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. 2019 Oct 31;18:988–1006. doi: 10.17179/excli2019-1825

Figure 3. Life cycle of CHIKV in infected cells. The majority of the cells that get infected by CHIKV express glycosaminoglycans that apparently act as a virus-cell binding factor, increasing infectivity. Once endocytosed inside the endosome, there is a reduction in pH level. Then the endosome releases the nucleocapsid and the genome; the nsP123 precursor is translated from the viral genome and it binds to free nsP4 along with some host proteins to form the replication complex. When nsP123 concentration is enough to support an efficient reaction, it is cleaved into mature non-structural proteins: nsP1-4. These proteins together with the host cell proteins act as plus-strand RNA replicase. The 26S sub-genomic RNA encodes for the polyprotein precursor for structural proteins, which is cleaved by an autoproteolytic serine protease in order to yield C, pE2, 6K, and E1. The C and 6K proteins are accumulated in the cell's cytoplasm for the formation of new nucleocapsids. The E3, E2, and E1 proteins are glycosylated at endoplasmic reticulum and then are sent, through the Golgi apparatus, in vesicles to the cell membrane, where can interact with the nucleocapsid, resulting in the viral particles maturation to be finally released by exocytosis.

Figure 3