کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2039820 1073083 2015 11 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Fatty Acid Elongase 7 Catalyzes Lipidome Remodeling Essential for Human Cytomegalovirus Replication
ترجمه فارسی عنوان
تری گلیسیرید اسید چرب 7 کاتالیز می کند ضروری ساختن لیپیدوم برای تکثیر سیتومگالوویروس انسان
موضوعات مرتبط
علوم زیستی و بیوفناوری علوم کشاورزی و بیولوژیک علوم کشاورزی و بیولوژیک (عمومی)
چکیده انگلیسی


• HCMV requires saturated very-long-chain fatty acids for virion envelope lipids
• During infection, these fatty acids are made by fatty acid elongase 7 (ELOVL7)
• SREBP1, mTOR, and the HCMV protein pUL38 induce ELOVL7 expression and activity
• Fatty acid elongation is required for the release of particles and their infectivity

SummaryHuman cytomegalovirus (HCMV) infection rewires host-cell metabolism, upregulating flux from glucose into acetyl-CoA to feed fatty acid metabolism, with saturated very-long-chain fatty acids (VLFCAs) required for production of infectious virion progeny. The human genome encodes seven elongase enzymes (ELOVL) that extend long-chain fatty acids into VLCFA. Here, we identify ELOVL7 as pivotal for HCMV infection. HCMV induces ELOVL7 by more than 150-fold. This induction is dependent on mTOR and SREBP-1. ELOVL7 knockdown or mTOR inhibition impairs HCMV-induced fatty acid elongation, HCMV particle release, and infectivity per particle. ELOVL7 overexpression enhances HCMV replication. During HCMV infection, mTOR activity is maintained by the viral protein pUL38. Expression of pUL38 is sufficient to induce ELOVL7, and pUL38-deficient virus is partially defective in ELOVL7 induction and fatty acid elongation. Thus, through its ability to modulate mTOR and SREBP-1, HCMV induces ELOVL7 to synthesize the saturated VLCFA required for efficient virus replication.

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ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: - Volume 10, Issue 8, 3 March 2015, Pages 1375–1385
نویسندگان
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