Mayaro virus (alphavirus) infection of Aedes albopictus cells results in inhibition of cell protein synthesis and viral proteins are preferably synthesized. When infected cells are heat shocked, however, there is also an inhibition of viral protein synthesis, and there is preferential synthesis of heat shock proteins. Based on these observations, the distribution of Mayaro viral RNA in polysomes and the association of p34 (capsid protein) with ribosomal fractions of the cells under such conditions have been analyzed. During infection, the viral RNA is mainly observed in light polysomes (60% of total viral RNA in the cell) and also in heavy polysomes (13%). However, when infected cells are heat-shocked, the viral RNA is strongly mobilized from heavy polysomes to the light polysomes fraction and an enrichment in the unbound fraction can be noticed. The amount of p34 associated with the ribosomal fraction was also shown to be decreased in the heat shocked cells. These data lead to the suggestion that two mechanisms could be involved in the inhibition of Mayaro virus protein synthesis in response to heat shock(1) mobilization of Mayaro virus RNA from heavy to light polysomes; (2) a decrease in the amount of the p34 within the ribosomal fraction.

译文

白纹伊蚊细胞的Mayaro病毒(alphavirus)感染导致细胞蛋白合成受到抑制,并且优选合成病毒蛋白。然而,当热激感染的细胞时,也抑制了病毒蛋白的合成,并且优先合成了热激蛋白。基于这些观察,已经分析了在这种情况下Mayaro病毒RNA在多核糖体中的分布以及p34(衣壳蛋白)与细胞核糖体级分的关系。在感染过程中,病毒RNA主要在轻多核小体(细胞中总病毒RNA的60%)和重多核小体(13%)中观察到。然而,当受热细胞受到热激时,病毒RNA从重多囊泡强烈地转移到轻多囊泡部分,未结合的部分富集。在热激细胞中,与核糖体级分相关的p34的量也显示减少。这些数据表明,响应热休克反应,Mayaro病毒蛋白合成的抑制可能涉及两种机制(1)Mayaro病毒RNA从重链体到轻链体的动员; (2)核糖体组分中p34的含量减少。

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