N 6 -methyladenosine (m 6 A) modification is the most common and reversible posttranscriptional modification of RNA in eukaryotes, which is mainly regulated by methyltransferase, demethylase, and specific binding protein. The replication of the virus and host immune response to the virus are affected by m 6 A modification. In different kinds of viruses, m 6 A modification has two completely opposite regulatory functions. This paper reviews the regulatory effects of m 6 A modification on different viruses and provides a reference for studying the regulatory effects of RNA epitranscriptomic modification.
IntroductionPseudorabies virus (PRV) is the pathogenic virus of porcine pseudorabies (PR), belonging to the Herpesviridae family. PRV has a wide range of hosts and in recent years has also been reported to infect humans. N6-methyladenosine (m6A) modification is the major pathway of RNA post-transcriptional modification. Whether m6A modification participates in the regulation of PRV replication is unknown.MethodsHere, we investigated that the m6A modification was abundant in the PRV transcripts and PRV infection affected the epitranscriptome of host cells. Knockdown of cellular m6A methyltransferases METTL3 and METTL14 and the specific binding proteins YTHDF2 and YTHDF3 inhibited PRV replication, while silencing of demethylase ALKBH5 promoted PRV output. The overexpression of METTL14 induced more efficient virus proliferation in PRV-infected PK15 cells. Inhibition of m6A modification by 3-deazaadenosine (3-DAA), a m6A modification inhibitor, could significantly reduce viral replication.Results and DiscussionTaken together, m6A modification played a positive role in the regulation of PRV replication and gene expression. Our research revealed m6A modification sites in PRV transcripts and determined that m6A modification dynamically mediated the interaction between PRV and host.
Background Feline panleukopenia (FP) is a highly contagious acute infectious disease caused by feline parvovirus (FPV). Parvovirus has a wide range of hosts, can infect many carnivores, and can remain infectious in the natural environment for a long time. Giant pandas are also susceptible to parvovirus. The viral enteritis of giant pandas caused by the virus infection poses a great threat to the survival of giant pandas. Therefore, screening out effective disinfectants is of great help for giant panda feeding management. Results The efficacy of four disinfectants against giant panda-derived FPV by determining viral titers, viral copies and viral hemagglutination after interacting virus with different disinfectants in the same amounts was evaluated. The virus titers decreased to 0 after treatment with peracetic acid (PAA), DuPont Virkon S (Virkon S) and glutaral and deciquam solution (JM). The inhibition by PAA was finally found to be most pronounced by determining viral copies. The virus hemagglutination titers decreased by 2 titers after 2 h of PAA treatment, and the virus hemagglutination titers decreased by 1 titer after Virkon S treatment. The immunofluorescence analysis showed that the PAA could effectively kill the virus within 1 h, while the JM and Virkon S took 2 h to achieve the killing effect. PAA, Virkon S, and glutaral and JM inhibited the production of viral structural protein within 1 h. Conclusions In this study, through multi-faceted comparison, the most effective disinfectant could be screened out, which could be used as a prevention and control disinfectant on panda origin feline panleukopenia virus, and provide reference opinions for giant panda disease control and prevention.
Feline panleukopenia (FPL) is a highly contagious acute infectious disease caused by feline parvovirus (FPV). FPV has also been found in giant pandas with clinical signs of vomiting and mild diarrhea, posing a threat to this vulnerable species. Cleaning and disinfection may be one of the most efficacious ways to prevent FPV spread in the habitat of giant pandas. This study evaluated the inactivation effect of peracetic acid (PAA), povidone-iodine (PVP-I), glutaral and deciquam solution (JM) and Virkon S. The tissue culture infective dose (TCID50) assay indicated that the virus may be totally inactivated by JM, PAA and Virkon S. Meanwhile, the hemagglutination (HA) assay showed a high inactivation efficiency of PAA and Virkon S. The analysis of Western blot revealed that PAA, Virkon S and JM can inhibit the structural protein synthesis. Taken together, our findings demonstrated that PAA could rapidly and efficiently inactivate FPV, representing an efficacious disinfectant for FPV control.
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