以前的研究已鉴别出病毒“隐藏”或“逃避”免疫系统的许多战略机制,但研究人员在8月出版的《自然—免疫学》期刊上报告说,他们鉴别出一种前所未知的感冒疮病毒逃避免疫系统的新机制。
单纯疱疹病毒1型(HSV-1)会导致感冒疮。被称为“自然杀手”的T细胞是一种免疫细胞,它能探测和牵制HSV-1。HSV-1颗粒通常出现在被感染细胞表面,因此T细胞能够区分感染和未感染细胞。CD1d是一种“展示”HSV-1的分子,它持续地从细胞表面到里面作环状运动,为T细胞采集和展示被感染细胞的内容。
Peter Cresswell 和同事发现,HSV-1阻断了这种环形运动,特别是阻断了CD1d分子回到细胞表面,结果导致T细胞不能探测到被HSV-1感染的细胞。虽然目前科学家们还不清楚这种病毒究竟是如何阻断CD1d的循环运动的,但是,新结果强调了病毒还有另外一种逃避免疫系统的新机制。
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.