The Zika virus (ZIKV) gained prominence as a significant global pathogen after the 2015–2016 outbreaks associated it with an increase in neurological complications in adults and congenital malformations. Different mechanisms have been proposed by which ZIKV may cross the blood–brain barrier and reach the central nervous system to cause neuroinflammation. Although ZIKV infection triggers a robust immune response, the virus has developed different strategies to escape it. Furthermore, although the virus is present in areas with cocirculation of other pathogenic agents, few studies have evaluated the cross-immune reactions and coinfection of ZIKV. Coinfections of ZIKV with other viruses, parasites, and bacteria are described. Such interactions can worsen infections and alter the immune response, imposing new therapeutic challenges and highlighting the need for more studies in the field. In this review, we discuss various aspects of ZIKV biology, focusing on the impacts of coinfections.

This study aimed to develop films of chitosan (CSF) associated with pentoxifylline (PTX) for healing cutaneous wounds. These films were prepared at two concentrations, F1 (2.0 mg/mL) and F2 (4.0 mg/mL), and the interactions between the materials, structural characteristics, in vitro release, and morphometric aspects of skin wounds in vivo were evaluated. The formation of the CSF film with acetic acid modifies the polymeric structure, and the PTX demonstrates interaction with the CSF, in a semi-crystalline structure, for all concentrations. The release for all films was proportional to the concentration, with two phases: a fast one of ≤2 h and a slow one of >2 h, releasing 82.72 and 88.46% of the drug after 72 h, being governed by the Fickian diffusion mechanism. The wounds of the mice demonstrate a reduction of up to 60% in the area on day 2 for F2 when compared to CSF, F1, and positive control, and this characteristic of faster healing speed for F2 continues until the ninth day with wound reduction of 85%, 82%, and 90% for CSF, F1, and F2, respectively. Therefore, the combination of CSF and PTX is effective in their formation and incorporation, demonstrating that a higher concentration of PTX accelerates skin-wound reduction.

The chikungunya arbovirus (CHIKV) is a persistent health problem with an expanding geographical range of mosquito vectors, but with poorly understood mechanisms regarding insect host specificity. Here, we sought to investigate an alternative model for CHIKV studies, aiming to improve our understanding of its biology in insects. We therefore set out to assess the ability of viruses to multiply in the lepidopteran Sf9 cells, comparing viral infection with C6/36 mosquito cells, commonly used for CHIKV maintenance. Viral exposure of Sf9 cells led to impaired viability and cytopathic effects, with RT-qPCR and immunofluorescence confirming CHIKV infection and production of viral particles, although with yields lower than those observed in C6/36 cells. Transmission electron microscopy revealed infection-induced morphological alterations in Sf9 and C6/36 cells, particularly associated with the endoplasmic reticulum and mitochondria. Viral particles were observed in vesicles and also extracellularly, anchored to the cell membrane. Budding of vesicles containing multiple viral particles were noticeable in Sf9, but not in C6/36, while infectivity was confirmed for CHIKV derived from both cells. Autophagy-like structures were noticed in infected C6/36 cells, supported by expression of the LC3B marker in these cells only. The results validate Sf9 cells as a novel permissive model for the investigation of CHIKV interactions in insects.