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缺失 sgg1 的鼠巨细胞病毒进入唾液腺的能力降低。

Mouse cytomegalovirus lacking sgg1 shows reduced import into the salivary glands.

机构信息

School of Chemistry and Molecular Biosciences, University of Queensland, Brisbane, Australia.

出版信息

J Gen Virol. 2024 Aug;105(8). doi: 10.1099/jgv.0.002013.

Abstract

Cytomegaloviruses (CMVs) transmit via chronic shedding from the salivary glands. How this relates to the broad cell tropism they exhibit is unclear. Human CMV (HCMV) infection presents only after salivary gland infection is established. Murine CMV (MCMV) is therefore useful to analyse early infection events. It reaches the salivary glands via infected myeloid cells. Three adjacent spliced genes designated as m131/129 (MCK-2), sgg1 and sgg1.1, positional homologues of the HCMV UL128/130/131 tropism determinants, are implicated. We show that a sgg1 null mutant is defective in infected myeloid cell entry into the salivary glands, a phenotype distinct from MCMV lacking MCK-2. These data point to a complex, multi-step process of salivary gland colonization.

摘要

巨细胞病毒(CMVs)通过唾液腺的慢性脱落传播。它们表现出广泛的细胞嗜性,但目前尚不清楚这种传播方式与细胞嗜性之间的关系。人巨细胞病毒(HCMV)感染仅在唾液腺感染建立后才会发生。因此,鼠巨细胞病毒(MCMV)可用于分析早期感染事件。它通过受感染的髓样细胞到达唾液腺。三个相邻的剪接基因,命名为 m131/129(MCK-2)、sgg1 和 sgg1.1,与 HCMV UL128/130/131 倾向性决定因素的位置同源物有关。我们表明,sgg1 缺失突变体在感染的髓样细胞进入唾液腺方面存在缺陷,这是一种与缺乏 MCK-2 的 MCMV 不同的表型。这些数据表明,唾液腺定植是一个复杂的、多步骤的过程。

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