病原体と宿主の「永遠の軍拡競争」において、細胞はSARS-CoV-2とHIVの両方に同じ遺伝子で対抗しており、治療法の可能性を示す新たな道筋が明らかに In the ‘eternal arms race’ between pathogen and host, cells employ the same gene to fight both SARS-CoV-2 and HIV, revealing new avenues for potential therapies
2022-05-26 バッファロー大学(UB)
この研究結果は、ウイルスと宿主の細胞間相互作用に関する重要な特徴を明らかにし、SARS-CoV-2、COVID-19の原因ウイルス、およびHIVの両方の新しい治療法を開発するために利用できる可能性を示しています。
本研究は、バッファロー大学(UB)のジェイコブス医学・生物医学学部のウイルス学者によって報告され、Nature Communications誌に掲載されました。
<関連情報>
- https://www.buffalo.edu/news/releases/2022/05/020.html
- https://www.nature.com/articles/s41467-022-30609-9
SARS-CoV-2 ORF7aは宿主因子SERINC5の抗ウイルス作用を強力に阻害する SARS-CoV-2 ORF7a potently inhibits the antiviral effect of the host factor SERINC5
Uddhav Timilsina,Supawadee Umthong,Emily B. Ivey,Brandon Waxman & Spyridon Stavrou
Nature Communications Published:26 May 2022
DOI:https://doi.org/10.1038/s41467-022-30609-9
Abstract
Serine Incorporator 5 (SERINC5), a cellular multipass transmembrane protein that is involved in sphingolipid and phosphatydilserine biogenesis, potently restricts a number of retroviruses, including Human Immunodeficiency Virus (HIV). SERINC5 is incorporated in the budding virions leading to the inhibition of virus infectivity. In turn, retroviruses, including HIV, encode factors that counteract the antiviral effect of SERINC5. While SERINC5 has been well studied in retroviruses, little is known about its role in other viral families. Due to the paucity of information regarding host factors targeting Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), we evaluated the effect of SERINC proteins on SARS-CoV-2 infection. Here, we show SERINC5 inhibits SARS-CoV-2 entry by blocking virus-cell fusion, and SARS-CoV-2 ORF7a counteracts the antiviral effect of SERINC5 by blocking the incorporation of over expressed SERINC5 in budding virions.
