these results indicate that early expression of A33 and A36 are required to form actin projections to propel other virions away from cells that are already infected. This newly found mechanism partially? explains the rapid spread of vaccinia virus, which is correlated with virulence in vivo.