SARS-CoV-2 ORF7a potently inhibits the antiviral effect of the host factor SERINC5.
Uddhav TimilsinaSupawadee UmthongEmily B IveyBrandon WaxmanSpyridon StavrouPublished in: Nature communications (2022)
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.
Keyphrases
- sars cov
- respiratory syndrome coronavirus
- human immunodeficiency virus
- antiretroviral therapy
- hepatitis c virus
- hiv infected
- hiv positive
- coronavirus disease
- hiv aids
- healthcare
- hiv testing
- drug delivery
- bone marrow
- single cell
- men who have sex with men
- amino acid
- health information
- cell therapy
- small molecule
- stem cells
- quantum dots
- sensitive detection
- single molecule