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Identifying risk factors for impaired oral rotavirus vaccine (ORV) efficacy in low-income countries may lead to improvements in vaccine design and delivery. We measured maternal rotavirus antibodies, environmental enteric dysfunction (EED), and bacterial gut microbiota development among infants receiving two doses of Rotarix in India (n = 307), Malawi (n = 119), and the UK (n = 60), using standardised methods across cohorts. ORV shedding and seroconversion rates were significantly lower in Malawi and India than the UK. Maternal rotavirus-specific antibodies in serum and breastmilk were negatively correlated with ORV response in India and Malawi, and this was mediated partly by a reduction in ORV replication. In the UK, ORV replication was not inhibited despite comparable maternal antibody levels. In both India and Malawi, pre-vaccination microbiota diversity was negatively correlated with ORV immunogenicity, suggesting that high early-life microbial exposure may contribute to impaired vaccine efficacy.

Global poliovirus surveillance involves virus isolation from stool and environmental samples, intratypic differential (ITD) by PCR, and sequencing of the VP1 region to distinguish vaccine (Sabin), vaccine-derived, and wild-type polioviruses and to ensure an appropriate response. This cell culture algorithm takes 2 to 3 weeks on average between sample receipt and sequencing. Direct detection of viral RNA using PCR allows faster detection but has traditionally faced challenges related to poor sensitivity and difficulties in sequencing common samples containing poliovirus and enterovirus mixtures., Global poliovirus surveillance involves virus isolation from stool and environmental samples, intratypic differential (ITD) by PCR, and sequencing of the VP1 region to distinguish vaccine (Sabin), vaccine-derived, and wild-type polioviruses and to ensure an appropriate response. This cell culture algorithm takes 2 to 3 weeks on average between sample receipt and sequencing. Direct detection of viral RNA using PCR allows faster detection but has traditionally faced challenges related to poor sensitivity and difficulties in sequencing common samples containing poliovirus and enterovirus mixtures. We present a nested PCR and nanopore sequencing protocol that allows rapid (99.9%. This novel method shows promise as a faster and safer alternative to cell culture for the detection and real-time sequencing of polioviruses in stool and environmental samples.

Environmental enteropathy (EE) or environmental enteric dysfunction (EED) is a poorly defined condition of the small intestine usually associated with gut inflammation and increased gut permeability. This condition is common in less developed settings and has been hypothesized to be linked to the high enteropathogen load in infants in developing countries, which leads to chronic enteric T-cell–mediated inflammation.1 This, in turn, has been linked with linear growth failure, impaired cognition, and suboptimal response to oral vaccines.2 Although studies, such as the “Etiology, Risk Factors and Interactions of Enteric Infections and Malnutrition and Consequences for Child Health and Development” (MAL-ED), have looked at biomarkers of EE among children in deprived settings, there are few studies evaluating differences, if any, in the levels of proposed biomarkers of EE or EED in children living in different environments in the same geographic location. The MAL-ED study looked at the role played by enteropathogen infection in malnutrition, gut inflammation, and other long-term health outcomes by focusing on resource-deprived settings with high incidence of diarrheal disease.3 However, this and other such studies have not evaluated heterogeneity in enteropathogen exposure and its consequences in communities with varying access to clean water and sanitation. In the following study, we compared the prevalence of asymptomatic enteropathogens and biomarkers of gut inflammation as a component of EE/EED,4 among infants and children living in different environmental conditions in southern India.

Aim Beta asarone is the major constituent of oil obtained from Acorus calamus, the Indian traditional medicine plant. Several studies have shown that beta asarone causes liver and cardiac damages but the reproductive toxicity is not well understood. The present study was initiated to investigate whether beta asarone has the potential to cause reproductive toxicity by inducing oxidative stress in the testis of male Wistar albino rats. Materials and methods For this study, the animals were divided into six groups: Group I was treated with saline (normal saline), Group II with DMSO (vehicle control) and Group III with cisplatin (10 mg/kg b.wt.). Group IV, V and VI animals were administrated at three dose levels of beta asarone 12.5, 25 and 50 mg/kg b.wt. The treatment was carried out for 14 days and animals were sacrificed on 29th day and processed for sperm analysis, hormone assay, histopathological, and antioxidant enzymatic assays. We also used molecular docking studies to predict the binding nature of beta asarone with luteinizing hormone receptor (LHR) and follicle-stimulating hormone receptor (FSHR). Key findings Beta asarone administered at a dose of 50 mg/kg b.wt. was responsible for inducing certain noticeable degenerative changes in histopathological analysis of the tissue. This was supported by altered sperm morphology and hormonal variations when compared to the control groups. Antioxidant enzyme levels were also found to be decreased. This was further validated by molecular docking studies. Significance The present study provides evidence that beta asarone administered at a dose of 50 mg/kg b.wt. is capable enough in bringing about moderate amount of degenerative changes in rat testis and altered antioxidant status. Therefore provides a suitable evidence to prove that beta asarone causes reproductive toxicity.