Commentary: Early-in-life Isoflurane Exposure Alters Resting-state Functional connectivity in Juvenile Non-human Primates - a Role for Neuroinflammation?
Viola Neudecker1#, Jose F. Perez-Zoghbi1# and Ansgar M. Brambrink1*
Department of Anesthesiology, Columbia University Medical Center, New York, NY 10032, USA.;
The concern about anesthesia-induced developmental neurotoxicity (AIDN) in infants and young children arises from animal studies indicating potential long-term neurobehavioral impairments following early-in-life anesthesia exposure. While initial clinical studies provided ambiguous results, recent prospective assessments in children indicate associations between early-in-life anesthesia exposure and later behavioral alterations. Ethical constraints and confounding factors in clinical studies pose challenges in establishing a direct causal link and in investigating its mechanisms. This commentary on a recent study in non-human primates (NHPs) focuses on exploring the role of neuroinflammation and alterations in brain functional connectivity in the behavioral impairments following early-in-life anesthesia exposure. In juvenile NHPs, chronic astrogliosis in the amygdala correlates with alterations in functional connectivity between this area with other regions of the brain and with the behavioral impairments, suggesting a potential mechanism for AIDN. Despite acknowledging the study's limitations, these findings emphasize the need for further research with larger cohorts to confirm these associations and to establish a causal link between the neuroinflammation and the behavioral alterations associated with early-in-life anesthesia exposure.
DOI: 10.29245/2578-3009/2024/2.1255 View / Download PdfAdvances in Understanding the Envelope Protein in Coronavirus Infection
Aakanksha Agarwal1 and Ashley L. Steed1*
1Department of Pediatrics, Washington University School of Medicine, Saint Louis, Missouri, United States of America
The COVID-19 pandemic continues to impart devastating effects on human health, healthcare systems, and the economy. Vaccination, monoclonal antibodies, and antiviral therapies prevent and limit early infection. Unfortunately, few strategies exist to mitigate the disease burden in the vast number of individuals who seek medical attention with established infection and severe disease. While we have a limited understanding of the mechanistic basis by which SARS-CoV-2 causes critical illness, increasing evidence suggests that host-pathogen interactions shape immune responses that drive the pathogenesis of COVID-19. Therefore, it is imperative to understand the roles of the viral proteins and how they shape the course of infection. One interesting protein is the envelope (E) protein of SARS-CoV-2; this tiny structural protein has been implicated in many phases of the viral life cycle. Importantly, the E protein facilitates viral packaging and replication, and its deletion reduces viral pathogenicity. The E protein also possesses ion channel functions, interacts with host proteins, and has the potential to have various structural topologies. This review aims to establish an updated understanding by highlighting recent developments in the investigation of the SARS-CoV-2 E protein, particularly in comparison to the envelope protein of SARS-CoV. thorough knowledge of this protein will enable targeted studies in hopes of tailored efficacious treatments.
DOI: 10.29245/2578-3009/2024/1.1256 View / Download Pdf