Background Zika virus (ZIKV) infection and ZIKV epidemic have been continuously spreading silently throughout the world and its associated microcephaly and other serious congenital neurological complications poses a significant global threat to public health. Type I interferon response to ZIKV infection in host cells suppresses viral replication by inducing the expression of interferon-stimulated genes (ISGs). Methods The study aims to demonstrate the anti-ZIKV mechanism of PARP11. PARP11 knock out and overexpressing A549 cell lines were constructed to evaluate the anti-ZIKV function of PARP11. PARP11−/−, PARP12−/− and PARP11−/−PARP12−/− HEK293T cell lines were constructed to explain the synergistic effect of PARP11 and PARP12 on NS1 and NS3 protein degradation. Western blotting, immunofluorescence and immunoprecipitation assay were performed to illustrate the interaction between PARP11 and PARP12. Results Both mRNA and protein levels of PARP11 were induced in WT but not IFNAR1−/− cells in response to IFNα or IFNβ stimulation and ZIKV infection. ZIKV replication was suppressed in cells expressed PARP11 but was enhanced in PARP11−/− cells. PARP11 suppressed ZIKV independently on itself PARP enzyme activity. PARP11 interacted with PARP12 and promoted PARP12-mediated ZIKV NS1 and NS3 protein degradation. Conclusion We identified ADP-ribosyltransferase PARP11 as an anti-ZIKV ISG and found that it cooperated with PARP12 to enhance ZIKV NS1 and NS3 protein degradation. Our findings have broadened the understanding of the anti-viral function of ADP-ribosyltransferase family members, and provided potential therapeutic targets against viral ZIKV infection.

Six bacteria strains from heavy-metal-polluted ramie rhizosphere soil were isolated through Cd2+ stress, which were numbered as JJ1, JJ2, JJ10, JJ11, JJ15, and JJ18. Sequence alignment and phylogenic analysis showed that strain JJ1 belonged to Pseudomonas, strain JJ2 belonged to Cupriavidus, strains JJ11 and JJ15 belonged to Bacillus, and strains JJ10 and JJ18 belonged to Acinetobacter. The tolerance capability of all the strains was the trend of Pb2+ > Zn2+ > Cu2+ > Cd2+, the maximum tolerance concentration to Cd2+ was 200 mg/L, to Pb2+ was 1600 mg/L, to Zn2+ was 600 mg/L, and to Cu2+ was 265 mg/L. Strains JJ1, JJ11, JJ15, and JJ18 could grow well under pH 9.0, and strains JJ2, JJ11, and JJ18 could grow well under 7% of NaCl. The results showed that as a whole these strains had high environmental adaptability. This is the first report that heavy-metal-tolerant bacteria were found from ramie rhizosphere soil, which could be as a foundation to discover the relationship between ramie, rhizosphere bacteria and heavy metals.

Highlights d HDAC3 deficiency impairs the antiviral immunity of macrophages in vivo and in vitro d HDAC3 interacts with FOXK1 and co-localizes at the promoters of STAT1 and STAT2 d HDAC3 and FOXK1 positively regulate the expression of STAT1/2 and downstream ISGs d HDAC3 is required for preventing FOXK1 from lysosomal degradation