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is not known whether they edit RNA genomes through cytidine deamination. Here, we investigated APOBEC3-mediated restriction of Coronaviridae. In experiments in vitro, three human APOBEC3 proteins (A3C, A3F and A3H) inhibited HCoV-NL63 infection and limited production of progeny virus, but did not cause hypermutation of the coronaviral genome. APOBEC3-mediated restriction was partially dependent on enzyme activity, and was reduced by the use of enzymatically inactive APOBEC3. Moreover, APOBEC3 proteins bound to the coronaviral nucleoprotein, and this interaction also affected viral replication. Although the precise molecular mechanism of deaminasedependent inhibition of coronavirus replication remains elusive, our results further our understanding of APOBEC-mediated restriction of RNA virus infections. Apolipoprotein B mRNA-editing enzyme, catalytic polypeptide-like type 3 (APOBEC3) proteins are Zn 2+dependent cytidine deaminases that belong to the APOBEC superfamily. APOBEC3 enzymes are considered to be part of the intrinsic defense system in eukaryotic cells, and can inhibit replication of some viruses and restrict mobile genetic elements. All APOBEC3 proteins share a cytidine-deaminase domain, which is identifiable by the primary amino acid motif His-Xaa-Glu-Xaa 23-28 -Pro-Cys-Xaa 2-4 -Cys, in which Zn 2+ is coordinated. Deamination of cytidine results in its conversion to uridine. During this process, the ammonium group on C 4 of cytidine undergoes nucleophilic attack by an activated water molecule and the APOBEC3 glutamate residue. A single copy of a gene encoding APOBEC3 is found in the genomes of rodents, cats, pigs and sheeps, with two genes in the genomes of cows, three the genomes of dogs and horses and seven genes in the human genome, encoding A3A, A3B, A3C, A3D, A3F, A3G and A3H 1 . The mechanisms and selective pressures that led to the APOBEC3 gene expansion in humans are unclear, but it is believed that all the genes originated from duplication of a single-copy primordial APOBEC3 gene. This multiplication may have provided protection from genomic instability caused by human endogenous retroviruses and retrotransposons 2 . The best-studied protein within the human APOBEC3 family is A3G. Its function as an antiviral factor was discovered in 2002 through cDNA-transfer experiments that were designed to identify a cellular suppressor of an HIV-1 accessory protein, the virion infectivity factor (Vif). The primary antiretroviral activity of A3G requires its encapsidation into HIV-1 particles, and involves cytidine deamination of the reverse-transcribed first viral DNA strand, with mutations becoming fixed as G to A changes upon second-strand synthesis. Mutational frequencies can exceed 10% of all G residues (hypermutation), and may result in inhibition of viral replication. This activity is blocked by Vif protein, which specifically binds to and ubiquitinates A3G, directing it for degradation in the Published: xx xx xxxx OPEN www.nature.com/scientificreports/ 2 ScIentIFIc REPORts | (2018) 8:5960 |
APOBEC3-mediated restriction of RNA virus replication OPEN