In a new paper published Jan. 21 in the journal Science, a team of researchers led by Microbiology and Immunology professor Blossom Damania, PhD, has shown for the first time that the Kaposi sarcoma virus has a decoy protein that impedes a key molecule involved in the human immune response.
The work was performed in collaboration with W.R. Kenan, Jr. Distinguished Professor, Jenny Ting, PhD. First author, Sean Gregory, MS, a graduate student in UNC's Department of Microbiology and Immunology played a critical role in this work.
The virus-produced protein, called a homolog, binds to the cellular protein that normally triggers an inflammatory response, a key immune system weapon for fighting viral infection. However, the homolog lacks a key part of the cellular protein that triggers the inflammation process. Inflammasome activation leads to the production of proinflammatory cytokines and eventual cell death.
The work was performed in collaboration with W.R. Kenan, Jr. Distinguished Professor, Jenny Ting, PhD. First author, Sean Gregory, MS, a graduate student in UNC's Department of Microbiology and Immunology played a critical role in this work.
The virus-produced protein, called a homolog, binds to the cellular protein that normally triggers an inflammatory response, a key immune system weapon for fighting viral infection. However, the homolog lacks a key part of the cellular protein that triggers the inflammation process. Inflammasome activation leads to the production of proinflammatory cytokines and eventual cell death.
