Insights into the mechanisms of apoptosis and pathogenesis in enterovirus 71 infections: A review

Abstract

This study examines the intricate interactions between enterovirus 71 (EV71) and various programmed cell death pathways, specifically apoptosis, necroptosis, and pyroptosis, which collectively shape the pathogenesis and severity of EV71 infections. Primarily affecting children under 5 years of age, EV71 is a leading cause of hand, foot, and mouth disease and has been linked to severe neurological and systemic complications. This paper highlights how EV71 leverages distinct cell death mechanisms to enhance viral replication and amplify disease pathology. Apoptosis, for example, may restrict viral dissemination by systematically eliminating infected cells; however, EV71's activation of necroptosis and pyroptosis induces robust inflammatory responses, potentially resulting in extensive tissue damage and adverse health outcomes. Additionally, this study also summarizes recent advancements in the field, with an emphasis on experimental studies and clinical trials focused on vaccine and antiviral therapy development. Despite substantial progress, challenges persist, notably in achieving reliable vaccine efficacy and formulating safe treatment options specifically for pediatric populations. Moving forward, the review suggests that future research should delve further into understanding EV71-related complications, developing broad-spectrum antiviral agents, and investigating host genetic factors that may influence disease progression and outcomes. Ultimately, this research is essential for the development of targeted interventions capable of reducing severe symptoms without compromising the immune response, underscoring the importance of these efforts for public health and the management of infectious diseases.

Keywords: advance; apoptosis; enterovirus 71; pathogenesis; programmed cell death.

Figure 1.

Interplay between EV71 infection and PCD. EV71 = enterovirus 71, PCD = programmed cell death.