ABSTRACT
Background: Cytomegalovirus (CMV) is known to cause symptomatic disease in immunocompromised individuals. We present a rare case of CMV myopericarditis with findings of acute pulmonary embolism (PE) thought to be from the procoagulant effect of CMV in an immunocompetent middle-aged female. Case: 55-year-old female who presented to the ED for chest pain. Found to have non-specific EKG changes in V4-V6, troponin and COVID negative. TTE with EF 68% and pericardial effusion. ESR and CRP were elevated. Started on treatment for viral myopericarditis with colchicine, unfortunately developed diarrhea and was switched to high dose aspirin. CT coronary angiogram was performed to rule out ischemia. Calcium score of 0 and non-obstructive CAD in the LAD. CT also showed a new acute PE with no RV strain and she was started on Xarelto for anticoagulation. Infectious work up was performed, serum CMV IgM positive and CMV DNA of 18,205 copies. Oral valganciclovir was started for a total 21-day course for CMV myopericarditis. Patient was discharged with improvement of symptoms and plan for follow up with infectious diseases and cardiology for follow-up cardiac MRI. Decision-making: Symptomatic CMV infection is common in immunocompromised individuals. Immunocompetent patients that present with pulmonary embolism are far fewer. Cardiovascular complications have only been mentioned a handful of times in literature. In addition, and to the best of our knowledge, this is only the second known description of a patient to experience both myo-pericarditis and pulmonary embolism simultaneously from a symptomatic CMV infection. Conclusion: It is important for clinicians to be aware of this rare presentation of CMV, adding this to the differential diagnosis when an immunocompetent patient presents with symptoms concerning for viral pericarditis and/or evidence of pulmonary embolus.
ABSTRACT
The emergence of SARS-CoV-2 virus has resulted in a worldwide pandemic, but effective antiviral therapies are not widely available. To improve treatment options, we conducted a high-throughput screen to uncover compounds that block SARS-CoV-2 infection. A minimally pathogenic human betacoronavirus (OC43) was used to infect physiologically-relevant human pulmonary fibroblasts (MRC5) to facilitate rapid antiviral discovery in a preclinical model. Comprehensive profiling was conducted on more than 600 compounds, with each compound arrayed across 10 dose points. Our screening revealed several FDA-approved agents that can attenuate both OC43 and SARS-CoV-2 viral replication, including lapatinib, doramapimod, and 17-AAG. Importantly, lapatinib inhibited SARS-CoV-2 RNA replication by over 50,000-fold. Further, both lapatinib and doramapimod could be combined with remdesivir to improve antiviral activity in cells. These findings reveal novel therapeutic avenues that could limit SARS-CoV-2 infection.