Department of Microbiology and Immunology, Witebsky Center for Microbial Pathogenesis and Immunology, School of Medicine and Biomedical Sciences, State University of New York at Buffalo, 109 BRB, 3435 Main Street, Buffalo, NY 14214, USA.
Microb Pathog. 2012 Jan;52(1):25-30. doi: 10.1016/j.micpath.2011.09.007. Epub 2011 Oct 2.
Cryptococcosis, caused by Cryptococcus neoformans, is the most common opportunistic fungal disease in HIV/AIDS patients. The prognosis of AIDS patients with Cryptococcus infection is very poor. One of the major characteristics in cryptococcosis patients is the presence of high concentrations of the cryptococcal capsule polysaccharide (CCP) in the serum and cerebrospinal fluid. CCP enhances HIV replication in H9 T-cells, but the mechanism is unknown. In this study, we tested whether extracellular glucuronoxylomannan (GXM), a major component of CCP, enhances HIV entry using replication-incompetent HIV and a cell line which expresses a stable amount of CD4 and both of the HIV co-receptors. Extracellular GXM had no effect on cell-cell fusion however; viral entry surprisingly was inhibited by GXM. Hence, any enhancement of replication must be due to an effect that occurs post-entry.
新型隐球菌病是由新型隐球菌引起的，是 HIV/AIDS 患者中最常见的机会性真菌感染病。艾滋病合并隐球菌感染者的预后极差。隐球菌病患者的主要特征之一是血清和脑脊液中存在高浓度的隐球菌荚膜多糖（CCP）。CCP 可增强 H9 T 细胞中的 HIV 复制，但具体机制尚不清楚。在本研究中，我们使用复制缺陷型 HIV 和表达稳定量 CD4 和两种 HIV 共受体的细胞系来检测细胞外葡聚糖（GXM），即 CCP 的主要成分，是否会增强 HIV 进入。然而，细胞外 GXM 对细胞-细胞融合没有影响；出人意料的是，GXM 抑制了病毒进入。因此，任何复制的增强都必须归因于进入后的影响。
