cThe Chinese virulent (CHv) strain of duck enteritis virus (DEV) has a genome of approximately 162,175 nucleotides with a GC content of 44.89%. Here we report the complete genomic sequence and annotation of DEV CHv, which offer an effective platform for providing authentic research experiences to novice scientists. In addition, knowledge of this virus will extend our general knowledge of DEV and will be useful for further studies of the mechanisms of virus replication and pathogenesis. D uck viral enteritis (DVE) is an acute, septic, contagious, and lethal disease that attacks ducks, geese, swans, and other members of the family Anatidae, order Anseriformes (6). The first known occurrence of DVE in the world was a major outbreak in the Netherlands in 1923 (1), and the first instance of DVE in China was reported in 1957. Nowadays, it is one of the most widespread and devastating diseases of waterfowl in the Anatidae family and has severely affected the waterfowl industry because of its relatively high mortality and wide host range.Duck enteritis virus (DEV) is the causative agent of DVE and was alternatively known as anatid herpesvirus 1 (AnHV-1) and duck plague virus (DPV). It has been clustered in the Alphaherpesvirinae subfamily, according to the eighth report of the International Committee on Taxonomy of Viruses (ICTV) (3). DEV may be closely related to mardiviruses, but it has not yet been classified in any genus. Lack of a genome sequence and genomic organization information is a factor that limits DEV taxonomy. Here we report the complete genomic sequence of the DEV Chinese virulent strain (CHv), which was isolated from infected ducks that showed a characteristic hemorrhagic button or bandlike lesions on the mucosal surface of the intestines.Construction of the library and sequencing of the DEV genome were performed as previously described (2). Considering the tandem duplication pattern of the DEV genome (5), we amplified the 5= and 3= ends of the DEV genome using a pair of primers. The shotgun library was sequenced and assembled.The DEV genome is linear, double-stranded DNA which consists of two covalently linked components, designated unique long (UL) and unique short (US), with each component consisting of unique sequences bracketed by the internal and terminal inverted repeat sequences (IRS and TRS, respectively): UL-IRS-US-TRS. The 5=-untranslated region (UTR) is 5,686 bp in length and contains 25 TATA boxes, 8 CAAT boxes, 8 poly(A)s, and 1 GC box, while the corresponding component of 3= UTR has 3, 13, 4, and 7, respectively. All of them are regarded as potential transcriptional regulatory elements. Also, the 3= UTR possesses seven tandem repeats which can be defined as minisatellites, since the length of the repeat unit reaches up to 40 nt (4).A total of 78 ORFs were predicted to code the potential functional protein. Of these ORFs, 65 and 11 ORFs are located in the UL and US regions, respectively, whereas the remaining two (ICP4/IE180) are located completely in the IRS and TRS regions. It is worth n...

Background eIF2α is a regulatory node that controls protein synthesis initiation by its phosphorylation or dephosphorylation. General control nonderepressible-2 (GCN2), protein kinase R-like endoplasmic reticulum kinase (PERK), double-stranded RNA (dsRNA)-dependent protein kinase (PKR) and heme-regulated inhibitor (HRI) are four kinases that regulate eIF2α phosphorylation. Main body In the viral infection process, dsRNA or viral proteins produced by viral proliferation activate different eIF2α kinases, resulting in eIF2α phosphorylation, which hinders ternary tRNAMet-GTP-eIF2 complex formation and inhibits host or viral protein synthesis. The stalled messenger ribonucleoprotein (mRNP) complex aggregates under viral infection stress to form stress granules (SGs), which encapsulate viral RNA and transcription- and translation-related proteins, thereby limiting virus proliferation. However, many viruses have evolved a corresponding escape mechanism to synthesize their own proteins in the event of host protein synthesis shutdown and SG formation caused by eIF2α phosphorylation, and viruses can block the cell replication cycle through the PERK-eIF2α pathway, providing a favorable environment for their own replication. Subsequently, viruses can induce host cell autophagy or apoptosis through the eIF2α-ATF4-CHOP pathway. Conclusions This review summarizes the role of eIF2α in viral infection to provide a reference for studying the interactions between viruses and hosts.

Nuclear factor-κB (NF-κB) is an important transcription factor that induces the expression of antiviral genes and viral genes. NF-κB activation needs the activation of NF-κB upstream molecules, which include receptors, adaptor proteins, NF-κB (IκB) kinases (IKKs), IκBα, and NF-κB dimer p50/p65. To survive, viruses have evolved the capacity to utilize various strategies that inhibit NF-κB activity, including targeting receptors, adaptor proteins, IKKs, IκBα, and p50/p65. To inhibit NF-κB activation, viruses encode several specific NF-κB inhibitors, including NS3/4, 3C and 3C-like proteases, viral deubiquitinating enzymes (DUBs), phosphodegron-like (PDL) motifs, viral protein phosphatase (PPase)-binding proteins, and small hydrophobic (SH) proteins. Finally, we briefly describe the immune evasion mechanism of human immunodeficiency virus 1 (HIV-1) by inhibiting NF-κB activity in productive and latent infections. This paper reviews a viral mechanism of immune evasion that involves the suppression of NF-κB activation to provide new insights into and references for the control and prevention of viral diseases.

Riemerella anatipestifer is a member of the family Flavobacteriaceae and a major causative agent of duck serositis. Little is known about its genetics and pathogenesis. Several bacteria are competent for natural transformation; however, whether R. anatipestifer is also competent for natural transformation has not been investigated. Here, we showed that R. anatipestifer strain ATCC 11845 can uptake the chromosomal DNA of R. anatipestifer strain RA-CH-1 in all growth phases. Subsequently, a natural transformation-based knockout method was established for R. anatipestifer ATCC 11845. Targeted mutagenesis gave transformation frequencies of ϳ10 Ϫ5 transformants. Competition assay experiments showed that R. anatipestifer ATCC 11845 preferentially took up its own DNA rather than heterogeneous DNA, such as Escherichia coli DNA. Transformation was less efficient with the shuttle plasmid pLMF03 (transformation frequencies of ϳ10 Ϫ9 transformants). However, the efficiency of transformation was increased approximately 100-fold using pLMF03 derivatives containing R. anatipestifer DNA fragments (transformation frequencies of ϳ10 Ϫ7 transformants). Finally, we found that the R. anatipestifer RA-CH-1 strain was also naturally transformable, suggesting that natural competence is widely applicable for this species. The findings described here provide important tools for the genetic manipulation of R. anatipestifer.IMPORTANCE Riemerella anatipestifer is an important duck pathogen that belongs to the family Flavobacteriaceae. At least 21 different serotypes have been identified. Genetic diversity has been demonstrated among these serotypes. The genetic and pathogenic mechanisms of R. anatipestifer remain largely unknown because no genetic tools are available for this bacterium. At present, natural transformation has been found in some bacteria but not in R. anatipestifer. For the first time, we showed that natural transformation occurred in R. anatipestifer ATCC 11845 and R. anatipestifer RA-CH-1. Then, we established an easy gene knockout method in R. anatipestifer based on natural transformation. This information is important for further studies of the genetic diversity and pathogenesis in R. anatipestifer.KEYWORDS Riemerella anatipestifer, natural transformation, targeted mutagenesis R iemerella anatipestifer is a Gram-negative, non-spore-forming, rod-shaped bacterium that is a major causative agent of septicemia in waterfowl, turkey, and other birds (1). R. anatipestifer infection leads to great economic losses due to its high mortality in ducklings and poor feed conversion (2). At present, at least 21 serotypes of

The host immune system has multiple innate immune receptors that can identify, distinguish and react to viral infections. In innate immune response, the host recognizes pathogen-associated molecular patterns (PAMP) in nucleic acids or viral proteins through pathogen recognition receptors (PRRs), especially toll-like receptors (TLRs) and induces immune cells or infected cells to produce type I Interferons (IFN-I) and pro-inflammatory cytokines, thus when the virus invades the host, innate immunity is the earliest immune mechanism. Besides, cytokine-mediated cell communication is necessary for the proper regulation of immune responses. Therefore, the appropriate activation of innate immunity is necessary for the normal life activities of cells. The suppressor of the cytokine signaling proteins (SOCS) family is one of the main regulators of the innate immune response induced by microbial pathogens. They mainly participate in the negative feedback regulation of cytokine signal transduction through Janus kinase signal transducer and transcriptional activator (JAK/STAT) and other signal pathways. Taken together, this paper reviews the SOCS proteins structures and the function of each domain, as well as the latest knowledge of the role of SOCS proteins in innate immune caused by viral infections and the mechanisms by which SOCS proteins assist viruses to escape host innate immunity. Finally, we discuss potential values of these proteins in future targeted therapies.