Juliane Santos de França da Silva
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Juliane Santos de França da Silva has a total of 9 co-authors. Here are the top co-authors by number of shared publications:
- Célio Valdevino Ferreira Junior
Department of Microbiology and Parasitology, Biosciences Center, Federal University of Rio Grande do Norte, Natal 59078-970, Rio Grande Do Norte, Brazil
1 shared publication - José L. Andrade
Department of Microbiology and Parasitology, Biosciences Center, Federal University of Rio Grande do Norte, Natal 59078-970, Rio Grande Do Norte, Brazil
1 shared publication - Juliana Navarro Ueda Yaochite
Universidade Federal do Ceará, Brasil
1 shared publication - Livian Maria Silva dos Santos
Department of Microbiology and Parasitology, Biosciences Center, Federal University of Rio Grande do Norte, Natal 59078-970, Rio Grande Do Norte, Brazil
1 shared publication - Manuela Sales Lima Nascimento
Departamento de Microbiologia e Parasitologia Centro de Biociências, UFRN Natal Rio Grande do Norte Brazil
1 shared publication - Nathalie de Sena Pereira
Department of Microbiology and Parasitology, Biosciences Center, Federal University of Rio Grande do Norte, Natal 59078-970, Rio Grande Do Norte, Brazil
1 shared publication
Latest Publications
- Open Access
The Role of Innate Cells During Alphavirus Chikungunya Infection
Alphavirus chikungunya (CHIKV) is an arthropod-borne alphavirus of the Togaviridae family, transmitted primarily by Aedes aegypti and Ae. albopictus mosquitoes. CHIKV infection often results in debilitating manifestations that compromise quality of life and generate significant socioeconomic impacts. Recurrent epidemics in tropical and subtropical regions underscore the urgent need to better understand the host immune responses and their contribution to disease outcome. CHIKV establishes infection by overcoming the host’s initial immunological barriers. Innate immune cells, including fibroblasts, dendritic cells, macrophages, monocytes, neutrophils and natural killer (NK) cells, are among the first to respond to infection, ensuring a rapid antiviral defense and supporting the development of adaptive immune responses. However, excessive release of inflammatory mediators and prolonged infiltration of innate cells into joint tissues contribute to disease chronicity and the persistence of arthralgia. In this review, we provide a comprehensive synthesis of current evidence on innate cells that serve as targets for CHIKV infection, highlighting mechanisms that promote effective antiviral defense as well as those responsible for pathological inflammation and chronic disease and identifying key gaps that remain to be addressed.
Open AccessThe Role of Innate Cells During Alphavirus Chikungunya Infection
Alphavirus chikungunya (CHIKV) is an arthropod-borne alphavirus of the Togaviridae family, transmitted primarily by Aedes aegypti and Ae. albopictus mosquitoes. CHIKV infection often results in debilitating manifestations that compromise quality of life and generate significant socioeconomic impacts. Recurrent epidemics in tropical and subtropical regions underscore the urgent need to better understand the host immune responses and their contribution to disease outcome. CHIKV establishes infection by overcoming the host’s initial immunological barriers. Innate immune cells, including fibroblasts, dendritic cells, macrophages, monocytes, neutrophils and natural killer (NK) cells, are among the first to respond to infection, ensuring a rapid antiviral defense and supporting the development of adaptive immune responses. However, excessive release of inflammatory mediators and prolonged infiltration of innate cells into joint tissues contribute to disease chronicity and the persistence of arthralgia. In this review, we provide a comprehensive synthesis of current evidence on innate cells that serve as targets for CHIKV infection, highlighting mechanisms that promote effective antiviral defense as well as those responsible for pathological inflammation and chronic disease and identifying key gaps that remain to be addressed.