Abstract

Autism spectrum disorder (ASD) is a neurodevelopmental condition of the central nervous system (CNS) that presents with severe communication problems of unknown cause. Few studies have explored the role of some herpesviridae members as potential etiological factors of ASD and phosphatase and tensin homolog (PTEN), a critical regulator of immune function, cellular growth, and neurodevelopment. This study aimed to assess the seropositivity of Herpes simplex virus-I (HSVI), Herpes simplex virus-II (HSVII), Epstein–Barr virus (EBV), and cytomegalovirus (CMV) in children with ASD. Also, the goal of the study was to explore whether viral exposure contributes to ASD through PTEN downregulation and neuroimmune disruption. Serum PTEN levels and their correlation with viral infections were examined. The seropositivity rate to HSV-I, HSV-II, EBV, CMV, and PTEN serum levels was estimated in 100 blood samples from autistic children (65 males and 35 females). The age range was 3 to 14 years, with a mean age of 5.87 ± 2.544 years. An enzyme-linked immunosorbent assay (ELISA) was used. Interestingly, the results demonstrated statistically significant negative correlations across all viral markers, indicating that higher levels of viral infection are associated with lower PTEN expression. Specifically, HSV I showed the strongest negative correlation with PTEN levels (r = –0.48, p < 0.001), followed by EBV (r = –0.45, p < 0.001), HSV II (r = –0.41, p = 0.001), and CMV (r = –0.39, p = 0.002). These findings suggest a consistent pattern in which increased viral load may be contributing to the downregulation of PTEN. This relationship reinforces the hypothesis that viral infections may contribute to reducing PTEN signaling, which could play a role in the pathophysiology of ASD through immune dysregulation or altered neurodevelopmental pathways.

Key words: Autism spectrum disorder, Cytomegalovirus, Epstein–Barr virus, Herpes simplex virus, PTEN