| Full text | |
| Author(s): |
Total Authors: 2
|
| Affiliation: | [1] Univ Sao Paulo, Dept Immunol, Inst Biomed Sci, Neuroimmune Interact Lab, Sao Paulo - Brazil
[2] Univ Sao Paulo, Sch Med, Immunopathol & Alergy PostGrad Program, Sao Paulo - Brazil
[3] Univ Sao Paulo, Sci Platform Pasteur, Sao Paulo - Brazil
Total Affiliations: 3
|
| Document type: | Review article |
| Source: | Journal of Leukocyte Biology; v. 106, n. 3, SI, p. 695-701, SEP 2019. |
| Web of Science Citations: | 1 |
| Abstract | |
Arboviruses have been a huge threat for human health since the discovery of yellow fever virus in 1901. Arboviruses are arthropod born viruses, mainly transmitted by mosquitoes and ticks, responsible for more than thousands of deaths annually. The Flavivirideae family is probably the most clinically relevant, as it is composed of very important agents, such as dengue, yellow fever, West Nile, Japanese encephalitis, and, recently, Zika virus. Intriguingly, despite their structural and genomic similarities, flaviviruses may cause conditions ranging from mild infections with fever, cutaneous rash, and headache, to very severe cases, such as hemorrhagic fever, encephalitis, Guillain-Barre syndrome, and microcephaly. These differences may greatly rely on viral burden, tissue tropism, and mechanisms of immune evasion that may depend on both viral and host genetic factors. Unfortunately, very little is known about the biology of these factors, and how they orchestrate these differences. In this context, viral structural proteins and host cellular receptors may have a great relevance, as their interaction dictates not only viral tissue tropism, but also a plethora on intracellular mechanisms that may greatly account for either failure or success of infection. A great number of viral receptors have been described so far, although there is still a huge gap in understanding their overall role during infection. Here we discuss some important aspects triggered after the interaction of flaviviruses and host membrane receptors, and how they change the overall outcome of the infection. (AU) | |
| FAPESP's process: | 17/26170-0 - Neuroimmunology in experimental models of Autoimmune Encephalomyelitis and Congenital Zika Syndrome: physiopathogenesis, susceptibility, cellular therapy, vaccination |
| Grantee: | Jean Pierre Schatzmann Peron |
| Support type: | Research Projects - Thematic Grants |
| FAPESP's process: | 17/22504-1 - TAM receptors and their ligands Gas6 and Pros1 on the ZIKV Congenital Syndrome in Experimental Models |
| Grantee: | Jean Pierre Schatzmann Peron |
| Support type: | Regular Research Grants |
| FAPESP's process: | 16/21259-0 - The role of TAM receptors and their ligands, Gas6 and Pros 1 during infection by Zika virus in bone marrow-derived dendritic cells and macrophages of SJL and C57BL/6 mice |
| Grantee: | Lilian Gomes de Oliveira |
| Support type: | Scholarships in Brazil - Master |