Background The IL‐33/ST2 immune axis plays crucial roles in infection and immunity. A dysregulated IL‐33/ST2 axis can induce autoimmune reaction and inflammatory responses. Guillain‐Barré syndrome (GBS) is an acute peripheral neuropathy, mostly caused by post‐infection autoimmunity. The role of IL‐33/ST2 axis is not known in GBS. This study aimed to explore the role of IL‐33/ST2 axis in GBS. Methods Three single nucleotide polymorphisms (SNPs) of Il33 gene (rs16924159, rs7044343, rs1342336) and three SNPs of Il1rl1 gene (rs10192157, rs1041973, rs10206753) coding for suppressor of tumorigenicity 2 (ST2) were genotyped in 179 GBS patients and 186 healthy controls by TaqMan Allelic Discrimination Assay. Plasma levels of IL‐33 and sST2 were measured in a subset of GBS patients (n = 80) and healthy controls (n = 80) by ELISA. Results The frequencies of CC genotype of rs10192157 (p = 0.043) and TT genotype of rs10206753 (p = 0.036) SNPs of Il1rl1 gene differed significantly between GBS patients and healthy controls. Gene–gene interaction between Il33 and Il1rl1 genes also conferred significant risk for GBS. In addition, the plasma sST2 levels were significantly elevated in GBS patients compared to healthy subjects (24,934.31 ± 1.81 pg/ml vs. 12,518.97 ± 1.51 pg/ml, p < 0.001). Plasma sST2 levels showed a significant correlation with the disability scores at the peak of neurological deficit in GBS patients. Conclusions The IL‐33/ST2 axis is suggested to influence the immunopathogenesis of GBS. Genetic variants of Il1rl1 gene might serve as a risk determinant of GBS and plasma sST2 levels might emerge as a biomarker of severity of GBS, if replicated further by other studies.

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Chikungunya virus (CHIKV) is primarily transmitted by Aedes spp. mosquitoes. The present study investigated vector competence for CHIKV in Aedes aegypti and Aedes albopictus mosquitoes found in Madurai, South India. The role of receptor proteins on midguts contributing to permissiveness of CHIKV to Aedes spp. mosquitoes was also undertaken. Mosquitoes were orally infected with CHIKV DRDE‐06. Infection of midguts and dissemination to heads was confirmed by immunofluorescence assay at different time points. A plaque assay was performed from mosquito homogenates at different time points to study CHIKV replication. Presence of putative CHIKV receptor proteins on mosquito midgut epithelial cells was detected by virus overlay protein binding assay (VOPBA). The identity of these proteins was established using mass spectrometry. CHIKV infection of Ae. aegypti and Ae. albopictus midguts and dissemination to heads was observed to be similar. A plaque assay performed with infected mosquito homogenates revealed that CHIKV replication dynamics was similar in Aedes sp. mosquitoes until 28 days post infection. VOPBA performed with mosquito midgut membrane proteins revealed that prohibitin could serve as a putative CHIKV receptor on Aedes mosquito midguts, whereas an absence of CHIKV binding protein/s on Culex quinquefasciatus midguts can partially explain the non‐permissiveness of these mosquitoes to infection.

Introduction Schizophrenia is one of the most severe mental disorders with a prevalence of about 1% and a leading cause of disability among young adults. Pharmacotherapy is the mainstay in the management of schizophrenia. However, even with the best of medication, several problems like refractoriness, negative symptoms, frequent relapses, and cognitive impairments persist. Methods This is a randomized-controlled clinical study including patients from an urban tertiary hospital and a semi-urban community center, with a between-group, repeated-measures, longitudinal design. This study will recruit 160 patients with DSM 5 diagnosis of schizophrenia who are on stable medication for a minimum of 6 weeks; they will be randomly assigned into 2 arms viz., yoga therapy (YT), and treatment-as-usual (TAU) with 80 patients in each arm. Participants will undergo Clinical, Laboratory, and Radiological assessments at baseline and at intervals of 1 month, 3 months, and 6 months from the baseline. It is hypothesized that yoga will improve psychopathology and emotion processing, increase serum brain derived neurotrophic factor (BDNF) and plasma oxytocin levels and effect changes in cerebral activation in areas of the brain associated with schizophrenia. Discussion This study aims to measure the efficacy of a Yoga-based intervention as an adjunct in patients with schizophrenia as well as the mechanisms of these effects. Trial registration Registered retrospectively with Clinical Trial Registry – India (CTRI) with registration number CTRI/2017/08/009219.

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