Abstract
During flavivirus infection, some viral proteins move to the nucleus and cellular components are relocated from the nucleus to the cytoplasm. Thus, the integrity of the main regulator of the nuclear-cytoplasmic transport, the nuclear pore complex (NPC), was evaluated during infection with dengue virus (DENV) and Zika virus (ZIKV). We found that while during DENV infection the integrity and distribution of at least three nucleoporins (Nup), Nup153, Nup98, and Nup62 were altered, during ZIKV infection, the integrity of TPR, Nup153, and Nup98 were modified. In this work, several lines of evidence indicate that the viral serine protease NS2B3 is involved in Nups cleavage. First, the serine protease inhibitors, TLCK and Leupeptin, prevented Nup98 and Nup62 cleavage. Second, the transfection of DENV and ZIKV NS2B3 protease was sufficient to inhibit the nuclear ring recognition detected in mock-infected cells with the Mab414 antibody. Third, the mutant but not the active (WT) protease was unable to cleave Nups in transfected cells. Thus, here we describe for the first time that the NS3 protein from flavivirus plays novel functions hijacking the nuclear pore complex, the main controller of the nuclear-cytoplasmic transport.
Highlights
Viral infections transmitted by mosquitoes, for example those caused by flaviviruses such as dengue virus (DENV), yellow fever virus (YFV), West Nile virus (WNV), and Zika virus (ZIKV)represent important health challenges worldwide [1,2,3]
Flavivirus replication occurs in the endoplasmic reticulum (ER), in close proximity to the during infection was evaluated byfor transmission electron nucleusZIKV
During the flavivirus replicative cycle, some viral proteins are relocated to the nucleus
Summary
Viral infections transmitted by mosquitoes, for example those caused by flaviviruses such as dengue virus (DENV), yellow fever virus (YFV), West Nile virus (WNV), and Zika virus (ZIKV)represent important health challenges worldwide [1,2,3]. Flaviviruses have a positive-strand RNA genome, which encodes a polyprotein that gives rise to three structural proteins (C, E and prM). Involved in the formation of viral particles and seven non-structural proteins (NS1, NS2A, NS2B, NS3, NS4A, NS4B, and NS5) essential for the replication of the viral genome [4,5,6,7]. The viral genome is translated and replicated in the endoplasmic reticulum (ER) [8], while viral morphogenesis takes place in the ER and the Golgi apparatus [9,10]. Every step of the flaviviral life cycle, from entry. Viruses hijack cellular proteins, components, and processes to be replicated in the host cell. The flaviviral replicative cycle takes place in the cytoplasm, at least three viral proteins
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