Advances in the mechanism of inflammasomes activation in herpes virus infection.

Herpesviruses, prevalent DNA viruses with a double-stranded structure, establish enduring infections and play a part in various diseases. Despite their deployment of multiple tactics to evade the immune system, both localized and systemic inflammatory responses are triggered by the innate immune system's recognition of them. Recent progress has offered more profound understandings of the mechanisms behind the activation of the innate immune system by herpesviruses, specifically through inflammatory signaling. This process encompasses the initiation of an intracellular nucleoprotein complex, the inflammasome associated with inflammation.Following activation, proinflammatory cytokines such as IL-1ß and IL-18 are released by the inflammasome, concurrently instigating a programmed pathway for cell death. Despite the structural resemblances between herpesviruses, the distinctive methods of inflammatory activation and the ensuing outcomes in diseases linked to the virus exhibit variations.The objective of this review is to emphasize both the similarities and differences in the mechanisms of inflammatory activation among herpesviruses, elucidating their significance in diseases resulting from these viral infections.Additionally, it identifies areas requiring further research to comprehensively grasp the impact of this crucial innate immune signaling pathway on the pathogenesis of these prevalent viruses.

Isolation and pathogenicity comparison of two novel natural recombinant porcine reproductive and respiratory syndrome viruses with different recombination patterns in Southwest China.

Porcine reproductive and respiratory syndrome virus (PRRSV) causes significant economic losses in the swine industry. Frequent mutations and recombinations account for PRRSV immune evasion and the emergence of novel strains. In this study, we isolated and characterized two novel PRRSV-2 strains from Southwest China exhibiting distinct recombination patterns. They were designated SCABTC-202305 and SCABTC-202309. Phylogenetic results indicated that SCABTC-202305 was classified as lineage 8, and SCABTC-202309 was classified as lineage 1.8. Amino acid mutation analysis identified unique amino acid substitutions and deletions in ORF5 and Nsp2 genes. The results of the recombination analysis revealed that SCABTC-202305 is a recombinant with JXA1 as the major parental strain and NADC30 as the minor parental strain. At the same time, SCABTC-202309 is identified as a recombinant with NADC30 as the major parental strain and JXA1 as the minor parental strain. In this study, we infected piglets with SCABTC-202305, SCABTC-202309, or mock inoculum (control) to study the pathogenicity of these isolates. Although both isolated strains were pathogenic, SCABTC-202305-infected piglets exhibited more severe clinical signs and higher mortality, viral load, and antibody response than SCABTC-202309-infected piglets. SCABTC-202305 also caused more extensive lung lesions based on histopathology. Our findings suggest that the divergent pathogenicity observed between the two novel PRRSV isolates may be attributed to variations in the genetic information encoded by specific genomic regions. Elucidating the genetic determinants governing PRRSV virulence and transmissibility will inform efforts to control this devastating swine pathogen.IMPORTANCEPorcine reproductive and respiratory syndrome virus (PRRSV) is one of the most critical pathogens impacting the global swine industry. Frequent mutations and recombinations have made the control of PRRSV increasingly difficult. Following the NADC30-like PRRSV pandemic, recombination events involving PRRSV strains have further increased. We isolated two novel field PRRSV recombinant strains, SCABTC-202305 and SCABTC-202309, exhibiting different recombination patterns and compared their pathogenicity in animal experiments. The isolates caused higher viral loads, persistent fever, marked weight loss, moderate respiratory clinical signs, and severe histopathologic lung lesions in piglets. Elucidating correlations between recombinant regions and pathogenicity in these isolates can inform epidemiologic tracking of emerging strains and investigations into viral adaptive mechanisms underlying PRRSV immunity evasion. Our findings underscore the importance of continued genomic surveillance to curb this economically damaging pathogen.

Transcriptome and metabolome analysis reveals PRV XJ delgE/gI/TK protects intracranially infected mice from death by regulating the inflammation.

Pseudorabies virus can cause inflammation in the central nervous system and neurological symptoms. To further investigate the protective mechanism of PRV XJ delgE/gI/TK in the central nervous system, an intracranial PRV-infection mice model was developed. The results demonstrated that immunization with PRV XJ delgE/gI/TK successfully prevented death caused by PRV-intracranial infection. Subsequently, the brains were collected for transcriptome and metabolome analysis. GO and KEGG enrichment analysis indicated that the differentially expressed genes were primarily enriched in pathways such as TNF, NOD-like receptor, JAK-STAT, MAPK, IL-17 and apoptosis signaling. Metabolomics analysis revealed that the differential metabolites were mainly associated with pathways such as fatty acid degradation, arachidonic acid metabolism, linoleic acid metabolism and unsaturated fatty acid biosynthesis. The combined analysis of metabolites and differentially expressed genes revealed a strong correlation between the differential metabolites and TNF, PI3K, and MAPK signaling pathways. Anti-inflammatory metabolites have been shown to inhibit the inflammatory response and prevent mouse death caused by PRV infection. Notably, when glutathione was injected intracranially and dihydroartemisinin was injected intraperitoneally, complete protection against PRV-induced death in mice was observed. Moreover, PRV activates the PI3K/AKT signaling pathway. In conclusion, our study demonstrates that PRV XJ delgE/gI/TK can protects intracranially infected mice from death by regulating various metabolites with anti-inflammatory functions post-immunization.

First report on identification and genomic analysis of a novel porcine circovirus (porcine circovirus 4) in cats.

Porcine circovirus type 4 (PCV4) is an emerging circovirus, which has been detected in domestic pigs across various provinces in China and Korea. In this study, we aimed to investigate whether cats are susceptible to PCV4. For this purpose, we collected 116 cat samples from animal hospitals in Sichuan Province, China, between 2021 and 2022. Using a SYBR Green-based real-time PCR assay, we detected PCV4 in 5 out of the 116 clinical samples, indicating a positive rate of 4.31% (5/116) and confirming the presence of PCV4 in cats from Sichuan Province, China. Moreover, we successfully sequenced and analyzed the complete genome of one PCV4 strain (SCGA-Cat) along with 60 reference sequences deposited in the GenBank database. SCGA-Cat exhibited high nucleotide homology (98.2-99.0%) with PCV4 strains from other species, including dogs, pigs, dairy cows, and fur animals. Notably, the SCGA-Cat strain from cats clustered closely with a PCV4 strain derived from a pig collected in Fujian Province, China. To the best of our knowledge, this study represents the first report on the molecular detection of PCV4 in cats worldwide, which prompted us to understand the genetic diversity and cross-species transmission of the ongoing PCV4 cases. However, further investigations are needed to explore the association between PCV4 infection and clinical syndromes in cats.

Intranasal administration with recombinant vaccine PRVXJ-delgE/gI/TK-S induces strong intestinal mucosal immune responses against PDCoV.

Porcine deltacoronavirus (PDCoV) is a novel coronavirus that causes enteric diseases in pigs leading to substantial financial losses within the industry. The absence of commercial vaccines and limited research on PDCoV vaccines presents significant challenges. Therefore, we evaluated the safety and immunogenicity of recombinant pseudorabies virus (PRV) rPRVXJ-delgE/gI/TK-S through intranasal mucosal immunization in weaned piglets and SPF mice. Results indicated that rPRVXJ-delgE/gI/TK-S safely induced PDCoV S-specific and PRV gB-specific antibodies in piglets, with levels increasing 7 days after immunization. Virus challenge tests demonstrated that rPRVXJ-delgE/gI/TK-S effectively improved piglet survival rates, reduced virus shedding, and alleviated clinical symptoms and pathological damage. Notably, the recombinant virus reduced anti-inflammatory and pro-inflammatory responses by regulating IFN-γ, TNF-α, and IL-1ß secretion after infection. Additionally, rPRVXJ-delgE/gI/TK-S colonized target intestinal segments infected with PDCoV, stimulated the secretion of cytokines by MLVS in mice, stimulated sIgA secretion in different intestinal segments of mice, and improved mucosal immune function. HE and AB/PAS staining confirmed a more complete intestinal mucosal barrier and a significant increase in goblet cell numbers after immunization. In conclusion, rPRVXJ-delgE/gI/TK-S exhibits good immunogenicity and safety in mice and piglets, making it a promising candidate vaccine for PDCoV.

Immunogenic response of recombinant pseudorabies virus carrying B646L and B602L genes of African swine fever virus in mice.

African swine fever (ASF) is an acute infectious disease that poses a high lethality risk to domestic pigs and wild boars, causing substantial economic losses to the global pig industry. The prevention and control of ASF remain challenging, necessitating the urgent development of a safe and effective vaccine. This study focused on the essential structural protein p72 of ASFV (encoded by the B646L gene) and its chaperone protein pB602L (encoded by the B602L gene) as the target antigenic proteins. Based on CRISPR/Cas9 gene-editing technology, we constructed a live attenuated recombinant pseudorabies virus vector expressing the p72 and pB602L proteins (designated as rPRVXJ-EGFP/B602L/B646L), and assessed its immunization effect in mice. The recombinant virus rPRVXJ-EGFP/B602L/B646L successfully proliferated and demonstrated stable expression of the p72 and pB602L proteins in BHK-21 cells. Moreover, it exhibited excellent safety when used in mice and induced specific humoral and cellular immune responses targeting p72 and pB602L. In addition, it provided complete protection (100%) against the virulent PRV strain (PRV-XJ). These results indicate that the recombinant virus rPRVXJ-EGFP/B602L/B646L possesses robust immunogenicity and safety in mice. In conclusion, PRV represents a promising viral vector for expressing ASFV gene, and our study serves as an essential reference for the development of viral vector vaccines against ASFV.

The Construction and Immunogenicity Analyses of a Recombinant Pseudorabies Virus with Senecavirus A VP2 Protein Coexpression.

Senecavirus A (SVA)-associated porcine idiopathic vesicular disease (PIVD) and pseudorabies (PR) are highly contagious swine diseases that pose a significant threat to the swine industry in China. Since there is currently no effective commercial vaccine against SVA, the virus has spread widely throughout China and its pathogenicity has increased over the last decade. In this study, a recombinant strain named rPRV-XJ-ΔTK/gE/gI-VP2 was constructed by using the pseudorabies virus (PRV) variant strain XJ as the parental virus and by deleting the TK/gE/gI gene while coexpressing SVA VP2. The recombinant strain can stably proliferate and express foreign protein VP2 in BHK-21 cells while having a similar virion appearance to that of the parental strain. rPRV-XJ-ΔTK/gE/gI-VP2 is safe and effective for BALB/c mice, inducing high levels of neutralizing antibodies against both PRV and SVA, providing 100% protection from the virulent PRV strain. Histopathological examination and quantitative PCR (qPCR) assay have demonstrated that SVA can infect mice through intranasal inoculation, while the vaccination of mice with rPRV-XJ-ΔTK/gE/gI-VP2 can significantly reduce SVA virus copies and alleviate the pathological inflammatory changes in the heart and liver. The evaluation of the safety and immunogenicity indicates that rPRV-XJ-ΔTK/gE/gI-VP2 holds promise as a candidate vaccine against PRV and SVA. IMPORTANCE This study reports the construction of a recombinant PRV with SVA for the first time, and the resulting virus, rPRV-XJ-ΔTK/gE/gI-VP2, can induce high levels of neutralizing antibodies against both PRV and SVA in model mice. These findings provide valuable insights for evaluating the effectiveness of rPRV-XJ-ΔTK/gE/gI-VP2 as a vaccine for pigs. Additionally, this study reports transient SVA infection in mice, with qPCR assays showing that the copies of the SVA 3D gene peaked at 3 to 6 days postinfection and fell below the sensitivity threshold by 14 days postinfection. The copies of the gene were more regular and at a higher level in the heart, liver, spleen, and lung tissue.

Macrophage Polarization: An Important Candidate Regulator for Lung Diseases.

Macrophages are crucial components of the immune system and play a critical role in the initial defense against pathogens. They are highly heterogeneous and plastic and can be polarized into classically activated macrophages (M1) or selectively activated macrophages (M2) in response to local microenvironments. Macrophage polarization involves the regulation of multiple signaling pathways and transcription factors. Here, we focused on the origin of macrophages, the phenotype and polarization of macrophages, as well as the signaling pathways associated with macrophage polarization. We also highlighted the role of macrophage polarization in lung diseases. We intend to enhance the understanding of the functions and immunomodulatory features of macrophages. Based on our review, we believe that targeting macrophage phenotypes is a viable and promising strategy for treating lung diseases.

Histopathological Changes and Inflammatory Response in Specific Pathogen-Free (SPF) with Porcine Circovirus Type 3 Infection.

Since the first report of PCV3 virus infection in 2016, it has been linked to multisystemic inflammation, reproductive failure, cardiac pathology, and clinical indications resembling porcine dermatitis and nephropathy syndrome (PDNS). However, the pathogenesis and clinical significance of PCV3 is still unclear. In this study, a PCV3 infection model was created using SPF pigs, and histopathology and fluorescence quantitative PCR were utilized to examine PCV3's pathogenicity. Reductions in body weight gain and fever were observed during this study. However, other clinical signs such as Dermatitis and Nephropathy Syndrome were not observed through the study. Viremia was detected in the PCV3-inoculated group from 17 days post-inoculation (p.i.) until the end of the study. Nasal shedding was detected from 21 to 35 dpi and fecal shedding was detected during 25-33 days and 39 days, respectively. Gross lesions and histological evaluation were detected in various tissues and organs, including the lung, heart, kidney, lymph nodes, spleen, liver, small intestine, and testis. The heart, lung, liver, kidney, lymph nodes, and spleen showed pathological changes. The pathological features include swelling, inflammation, cell degeneration, necrosis, and hemorrhage. The lesions are consistent with multisystemic inflammation. Tissue viral load results showed only heart, lung, liver, kidney, lymph nodes, and spleen was positive by qRT-PCR. Moreover, the pro-inflammation cytokines in serum increased a lot in the PCV3-inoculated group compared to the control group, demonstrating that the induced inflammation response may be the cause of tissue damage in PCV3-infection. This study demonstrated that PCV3 can produce mild pathological damage to multiple organs, especially multisystemic inflammatory cell infiltration and prolonged viremia, viral shedding in nasal secretions. This is the first in vivo characterization of PCV3 infection in the SPF piglets model using isolated PCV3 strain, and this is also the first time to show the gross and pathological lesion with all tissue and organs in the PCV3-inoculated group. Our findings might serve as a starting point for more investigation into PCV3's pathogenic mechanism.

Evasion of interferon-mediated immune response by arteriviruses.

IFN is the most potent antiviral cytokine required for the innate and adaptive immune responses, and its expression can help the host defend against viral infection. Arteriviruses have evolved strategies to antagonize the host cell's innate immune responses, interfering with IFN expression by interfering with RIG, blocking PRR, obstructing IRF-3/7, NF-κB, and degrading STAT1 signaling pathways, thereby assisting viral immune evasion. Arteriviruses infect immune cells and may result in persistence in infected hosts. In this article, we reviewed the strategies used by Arteriviruses to antagonize IFN production and thwart IFN-activated antiviral signaling, mainly including structural and nonstructural proteins of Arteriviruses encoding IFN antagonists directly or indirectly to disrupt innate immunity. This review will certainly provide a better insight into the pathogenesis of the arthritis virus and provide a theoretical basis for developing more efficient vaccines.

Mfn2 is responsible for inhibition of the RIG-I/IRF7 pathway and activation of NLRP3 inflammasome in Seneca Valley virus-infected PK-15 cells to promote viral replication.

Seneca Valley virus (SVV), a non-enveloped positive single-stranded virus can cause vesicular disease in swine. However, the mechanisms by which SVV activates an innate immune response remain unknown. Mitofusin-2 (MFN2), a mitochondria-shaping protein regulating mitochondrial fusion and fission, plays a crucial role in innate immune responses. But, the roles of Mfn2 in SVV infection have not been elucidated. Here, we show that SVV inhibited Mfn2 expression and NLRP3 inflammasome, activating RIG-I/IRF7 signaling pathway to increase IFN-λ3 expression. Overexpression of Mfn2 inhibited RIG-I/IRF7 signaling pathway, thus decreasing IFN-λ3 expression and promoting SVV replication. Interestingly, overexpression of Mfn2 also activated NLRP3 inflammasome but did not inhibit SVV proliferation. That may mean the RIG-I/IRF7 signaling pathway plays a more important role in SVV proliferation in PK-15 cells. This study could provide important insights into the modulation of host metabolism during SVV infection and provide a strong theoretical basis for a better understanding of the pathogenic mechanism and immune activation mechanism of SVV.

Antiviral Activity of Porcine IFN-λ3 and IFN-α against Porcine Rotavirus In Vitro.

Interferons (IFNs) play a major role in the host's antiviral innate immunity. In response to viral infection, IFNs bind their receptors and initiate a signaling cascade, leading to the accurate transcriptional regulation of hundreds of IFN-stimulated genes (ISGs). Porcine rotavirus (PoRV) belongs to genus Rotavirus of the Reoviridae family; the infection is a global epidemic disease and a major threat to the pig industry. In this study, we found that IFN-λ3 inhibited the replication of PoRV in both MA104 cells and IPEC-J2 cells, and this inhibition was dose-dependent. Furthermore, the antiviral activity of IFN-λ3 was more potent in IPEC-J2 cells than in MA104 cells. Further research showed that IFN-λ3 and IFN-α might inhibit PoRV infection by activating ISGs, i.e., MxA, OASL and ISG15, in IPEC-J2 cells. However, the co-treatment of IFN-λ3 and IFN-α did not enhance the antiviral activity. Our data demonstrated that IFN-λ3 had antiviral activity against PoRV and may serve as a useful antiviral candidate against PoRV, as well as other viruses in swine.

Insights on the cGAS-STING Signaling Pathway During Herpesvirus Infections.

Herpesviruses belong to large double-stranded DNA viruses. They are under a wide range of hosts and establish lifelong infection, which creates a burden on human health and animal health. Innate immunity is the host's innate defense ability. Activating the innate immune signaling pathway and producing type I interferon is the host's first line of defense against infectious pathogens. Emerging evidence indicates that the cGAS-STING signaling pathway plays an important role in the innate immunity in response to herpesvirus infections. In parallel, because of the constant selective pressure imposed by host immunity, herpesvirus also evolves to target the cGAS-STING signaling pathway to inhibit or escape the innate immune responses. In the current review, we insight on the classical cGAS-STING signaling pathway. We describe the activation of cGAS-STING signaling pathway during herpesvirus infections and strategies of herpesvirus targeting this pathway to evade host antiviral response. Furthermore, we outline the immunotherapy boosting cGAS-STING signaling pathway.

Characterization of B cell receptor H-CDR3 repertoire of spleen in PRV-infected mice.

Pseudorabies virus (PRV), also known as suid Alphaherpesvirus 1 (SuHV-1), which is one of the most devastating infectious pathogen of swine industry worldwide. Vaccination is the safest and most effective PRV prevention and control strategy. B cell receptor (BCR) is membrane-bound immunoglobulin located on the surface of B cells capable of specifically binding foreign antigens, which is one of the most important molecules regulating the proliferation and function of B cells. Here, to assess the molecular diversity of BCR H-CDR3 repertoire after different PRV strains infection, we detected the IGHV, IGHD, IGHJ genes usage and CDR3 sequence changes of mice spleen with PRV vaccine strain (Bartha-K61), variant strain (XJ) and mock infection by high-throughput sequencing. We found that PRV-infected groups shared partial BCR sequences, which are most likely to be PRV-specific BCR candidates. However, there were still differences in the IGHV genes usage as well as the combined usage of IGHV and IGHJ genes between the Bartha-K61 strain and XJ strain infection groups. In addition, the CDR3 sequences exhibited large differences in the types and lengths in PRV infection groups. Our study contributes to a better understanding of the host adaptive immune response to PRV infection and provides a theoretical basis for further research on novel and efficient PRV vaccines in the future.

Autophagy induced by largemouth bass virus inhibits virus replication and apoptosis in epithelioma papulosum cyprini cells.

Autophagy and apoptosis play important roles in the occurrence and development of diseases. Largemouth bass virus (LMBV) is a primary agent that causes infectious skin ulcerative syndrome in largemouth bass and threatens the aquaculture of the species. We investigated the relationship between LMBV and autophagy, as well as the effect of autophagy on apoptosis induced by LMBV. Results showed that LMBV could induce autophagy in epithelioma papulosum cyprinid (EPC) cells. There was also an increase in LC3-II protein and decrease in p62 protein, along with autophagosome-like membranous vesicles and punctate autophagosomes fluorescent spots being observed in EPC cells. Enhancing autophagy inhibited the replication of LMBV and apoptosis in EPC cells while inhibiting autophagy produced the opposite effect. These results offer new insights into the pathogenesis of LMBV and anti-LMBV strategies.

Transcriptome Analyses of Senecavirus A-Infected PK-15 Cells: RIG-I and IRF7 Are the Important Factors in Inducing Type III Interferons.

Senecavirus A (SVA) is a new type of virus related to swine vesicular disease, which results in enormous economic losses worldwide. At present, the host transcriptional responses to SVA infection, host-SVA interactions, and the mechanism of SVA in innate immune modulation are not well understood. This study explores the gene expression profiles of PK-15 cells at 0, 6, 12, 18, 24, 36 h SVA post-infection by RNA sequencing. Our analysis identified 61, 510, 1,584, 2,460, and 2,359 differentially expressed genes (DEGs) in the comparison groups S6 vs. Control, S12 vs. Control, S18 vs. Control, S24 vs. Control, S36 vs. Control, respectively. The reproducibility and repeatability of the results were validated by RT-qPCR, and all DEGs exhibited expression patterns consistent with the RNA-seq results. According to GO enrichment analysis and KEGG pathway analysis of DEGs in different periods after SVA infection, we found that SVA infection significantly modified the host cell gene-expression patterns and the host cells responded in highly specific manners, including response to signal reception and transmission, external biotic stimulus, response to the virus and host immune defense response. Notably, we observed the specific induction of type III interferon IFN-λ1 and IFN-λ3, which indicated that type III interferon plays an important antiviral function in PK-15 cells. Furthermore, our results showed that SVA might be recognized by RIG-I/MDA-5 receptors first after infecting PK-15 cells and then activates downstream IRF7-mediated signaling pathways, causing an increase in the expression of type III interferon. This study could provide important insights into the modulation of host metabolism during SVA infection and provide a strong theoretical basis for a better understanding of the pathogenic mechanism and immune escape mechanism of SVA.

Development and use of a droplet digital PCR (ddPCR) assay to achieve sensitive and fast atypical porcine pestivirus detection.

Atypical porcine pestivirus (APPV) is a recently discovered RNA virus, which mainly caused congenital tremor in piglets. Droplet digital PCR (ddPCR) is an absolute quantitative method that does not rely on the standard curve but has high sensitivity and accuracy. The present study aimed to develop a ddPCR detection assay for APPV. Furthermore, we evaluated the limit of detection, sensitivity, specificity and reproducibility of the ddPCR and real-time quantitative PCR (qPCR) and tested 135 clinical samples to calculate the detection rate of the two methods. The results showed that both methods had a strong linear relationship and quantitative correlation. The ddPCR assay had a minimum detection limit of 0.15 copies/µL for APPV, with a sensitivity 100 times that of qPCR. We tested clinical samples and found that the APPV ddPCR had a 27.4% positive detection rate, noticeably higher than that of the qPCR (14.8%). Additionally, the APPV ddPCR method had excellent repeatability and specificity. In brief, our study provided a novel, feasible and sensitive diagnostic technique to identify and monitor APPV.

CMTV-like ranavirus infection associated with high mortality in captive catfish-like loach, Triplophysa siluorides, in China.

Ranaviruses are important emerging pathogens of ectothermic vertebrates that threaten aquaculture and wildlife worldwide. A mortality event occurred in a cultured population of catfish-like loach (Triplophysa siluorides) in Sichuan Province, China. Gross clinical signs of the affected fish included skin lesions and haemorrhagic ulcers, which are often associated with ranaviruses. Inoculation of liver, kidney and spleen tissue homogenates in epithelioma papulosum cyprini (EPC) cells at 25°C resulted in cytopathic effect within 24 hr. Transmission electron microscopy of infected EPC cells revealed hexagonal viral arrays in the cytoplasm and icosahedral geometry of the virions. Following exposure of T. siluroides to the isolated virus, similar clinical signs were observed and the fish experienced 40% and 90% mortality after 21 days at 103.58 and 107.8 TCID50 /0.1 ml doses, respectively, providing evidence the isolated virus was the main causative agent of the mortality event. Diagnostic PCR of the major capsid protein gene of ranavirus showed that all samples of diseased fish and isolated virus were positive. Phylogenetic analysis revealed that the isolated virus, designated as FYLl40220, was associated with the Common Midwife Toad Virus (CMTV)-like ranavirus clade. To our knowledge, this case represents the first report of CMTV-associated mortality in a fish species. Collectively, these results suggest that the host range of CMTV-like ranaviruses is greater than previously thought, and this clade of ranaviruses could have significant economic and biodiversity impacts.

[Determination of thermodynamic parameters for ionic liquid 1-hexyl-3-methylimidazolium trifluoromethansulfonate by inverse gas chromatography].

The thermodynamic parameters of ionic liquid 1-hexyl-3-methylimidazolium trifluoromethansulfonate ([HMIM] OTF) were investigated by inverse gas chromatography in the temperature range of 343.15-373.15 K. Eighteen probe solvents were used to calculate the molar enthalpy of sorption, molar enthalpy of mixing at infinite dilution, molar enthalpy of vaporization and the mass fraction activity coefficients. Furthermore, Flory-Huggins interaction parameters, the solubility parameter of the ionic liquid were calculated to judge the interactions between [HMIM] OTF and the 18 probes solvents. The results showed that among the selected solvents, n-C6-9, tetrahydrofuran, diethyl ether, cyclohexane and benzene are the poor solvents for [HMIM] OTF, while dichloromethane, acetone, chloroform, ethyl acetate, carbon tetrachloride, methyl acetate, toluene and methanol are the favorite solvents for [HMIM] OTF. In addition, the solubility parameter of [HMIM] OTF at room temperature (298.15 K), which was obtained by linear extrapolation method, was 20.74 (J/cm3)0.5. This study could be used as a reference to the application and research of the ionic liquids.

[Characterization of surface properties of 1-allyl-3-methylimidazolium chloride ionic liquid by inverse gas chromatography].

The determination of the dispersive component of surface free energies (gamma(s)d) at different temperatures and Lewis acid-base parameters of 1-allyl-3-methylimidazolium chloride ionic liquid ([AMIM]Cl) were investigated by means of inverse gas chromatography (IGC). Four n-alkanes, including n-hexane (C6), n-heptane (C7), n-octane (C8) and n-nonane (C9), were chosen as the apolar probes to characterize the dispersive component of the surface free energies at 343.15, 353.15, 363.15 and 373.15 K, respectively; and dichloromethane (DCM), trichloromethane (TCM), tetrahydrofuran (THF), ethyl acetate (EtAc), acetone (Acet) as the polar probes to estimate the Lewis acid-base parameters to judge the interactions between [AMIM] Cl and the solvents. The IGC characterizations encompassed the adsorption thermodynamic parameters to acid-base surface interactions, including the standard enthalpy (deltaHa(s)) and the free energy change of adsorption (deltaGa(s)) at different temperatures. The results showed that the Lewis acid parameter Ka of [AMIM] Cl was 0.34, and the base parameter Kb was 1.68, which indicated it was Lewis amphoteric with predominantly basic character. Furthermore, the free energy of adsorption deltaGa(s) was also figured out. It was found that the gamma(s)d of the [AMIM] Cl were 52.26, 50.82, 46.08 and 42.05 mJ/m2 at 343.15, 353.15, 363.15 and 373.15 K, respectively. The results are of great importance to the study of the surface properties and the application of ionic liquid.