No abstract

The cell biology of viral infections is the focus of this research, in which the role of the cytoskeleton in dengue virus (DENV) replication in cell cultures was evaluated by means of Nocodazole and Cytochalasin D treatments before and after of DENV infection. The potential contribution of cytoskeleton elements with/without the treatment of depolymerizing agents was evidenced and quantified by the subcellular distribution of viral proteins, virions produced, and viral protein quantification. The cytoskeleton is involved in DENV replication because treatments with actin microfilaments and microtubule depolymerizing agents in non-cytotoxic concentrations, affected DENV2 replication in Vero cells and decreased both the viral protein expression and infectious virion production, when compared with non-treated cells. The actin and microtubules are partly involved in DENV2 replication, since the treatment does not completely blocked viral replication, suggesting that these components are necessary but not sufficient alone for DENV2 replication in Vero cells. The structural and functional role of actin and the microtubules in replication are postulated here, opening new perspectives for understanding the architecture of the replicative complex and viral morphogenesis processes, due to the role of the cytoskeleton in the organization, recruitment, and function of the cellular elements necessary for the assembly of viral factories.

Dengue virus (DENV) is one of the most prevalent human pathogens worldwide. It causes a huge socioeconomic burden with approximately 400 million infections per year, but yet there is no vaccine or antiviral that is currently effective against the disease. DENV is spread by the mosquitoes Aedes aegypti and Aedes albopictus, and viral replication within the mosquito vector is required for transmission to human host. During its replication cycle, the virus cause significant changes to the host transcriptome profile, especially in the metabolic and trafficking pathways. Recent studies have shown a strong association between autophagy and lipid metabolism modulation. For many years, biochemistry studies have been forgotten and replaced by the most advanced techniques and theories in molecular biology and their promises for solving the "life code"; however, after many years of strong molecular biology research, it had not found the key of many problems with which we have the elemental biosystems like viruses. Decades of molecular virology investigations did not give more light about several cellular processes that occurred into the host cells when the infections happen. The molecular virologists have cloned many viral genes, manipulating full viral genomes, and engineering chimeric constructs to study many details at the molecular level, but the host cell and the encrypted viruses do not want to reveal their secrets.Only with the new perspective of complex diseases, a new approach has emerged: An integrative methodology wherein molecular cell biology is converging with the most pure and elegant biochemistry. In this way, more extensive research is necessary for future comparative analyses of the host and vector metabolic/signaling environments required for viral replication.

No abstract