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  1. Social interaction is inherently bidirectional, but research on autistic peer interactions often frames communication as unidirectional and in isolation from the peer context. This study investigated natural peer interactions among six autistic and six non-autistic adolescents in an inclusive school club over 5 months (14 45-min sessions in total) to examine the students’ peer preferences in real-world social interactions and how the preferences changed over time. We further examined whether social behavior characteristics differ between student and peer neurotype combinations. Findings showed that autistic students were more likely to interact with autistic peers then non-autistic peers. In both autistic and non-autistic students, the likelihood of interacting with a same-neurotype peer increased over time. Autistic and non-autistic students’ within-neurotype social interactions were more likely to reflect relational than functional purposes, be characterized as sharing thoughts and experiences rather than requesting help or objects, and be highly reciprocal, as compared with cross-neurotype interactions. These peer preferences and patterns of social interactions were not found among student-peer dyads with the same genders. These findings suggest that peer interaction is determined by more than just a student’s autism diagnosis, but by a combination of student and peer neurotypes. Lay abstract Autistic students often experience challengesmore »in peer interactions, especially for young adolescents who are navigating the increased social expectations in secondary education. Previous research on the peer interactions of autistic adolescents mainly compared the social behaviors of autistic and non-autistic students and overlooked the peers in the social context. However, recent research has shown that the social challenges faced by autistic may not be solely contributed by their social differences, but a mismatch in the social communication styles between autistic and non-autistic people. As such, this study aimed to investigate the student-and-peer match in real-world peer interactions between six autistic and six non-autistic adolescents in an inclusive school club. We examined the odds of autistic and non-autistic students interacting with either an autistic peer, a non-autistic peer, or multiple peers, and the results showed that autistic students were more likely to interact with autistic peers then non-autistic peers. This preference for same-group peer interactions strengthened over the 5-month school club in both autistic and non-autistic students. We further found that same-group peer interactions, in both autistic and non-autistic students, were more likely to convey a social interest rather than a functional purpose or need, be sharing thoughts, experiences, or items rather than requesting help or objects, and be highly reciprocal than cross-group social behaviors. Collectively, our findings support that peer interaction outcomes may be determined by the match between the group memberships of the student and their peers, either autistic or non-autistic, rather than the student’s autism diagnosis.« less
  2. Shenk, Thomas (Ed.)
    ABSTRACT During replication of herpesviruses, capsids escape from the nucleus into the cytoplasm by budding at the inner nuclear membrane. This unusual process is mediated by the viral nuclear egress complex (NEC) that deforms the membrane around the capsid by oligomerizing into a hexagonal, membrane-bound scaffold. Here, we found that highly basic membrane-proximal regions (MPRs) of the NEC alter lipid order by inserting into the lipid headgroups and promote negative Gaussian curvature. We also find that the electrostatic interactions between the MPRs and the membranes are essential for membrane deformation. One of the MPRs is phosphorylated by a viral kinase during infection, and the corresponding phosphomimicking mutations block capsid nuclear egress. We show that the same phosphomimicking mutations disrupt the NEC-membrane interactions and inhibit NEC-mediated budding in vitro , providing a biophysical explanation for the in vivo phenomenon. Our data suggest that the NEC generates negative membrane curvature by both lipid ordering and protein scaffolding and that phosphorylation acts as an off switch that inhibits the membrane-budding activity of the NEC to prevent capsid-less budding. IMPORTANCE Herpesviruses are large viruses that infect nearly all vertebrates and some invertebrates and cause lifelong infections in most of the world’s population. During replication,more »herpesviruses export their capsids from the nucleus into the cytoplasm by an unusual mechanism in which the viral nuclear egress complex (NEC) deforms the nuclear membrane around the capsid. However, how membrane deformation is achieved is unclear. Here, we show that the NEC from herpes simplex virus 1, a prototypical herpesvirus, uses clusters of positive charges to bind membranes and order membrane lipids. Reducing the positive charge or introducing negative charges weakens the membrane deforming ability of the NEC. We propose that the virus employs electrostatics to deform nuclear membrane around the capsid and can control this process by changing the NEC charge through phosphorylation. Blocking NEC-membrane interactions could be exploited as a therapeutic strategy.« less