Treatment options for viral infections are limited and viruses have proven adept at evolving resistance to many existing therapies, highlighting a significant vulnerability in our defenses. In response to this challenge, we explored the modulation of cellular RNA metabolic processes as an alternative paradigm to antiviral development. Previously, the small molecule 5342191 was identified as a potent inhibitor of HIV-1 replication by altering viral RNA accumulation at doses that minimally affect host gene expression. In this report, we document 5342191 as a potent inhibitor of adenovirus, coronavirus, and influenza replication. In each case, 5342191-mediated reduction in virus replication was associated with altered viral RNA accumulation and loss of viral structural protein expression. Interestingly, while resistant viruses were rapidly isolated for compounds targeting either virus-encoded proteases or polymerases, we have not yet isolated 5342191-resistant variants of coronavirus or influenza. As with HIV-1, 5342191’s inhibition of coronaviruses and influenza is mediated through the activation of specific cell signaling networks, including GPCR and/or MAPK signaling pathways that ultimately affect SR kinase expression. Together, these studies highlight the therapeutic potential of compounds that target cellular processes essential for the replication of multiple viruses. Not only do these compounds hold promise as broad-spectrum antivirals, but they also offer the potential of greater resilience in combating viral infections.

Background: There is some evidence of the association between ST‐segment elevation in the V4R chest lead and the likelihood of anterior wall myocardial infarction; however, the link of this phenomenon with the location and the severity of the coronary involvements in such patients remains uncertain. We aimed to investigate the ST‐segment elevation in V4R leads in patients with anterior myocardial infarction and also its effect on prognosis as well as the detection and prediction of the location of arterial stenosis in coronary angiography.Methods: Data collection was performed by reviewing the hospital recorded files of 195 patients’ suspicion of acute myocardial infarction who have been referred within 2 h of the onset of cardiac symptoms. The patients were then categorized into two groups with and without ST elevation in the V4R chest lead.Results: Comparing two groups showed a significantly higher rate of concurrent ST‐segment elevation in V₁ lead in those with ST‐segment elevation in V4R. Echocardiography on the day after anterior myocardial infarction showed LVEF <40% in 74% and 35.2% of patients with and without ST‐segment elevation in V4R, respectively, indicating a significant difference. The lesions on proximal LAD were more common in the group with ST‐segment elevation in V4R.Conclusion: Our study emphasized a high likelihood of ST‐segment elevation in V4R lead concurrently with ST‐elevation in V₁ lead. Also, the appearance of ST‐segment elevation in V4R lead can be accompanied with a lower LVEF, myocardial infarct size, involvement of proximal part of LAD, and Wrap around LAD.