key: cord-0858816-979qfbcg authors: Bizzotto, Juan; Sanchis, Pablo; Abbate, Mercedes; Lage-Vickers, Sofía; Lavignolle, Rosario; Toro, Ayelén; Olszevicki, Santiago; Sabater, Agustina; Cascardo, Florencia; Vazquez, Elba; Cotignola, Javier; Gueron, Geraldine title: SARS-CoV-2 infection boosts MX1 antiviral effector in COVID-19 patients date: 2020-09-23 journal: iScience DOI: 10.1016/j.isci.2020.101585 sha: 2b51f2290c9401ede3d4883a627c05ea9ced0db8 doc_id: 858816 cord_uid: 979qfbcg In a published case-control study (GSE152075) from SARS-CoV-2 positive (n=403) and negative patients (n=50), we analyzed the response to infection assessing gene expression of host cell receptors and antiviral proteins. The expression analysis associated with reported risk factors for COVID-19 was also assessed. SARS-CoV-2 cases had higher ACE2, but lower TMPRSS2, BSG/CD147 and CTSB expression compared with negative cases. COVID-19 patients’ age negatively affected ACE2 expression. MX1 and MX2 were higher in COVID-19 patients. A negative trend for MX1 and MX2 was observed as patients’ age increased. Principal Component Analysis determined that ACE2, MX1, MX2, and BSG/CD147 expression was able to cluster non-COVID-19 and COVID-19 individuals. Multivariable regression showed that MX1 expression significantly increased for each unit of viral load increment. Altogether, these findings support differences in ACE2, MX1, MX2, and BSG/CD147 expression between COVID-19 and non-COVID-19 patients and point out to MX1 as a critical responder in SARS-CoV-2 infection. There is controversial data concerning therapies that could modulate ACE2 expression, like In conclusion, these results highlight MX1 as a solid responder to SARS-CoV-2 pointing out to 265 the relevance of evaluating approved drugs able to boost MX1 expression and halt infection. Delayed 462 antiviral plus immunomodulator treatment still reduces mortality in mice infected by high 463 inoculum of influenza A/H5N1 virus Risk factors of critical & mortal COVID-19 467 cases: A systematic literature review and meta-analysis Protease inhibitors 471 targeting coronavirus and filovirus entry