以前的研究已鑒別出病毒“隱藏”或“逃避”免疫系統(tǒng)的許多戰(zhàn)略機制，但研究人員在8月出版的《自然—免疫學》期刊上報告說，他們鑒別出一種前所未知的感冒瘡病毒逃避免疫系統(tǒng)的新機制,。
單純皰疹病毒1型（HSV-1）會導致感冒瘡。被稱為“自然殺手”的T細胞是一種免疫細胞，它能探測和牽制HSV-1。HSV-1顆粒通常出現(xiàn)在被感染細胞表面,，因此T細胞能夠區(qū)分感染和未感染細胞。CD1d是一種“展示”HSV-1的分子,，它持續(xù)地從細胞表面到里面作環(huán)狀運動,，為T細胞采集和展示被感染細胞的內容。
Peter Cresswell 和同事發(fā)現(xiàn),，HSV-1阻斷了這種環(huán)形運動,，特別是阻斷了CD1d分子回到細胞表面，結果導致T細胞不能探測到被HSV-1感染的細胞,。雖然目前科學家們還不清楚這種病毒究竟是如何阻斷CD1d的循環(huán)運動的,，但是，新結果強調了病毒還有另外一種逃避免疫系統(tǒng)的新機制,。
英文原文：
Cold sore virus can evade immune system
NEW HAVEN, Conn., July 17 (UPI) -- U.S. scientists say they have found another method deployed by cold sore viruses to escape the body's immune system.
Immune cells called natural killer T cells are important in detecting and containing herpes simplex virus 1 infections, which cause cold sores.
HSV-1 particles are 'displayed' on the surface of infected cells, enabling the natural killer T cells to distinguish between infected and uninfected cells. The molecule CD1d, which presents HSV-1 particles, constantly moves in a loop from the cell surface to the interior of the cell to sample and display the contents of infected cells to natural killer T cells.
Peter Cresswell and colleagues at Yale University found HSV-1 blocks that loop; specifically preventing CD1d molecules from returning to the cell surface. As a result, HSV-1-infected cells appear to be uninfected and are, therefore, nearly 'invisible' to natural killer T cells.
Precisely how the virus blocks CD1d looping remains to be determined. However, the researchers say their findings emphasize an additional mechanism by which viruses can escape immune detection.
The study is reported in the August issue of the journal Nature Immunology.
