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Viral protein helps infected T cells stick to uninfected cells

body, the HTLV-1 mainly targets immune-system cells known as CD4 T lymphocytes. These immune cells coordinate immune responses in part through physical contact with other immune cells. The cells adhere to one another using a protein known as LFA-1, which is found on the cells' surface.

In this study, Lairmore and his collaborators examined the influence of the p12 protein on LFA-1 adhesion. The researchers compared cells infected with HTLV-1 that lacked the p12 protein to cells that were infected by normal HTLV-1.

They found that the p12 protein not only activated the T cells, but caused the cells infected with normal HTLV-1 to have far greater adherence than cells infected with viruses that lacked p12 in a standardized adherence test.

In addition, they showed that the greater adherence did not occur because the infected cells made more of the LFA-1 protein, but rather because already existing LFA-1 protein molecules gathered into large clusters on the cell surface.

(LFA-1 proteins float in the cell membrane like buoys in semisolid gelatin. They can move across the surface of the cell and form clusters when directed to do so by signals from within the cell.)

"Our study is the first to show that HTLV-1 p12 not only enhances the activity of infected T cells, but that it promotes the spread of the virus from cell to cell by causing LFA-1 receptors to cluster on the cell surface," Lairmore says.


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Source:Ohio State University


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