Abstract
BackgroundProteomic analysis was performed to identify proteins regulated during infection by Dengue serotypes 1 and 3 in an Aedes albopictus cell line. The potential of these viruses to cause severe disease at primary infection is of interest although few studies have been performed with these two Dengue serotypes.ResultsThe most relevant observation of our study is the significant overexpression of proteins involved in the cellular stress response and the glycolysis pathway after 48 hours of infection. Viral infection activates the translation of some host genes, which may result in stress due to responses involving unfolded proteins.ConclusionsTherefore, the oxidation reduction and glycolytic mechanisms could participate in the antiviral response against Dengue virus. The results of our study should help to improve our knowledge of the virus-mosquito interaction at a cellular level with the aim of designing efficient strategies for the control of Dengue virus.
Highlights
Proteomic analysis was performed to identify proteins regulated during infection by Dengue serotypes 1 and 3 in an Aedes albopictus cell line
The modulation of chaperone-associated proteins could protect cells from apoptosis, as does the overexpression of calreticulin, which is a Ca2+-binding chaperone protein [36]. These findings suggest that the activation of these two chaperone proteins in infected cells due to oxidative stress could induce unfolded protein response (UPR) to cope
The modulation of protein expression found in our study might be the strategy of the virus to overcome host pathways to facilitate survival at the expense of the host
Summary
Proteomic analysis was performed to identify proteins regulated during infection by Dengue serotypes 1 and 3 in an Aedes albopictus cell line. The potential of these viruses to cause severe disease at primary infection is of interest few studies have been performed with these two Dengue serotypes. Aedes albopictus (Diptera, Culicidae) is a less efficient vector for this virus, it was involved in Dengue outbreaks in Japan, Seychelles, Hawaii, and Reunion Island [2]. Dengue virus (DENV) can cause several clinical forms, ranging from an asymptomatic disease to severe Dengue hemorrhagic fever (DHF) or Dengue shock syndrome [5]. DENV dramatically expands each year into new territories [6,7] as a consequence of combined factors such as the rapid and easy mobility of human populations, the distribution of mosquito vectors, and the lack of herd immunity in unexposed populations [8]
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