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Dengue virus (DENV) is one of the most prevalent human pathogens worldwide. It caus‐ es 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 cy‐ cle, the virus cause significant changes to the host transcriptome profile, especially in the metabolic and trafficking pathways. Recent studies have shown a strong association be‐ tween autophagy and lipid metabolism modulation. For many years, biochemistry studies have been forgotten and replaced by the most ad‐ vanced 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 vi‐ ruses. 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 mo‐ lecular 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 in‐ tegrative 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.

Autophagy and Lipid Metabolism – A Cellular Platform where Molecular and Metabolic Pathways Converge to Explain Dengue Viral Infection