Although the influence of sleep quality on the immune system is well documented, the mechanisms behind its impact on natural host immunity remain unclear. Meanwhile, it has been suggested that neuroimmune interactions play an important role in this phenomenon. To evaluate the impact of stress-induced sleep disturbance on host immunity, we used a murine model of rapid eye movement sleep deprivation (RSD) integrated with a model of malaria blood-stage infection. We demonstrate that sleep disturbance compromises the differentiation of T follicular helper cells, increasing host susceptibility to the parasite. Chemical inhibition of glucocorticoid (Glcs) synthesis showed that abnormal Glcs production compromised the transcription of Tfh-associated genes resulting in impaired germinal center formation and humoral immune response. Our data demonstrate that RSD-induced abnormal activation of the hypothalamic-pituitary-adrenal axis drives host susceptibility to infection. Understanding the impact of sleep quality in natural resistance to infection may provide insights for disease management.

In 2015, the world witnessed the resurgence and global spread of Zika virus (ZIKV). This arbovirus infection is associated with Guillain-Barré syndrome in adults and with devastating congenital malformations during pregnancy. Despite scientific efforts, the development of a vaccine capable of inducing long-term protection has been challenging. Without a safe and efficacious licensed vaccine, control of virus transmission is based on vector control, but this strategy has been shown to be inefficient. An effective and protective vaccine relies on several requirements, which include: (i) induction of specific immune response against immunodominant antigens; (ii) selection of adjuvant-antigen formulation; and (iii) assessment of safety, effectiveness, and long-term protection. In this commentary, we provide a brief overview about the current efforts for the development of an efficacious ZIKV vaccine, covering the most important preclinical trials up to the formulations that are now being evaluated in clinical trials.

Chikungunya virus (CHIKV) is an arbovirus transmitted to humans mainly by the bite of infected Aedes aegypti and Aedes albopictus mosquitoes. CHIKV illness is characterized by fever and long-lasting arthritic symptoms, and in some cases it is a deadly disease. The CHIKV envelope E2 (E2_CHIKV) glycoprotein is crucial for virus attachment to the cell. Furthermore, E2_CHIKV is the immunodominant protein and the main target of neutralizing antibodies. To date, there is no available prophylactic vaccine or specific treatment against CHIKV infection. Here, we designed and produced a DNA vaccine and a recombinant protein containing a consensus sequence of E2_CHIKV. C57BL/6 mice immunized twice with the E2_CHIKV recombinant protein in the presence of the adjuvant Poly (I:C) induced the highest E2_CHIKV-specific humoral and cellular immune responses, while the immunization with the homologous DNA vaccine pVAX-E2_CHIKV was able to induce specific IFN-γ producing cells. The heterologous prime-boost strategy was also able to induce specific cellular and humoral immune responses that were, in general, lower than the responses induced by the homologous E2_CHIKV recombinant protein immunization. Furthermore, recombinant E2_CHIKV induced the highest titers of neutralizing antibodies. Collectively, we believe this is the first report to analyze E2_CHIKV-specific humoral and cellular immune responses after immunization with E2_CHIKV recombinant protein and DNA pVAX-E2_CHIKV vaccine platforms.