Phosphorylation Modifications and Their Role in Viral Pneumonia: Mechanisms and Therapeutic Implications

Abstract

Advances in diagnostic technologies have led to the identification of an increasing number of viruses associated with pneumonia, thereby drawing significant attention to viral pneumonia. The primary viral pathogens implicated in pneumonia include influenza virus, respiratory syncytial virus, coronavirus, adenovirus, parainfluenza virus, human metapneumovirus, and enterovirus. Post-translational modifications, especially phosphorylation, are pivotal in the lifecycle of these viruses. Phosphorylation affects key processes such as viral replication, transcription, assembly, and release, thereby influencing their propagation in host cells. Viral infection can also trigger kinase-associated pathways within host cells, activating host cell phosphatases and related signaling cascades. This results in alterations to host phosphorylation states, aggravating cellular pathology and facilitating viral proliferation. This review examines the common viral pathogens involved in pneumonia and highlights the role of phosphorylation in viral proliferation. Additionally, we explore the potential of phosphorylation inhibitors in controlling viral infections, with the aim of advancing our understanding of viral phosphorylation and promoting the use of these inhibitors in the treatment of viral pneumonia.