Evaluation of the in vivo role of vaccinia virus complement control protein (VCP) following renal ischemia

In transplantation, vascularized organs often suffer the consequences of ischemic damage as well as reperfusion injury following the reestablishment of blood flow. The induced ischemialreperfusion (I/R) damage is usually associated with the accumulation of injurious complement components. The vaccinia virus complement control protein (VCP) has the ability to simultaneously inhibit the classical and the alternative complement pathways by binding to the early components C3b and C4b. The complement component C3 is known to be the central route to all of the known complement activation pathways. As a result, it is involved in a number of complement-mediated ailments including renal ischemia/reperfusion injury. The objectives of this study were to initially evaluate the in vitro roles of the natural VCP and the humanized recombinant VCP (hrVCP), and then to establish their in vivo roles in a renal I/R injury model.

Grantor dc:publisher.institution

Division of Virology

Year dc:date.issued

2006

Author dc:creator

• Ghebremariam, Yohannes T

Advisors dc:contributor.advisor

• Kotwal, Girish J
• Kahn, Del

Language dc:language.iso

eng

Handle dc:identifier.uri

http://hdl.handle.net/11427/2726

OAI identifier oai:identifier

oai:open.uct.ac.za:11427/2726