Isolation and characterization of a novel parvovirus from a red-crowned crane, China, 2021.

BACKGROUND: Parvoviruses are icosahedral, nonenveloped viruses with single-stranded DNA genomes of approximately 5 kb in length. In recent years, parvoviruses have frequently mutated and expanded their host range to cause disease in many wild animals by altering their tissue tropism. Animal infection mainly results in acute enteritis and inflammation of other organs. In this study, we used a viral metagenomic method to detect a novel parvovirus species in a red-crowned crane that died due to severe diarrhea in China. RESULTS: The presence of the viral genome in the kidney, lung, heart, liver, and intestine were confirmed by PCR. Histopathological examination of the intestine showed a large number of infiltrated inflammatory cells. The JL21/10 strain of the red-crowned crane parvovirus was first isolated from the intestine. Whole-genome sequence analysis showed that JL21/10 shared high identity with the red-crowned crane Parvovirinae strains yc-8 at the nucleotide level (96.61%). Phylogenetic analysis of the complete genome and NS1 gene revealed that the JL21/10 strain clustered with strains in chicken and revealed a close genetic relationship with the red-crowned crane parvovirus strains.The complete of VP2 gene analysis showed that JL21/10 shared identity with the red-crowned crane yc-8 strains (97.7%), chicken (55.4%),ducks(31.0%) and geese(30.1%) at the amino acid level. The result showed that red-crowned crane parvovirus may be cross-species transmission to chicken. However, There is little possibility of transmission to ducks and geese. CONCLUSION: This is the first isolation and identification of a parvovirus in red-crowned crane that was associated with severe diarrhea.

Swine acute diarrhoea syndrome coronavirus (SADS-CoV) Nsp5 antagonizes type I interferon signaling by cleaving DCP1A.

Swine acute diarrhoea syndrome coronavirus (SADS-CoV), which is a recently discovered enteric coronavirus, is the major aetiological agent that causes severe clinical diarrhoea and intestinal pathological damage in pigs, and it has caused significant economic losses to the swine industry. Nonstructural protein 5, also called 3C-like protease, cleaves viral polypeptides and host immune-related molecules to facilitate viral replication and immune evasion. Here, we demonstrated that SADS-CoV nsp5 significantly inhibits the Sendai virus (SEV)-induced production of IFN-ß and inflammatory cytokines. SADS-CoV nsp5 targets and cleaves mRNA-decapping enzyme 1a (DCP1A) via its protease activity to inhibit the IRF3 and NF-κB signaling pathways in order to decrease IFN-ß and inflammatory cytokine production. We found that the histidine 41 and cystine 144 residues of SADS-CoV nsp5 are critical for its cleavage activity. Additionally, a form of DCP1A with a mutation in the glutamine 343 residue is resistant to nsp5-mediated cleavage and has a stronger ability to inhibit SADS-CoV infection than wild-type DCP1A. In conclusion, our findings reveal that SADS-CoV nsp5 is an important interferon antagonist and enhance the understanding of immune evasion by alpha coronaviruses.

Sandwich stent located in the iliac artery dislodged into the thoracic aorta and its remedy.

The sandwich stent technique is a commonly used method to preserve unilateral internal iliac artery flow when treating iliac artery aneurysm. In this case, covered stent grafts (Viabahn, Gore) were used to build the iliac limb of a sandwich stent. However, if Viabahn is released without long sheath protection, the trigger wire is easily wound on another stent, resulting in the Viabahn delivery system being inseparable from the stent. If we drag it forcefully, it would easily cause the entire sandwich stent graft to shift or even fall into the thoracic aorta. This complication is catastrophic. Here we report the case of a patient whose sandwich stent system disengaged and entered the thoracic aorta. We took corresponding measures to remedy it.

Seroepidemiological investigation of Getah virus in the China-Myanmar border area from 2022-2023.

Getah Virus (GETV) is an RNA virus that is transmitted by mosquitoes and can cause disease or death in a variety of vertebrates. Its prevalence is increasingly severe in Asia. This study conducted a GETV epidemiological investigation on 1,300 bovine sera collected in the Honghe Prefecture of Yunnan Province on the China-Myanmar border from 2022 to 2023. The positive rate of GETV antibodies in bovine serum in Honghe Prefecture was determined to be 20.25% through indirect Enzyme-linked immunosorbent test (ELISA) methods. Using Real-time PCR methods to detect GETV RNA in bovine serum, the positive rate was 0.23% (3/1300), and viral nucleic acids were only detected in three bovine sera in Jianshui area in 2022. The YN2305 strain was successfully isolated from mouse neuroblastoma (N2a) cells and the complete gene sequence was obtained. All the above results indicate the existence of GETV infection in cattle in Honghe Prefecture, Yunnan Province. Homology and genetic evolution analysis found that the isolated strain has a high homology with the JL1808 strain isolated from cattle in 2018, with a nucleotide identity of 100%, and a nucleotide identity of 99.8% with the SD17-09 strain isolated from foxes in 2017. Compared with the nucleotides of 44 virus strains published in Genbank, YN2305 has multiple nucleotide site mutations in the structural gene E2 and non-structural gene NS. The nucleotide and amino acid identity of the E2 gene are 94.2-100% and 96.4-100%, respectively. Genetic evolution analysis found that this virus strain is most closely related to the bovine origin JL1808, and it is in gene group III with HuN1, Kochi-01, SD17-09, MI-110-C1, and MI-110-C2 strains that causes significant clinical symptoms in Chinese pig, fox and horse populations, belonging to the same evolutionary branch. This study determined the infection rate, genotype, and main prevalence areas of GETV in bovine sera in the China-Myanmar border area. Therefore, the epidemiological investigation of GETV infection in multiple animal hosts should be further expanded, and research on its pathogenicity and vectors should be carried out.

Immunogenicity and protective efficacy of a DNA vaccine inducing optimal expression of the SARS-CoV-2 S gene in hACE2 mice.

The wide spread of coronavirus disease 2019 (COVID-19) has significantly threatened public health. Human herd immunity induced by vaccination is essential to fight the epidemic. Therefore, highly immunogenic and safe vaccines are necessary to control SARS-CoV-2, whose S protein is the antigenic determinant responsible for eliciting antibodies that prevent viral entry and fusion. In this study, we developed a SARS-CoV-2 DNA vaccine expressing the S protein, named pVAX-S-OP, which was optimized according to the human-origin codon preference and using polyinosinic-polycytidylic acid as an adjuvant. pVAX-S-OP induced specific antibodies and neutralizing antibodies in BALB/c and hACE2 transgenic mice. Furthermore, we observed 1.43-fold higher antibody titers in mice receiving pVAX-S-OP plus adjuvant than in those receiving pVAX-S-OP alone. Interferon gamma production in the pVAX-S-OP-immunized group was 1.58 times (CD3+CD4+IFN-gamma+) and 2.29 times (CD3+CD8+IFN-gamma+) lower than that in the pVAX-S-OP plus adjuvant group but higher than that in the control group. The pVAX-S-OP vaccine was also observed to stimulate a Th1-type immune response. When, hACE2 transgenic mice were challenged with SARS-CoV-2, qPCR detection of N and E genes showed that the viral RNA loads in pVAX-S-OP-immunized mice lung tissues were 104 times and 106 times lower than those of the PBS control group, which shows that the vaccine could reduce the amount of live virus in the lungs of hACE2 mice. In addition, pathological sections showed less lung damage in the pVAX-S-OP-immunized group. Taken together, our results demonstrated that pVAX-S-OP has significant immunogenicity, which provides support for developing SARS-CoV-2 DNA candidate vaccines.

Characterization of a new NSP2-deletion NADC34-Like Porcine Reproductive and Respiratory Syndrome Virus in China.

Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) is the causative agent of Porcine Reproductive and Respiratory Syndrome (PRRS), which has caused huge economic losses to the pig industry worldwide. PRRSV NADC34-Like PRRSV 2020-Acheng-1 strain, which caused high morbidity and high mortality were isolated from dead piglets (high-throughput sequencing to show that only PRRSV and TGEV) on a farm in northeastern China. The full-length genome sequence of 2020-Acheng-1 shares 95.6% nucleotide homology with NADC34 PRRSV without any gene insertion, but has a unique 17 amino acid (469aa to 486aa) deletion in Nsp2 compared with all NADC34-Like strains in NCBI and there are unique 100 amino acid deletions. In addition, difference degree of changes in signal peptide, trans-membrane region (TM), main neutralizing epitope (PNE), non-neutralizing epitope and N-glycosylation site were observed in GP5 of 2020-Acheng-1 and other PRRSV-2 strains, we only found a change in the fifteenth amino acid of signal peptide of in GP5 of 2020-Acheng-1 with NADC34 strains. Recombination analysis showed that 2020-Acheng-1 strain did not have any recombination events with representative PRRSV-2 strains in China. This study provided valuable evidence for understanding the role of NADC34-Like strain that impact on pathogenicity.

GII.P16-GII.2 Recombinant Norovirus VLPs Polarize Macrophages Into the M1 Phenotype for Th1 Immune Responses.

Norovirus (NoV) is a zoonotic virus that causes diarrhea in humans and animals. Outbreaks in nosocomial settings occur annually worldwide, endangering public health and causing serious social and economic burdens. The latter quarter of 2016 witnessed the emergence of the GII.P16-GII.2 recombinant norovirus throughout Asia. This genotype exhibits strong infectivity and replication characteristics, proposing its potential to initiate a pandemic. There is no vaccine against GII.P16-GII.2 recombinant norovirus, so it is necessary to design a preventive vaccine. In this study, GII.P16-GII.2 type norovirus virus-like particles (VLPs) were constructed using the baculovirus expression system and used to conduct immunizations in mice. After immunization of mice, mice were induced to produce memory T cells and specific antibodies, indicating that the VLPs induced specific cellular and humoral immune responses. Further experiments were then initiated to understand the underlying mechanisms involved in antigen presentation. Towards this, we established co-cultures between dendritic cells (DCs) or macrophages (Mø) and naïve CD4+T cells and simulated the antigen presentation process by incubation with VLPs. Thereafter, we detected changes in cell surface molecules, cytokines and related proteins. The results indicated that VLPs effectively promoted the phenotypic maturation of Mø but not DCs, as indicated by significant changes in the expression of MHC-II, costimulatory factors and related cytokines in Mø. Moreover, we found VLPs caused Mø to polarize to the M1 type and release inflammatory cytokines, thereby inducing naïve CD4+ T cells to perform Th1 immune responses. Therefore, this study reveals the mechanism of antigen presentation involving GII.P16-GII.2 recombinant norovirus VLPs, providing a theoretical basis for both understanding responses to norovirus infection as well as opportunities for vaccine development.

Lentogenic NDV V protein inhibits IFN responses and represses cell apoptosis.

The V protein of Newcastle disease virus (NDV) has been shown to inhibit the secretion of interferon (IFN) during infection, which is responsible for the promotion of NDV pathogenicity. However, the ability of the V protein to suppress host innate immunity is not well understood. In this study, we explored the function of V protein and its relationship with virulence by generating V protein-inserted recombinant (r) NDVs. Using rNDVs as a model, we examined the efficiency of infection, IFN responses, and apoptosis of host cells during infection. We found that viral propagation occurred smoothly when V protein from lentogenic NDV is inserted instead of the V protein from the velogenic strain. The infection of lentogenic V protein-inserted rNDV induced less expression of IFNs and downstream antiviral proteins via efficient degradation of p-STAT1 and MDA5. Moreover, velogenic V protein triggered a higher apoptosis rate during infection thereby restricting the replication of NDV. Conversely, lentogenic V protein inhibits IFN responses efficiently and induces less apoptosis compared to the velogenic strain. Our findings provide a novel understanding of the role of V protein in NDV pathogenicity.

Construction and Immunogenicity of Recombinant Vaccinia Virus Vaccine Against Japanese Encephalitis and Chikungunya Viruses Infection in Mice.

Japanese encephalitis virus (JEV) is recognized as a public health risk by the World Health Organization. In Asia, each year, ∼70,000 people become infected with JEV, which results in ∼10,000 deaths. Chikungunya virus (CHIKV) is an RNA virus, whose infection mainly causes fever, myalgia, and skin rash. Although the mortality rate is low, it seriously affects daily life. JEV and CHIKV infect humans through mosquitoes; therefore, a recombinant vaccinia virus coexpressing JEV E and CHIKV E1 proteins was constructed to prevent their concurrent infection. In this study, after mice first immunization, booster immunization was performed at 21 days postimmunization (dpi). At 35 dpi, mice were challenged with JEV and CHIKV. Specific antibodies significantly increased in the rVTT-CE1-JE-EGFP group, which were significantly (p < 0.01) higher than those of the control groups at 35 dpi. The plaque reduction neutralization tests (JEV) of rVTT-CE1-JE-EGFP group was 1:320 at 35 dpi. Furthermore, cytokine levels and the percentage of CD3+CD4+ and CD3+CD8+ T-lymphocytes in the rVTT-CE1-JE-EGFP group were significantly (p < 0.01) higher than those in the control groups at 35 dpi. After challenge, mice body weights in rVTT-CE1-JE-EGFP group were not significantly altered, and the survival rate was 100%. These results showed the rVTT-CE1-JE-EGFP group elicited significant humoral and cellular immune responses, thus indicating that the recombinant vaccine may serve as a candidate for effective prevention of CHIKV and JEV infection.

Management of injuries near the innominate artery bifurcation using an accurate kissing Viabahn stent technique.

OBJECTIVE: To evaluate the feasibility, safety, and efficacy of an accurate kissing Viabahn stent technique to manage injuries near the innominate artery bifurcation. METHODS: This retrospective study included patients with injuries near the innominate artery bifurcation who were treated with an accurate kissing Viabahn stent technique. Perioperative and follow-up data were extracted and analysed. RESULTS: A total of 10 patients were included (mean age, 52.8 years; six male and four female patients) with injuries at the following sites: the distal end of the innominate artery (n = 2), the innominate artery bifurcation (n = 5), the root of the right common carotid artery (n = 2) and the origin of the right subclavian artery (n = 1). All were successfully treated with the accurate kissing Viabahn stent technique. During follow-up (mean duration, 16.8 months), there were no complications, such as right upper limb ischaemia, neurological dysfunction, stent occlusion or migration. CONCLUSIONS: The accurate kissing Viabahn stent technique to manage injuries near the bifurcation of the innominate artery was safe and effective, with good perioperative and long-term follow-up results.

Pathogenicity of porcine reproductive and respiratory syndrome virus (ORF5 RFLP 1-7-4 viruses) in China.

Porcine reproductive and respiratory syndrome virus (PRRSV) is an RNA virus that causes reproductive failure in sows and respiratory problems in piglets. PRRSV infection leads to substantial pig mortality and causing huge economic losses so that disease outbreaks caused by the new PRRSV strain from other regions have caused great concern in China. In this study, we analysed the pathogenicity of the novel ORF5 RFLP 1-7-4-like PRRSV strain, named PRRSV-ZDXYL-China-2018-1 in pigs. The viral challenge test showed that PRRSV-ZDXYL-China-2018-1 infection can cause persistent fever, moderate dyspnoea, serum viraemia and interstitial pneumonia in piglets. The levels of viral loads in serum and PRRSV-specific antigen were also detected in lung tissues were used one-step Taq-Man RT-qPCR and Immunohistochemistry, respectively. At 28dpi, the level of specific antibodies was increased among infected piglets. Importantly, the new virus appeared be a moderately virulent isolate with pathogenicity compared to HP-PRRSV strain LQ (JXA1-like strain). Histological examination revealed severe monocyte haemorrhage and interstitial pneumonia associated with monocyte infiltration in the lung tissue of pigs infected with PRRSV-ZDXYL-China-2018-1 and LQ-JXA1 strains. Immunohistochemistry (IHC) results showed positive brown-red epithelial cells and macrophages in pig lungs. Therefore, it is critical to establish an effective strategy to control the spread of PRRSV in China.

First detection and genomic characterization of porcine circovirus 3 in mosquitoes from pig farms in China.

The porcine circovirus type 3 (PCV3) becomes an important causative agent of swine disease since its discovery in 2016. PCV3 infection exhibits a wide range of clinical syndromes causing substantial economic losses in swine industry. Previous studies have reported the detection of numerous known viruses including circovirus in mosquitoes. However, the transmission of PCV3 in field-caught mosquitoes remains largely unknown. This study aims to detect PCV3 infection in mosquitoes and analyze its genomic characteristics. Here, we performed a PCR to detect the PCV3 in 269 mosquito samples collected from pig farms located in Heilongjiang, Jilin, and Yunnan provinces. The proportion of PCV3-positive mosquitoes was 32.0 % (86/269), ranging from 21.4%-42.5% at farm level, which may imply that mosquito serves as a route of transmission for PCV3. To determine the possible origin of PCV3 in mosquitoes, 80 pig serum samples were collected from the pig farms where mosquito sampling was also performed. The proportion of PCV3-positive farms ranged from 15.0%-30.0 % in which infection of positive pigs positively correlated with mosquitoes carrying the virus. Additionally, we sequenced the entire genome of 6 strains of PCV3 in mosquitoes and 2 strains of PCV3 in pigs. Sequence analysis indicated a 100 % nucleotide similarity between mosquito and pig viral isolates that were all collected from similar farms. Phylogenetic analysis showed that PCV3 could be divided into two clades, PCV3a and PCV3b, and the PCV3 strains isolated in mosquitoes were distributed on the two clades. Our results demonstrate that mosquitoes may serve as a potential transmission vector in the life-cycle of PCV3, revealing possible transmission routes of PCV3.

Newcastle Disease Virus Inhibits the Proliferation of T Cells Induced by Dendritic Cells In Vitro and In Vivo.

Newcastle disease virus (NDV) infects poultry and antagonizes host immunity via several mechanisms. Dendritic cells (DCs) are characterized as specialized antigen presenting cells, bridging innate and adaptive immunity and regulating host resistance to viral invasion. However, there is little specific knowledge of the role of DCs in NDV infection. In this study, the representative NDV lentogenic strain LaSota was used to explore whether murine bone marrow derived DCs mature following infection. We examined surface molecule expression and cytokine release from DCs as well as proliferation and activation of T cells in vivo and in vitro in the context of NDV. The results demonstrated that infection with lentogenic strain LaSota induced a phenotypic maturation of immature DCs (imDCs), which actually led to curtailed T cell responses. Upon infection, the phenotypic maturation of DCs was reflected by markedly enhanced MHC and costimulatory molecule expression and secretion of proinflammatory cytokines. Nevertheless, NDV-infected DCs produced the anti-inflammatory cytokine IL-10 and attenuated T cell proliferation, inducing Th2-biased responses. Therefore, our study reveals a novel understanding that DCs are phenotypically mature but dysfunctional in priming T cell responses during NDV infection.

Molecular detection and genomic characterization of porcine circovirus 3 in pigs from Northeast China.

BACKGROUND: First identified in the United States in 2016, porcine circovirus type 3 (PCV3) is a newly emerging porcine circovirus exhibiting a wide range of clinical syndromes, which may be associated with the pathogenicity observed in pigs. RESULTS: The aim of this study was to identify and characterize the full genome sequence of PCV3 strains circulating in Northeast China. Herein, 105 lung samples isolated from sick pigs in Northeast China during 2018 were analyzed for PCV3. Using PCR, the total PCV3-positive rate was 33.3% (35/105), with rates of 17.8% (8/45), 66.7% (10/15), and 37.8% (17/45) in Heilongjiang, Jilin, and Liaoning province, respectively. Additionally, our findings showed that PCV3-positive samples had a high rate of co-infection with PCV2, PPV6, and PPV7. To study the evolution of the PCV3 in Northeast China, we sequenced the entire genome of 13 strains of PCV3. The results of phylogenetic analyses revealed that PCV3 could be divided into two clades, PCV3a and PCV3b. Interestingly, a G deletion at position 1072 was found in the 1999 nt genome of PCV3-CN2018LN-4 (MH277118). The G deletion terminated replicase protein translation and induced a truncated replicase protein. CONCLUSION: These results contribute to the understanding of PCV3 molecular epidemiology and evolution in Northeast China. A new strain of PCV3 with truncated replicase protein was identified.

Mapping the clinical outcomes and genetic evolution of Ebola virus in Sierra Leone.

Sierra Leone was the most severely affected country in Western Africa during the 2013-2016 outbreak of Ebola virus disease (EVD). Previous genome surveillance studies have revealed the origin, diversity, and evolutionary dynamics of the Ebola virus (EBOV); however, the information regarding EBOV sequences is insufficient, especially the clinical outcomes, given that the correlation between the clinical outcomes and the genetic evolution of EBOV is still not clear. Here, we collected and curated a comprehensive data set that includes 514 EBOV genome sequences from patients with confirmed EVD (including 60 sequences not previously studied), >87.5% of which have residence information and definitive clinical outcomes. Phylogenetic reconstruction revealed 11 lineages of EBOV in Sierra Leone. The median-joining haplotype network showed that haplotypes that are associated with lethal outcomes tend to contribute more to the spread of the EBOV in Sierra Leone than those with live outcomes. Analyses of the spatial-temporal distribution unraveled the lineage-distinctive distribution patterns. Different viral lineages have different case fatality rates (CFRs) during the same stage of the outbreak, implying that several lineages featuring SNPs may correlate with increased/decreased CFRs. This study provides invaluable data sets of EBOV infection and highlights the potential SNPs for further in-depth investigation.

Intra-host dynamics of Ebola virus during 2014.

Since 2013, West Africa has encountered the largest Ebola virus (EBOV) disease outbreak on record, and Sierra Leone is the worst-affected country, with nearly half of the infections. By means of next-generation sequencing and phylogeographic analysis, the epidemiology and transmission of EBOV have been well elucidated. However, the intra-host dynamics that mainly reflect viral-host interactions still need to be studied. Here, we show a total of 710 intra-host single nucleotide variations (iSNVs) from deep-sequenced samples from EBOV-infected patients, through a well-tailored bioinformatics pipeline. We present a comprehensive distribution of iSNVs during this outbreak and along the EBOV genome. Analyses of iSNV and its allele frequency reveal that VP40 is the most conserved gene during this outbreak, and thus it would be an ideal therapeutic target. In the co-occurring iSNV network, varied iSNV sites present different selection features. Intriguingly, the T-to-C substitutions at the 3'-UTR of the nucleoprotein (NP; positions 3008 and 3011), observed in many patients, result in the upregulation of the transcription of NP through an Ebola mini-genome reporting system. Additionally, no iSNV enrichment within B-cell epitopes of GP has been observed.

Clinical and Virological Characteristics of Ebola Virus Disease Patients Treated With Favipiravir (T-705)-Sierra Leone, 2014.

BACKGROUND: During 2014-2015, an outbreak of Ebola virus disease (EVD) swept across parts of West Africa. No approved antiviral drugs are available for Ebola treatment currently. METHODS: A retrospective clinical case series was performed for EVD patients in Sierra Leone-China Friendship Hospital. Patients with confirmed EVD were sequentially enrolled and treated with either World Health Organization (WHO)-recommended supportive therapy (control group) from 10 to 30 October, or treated with WHO-recommended therapy plus favipiravir (T-705) from 1 to 10 November 2014. Survival and virological characteristics were observed for 85 patients in the control group and 39 in the T-705 treatment group. RESULTS: The overall survival rate in the T-705 treatment group was higher than that of the control group (56.4% [22/39] vs 35.3% [30/85]; P = .027). Among the 35 patients who finished all designed endpoint observations, the survival rate in the T-705 treatment group (64.8% [11/17]) was higher than that of the control group (27.8% [5/18]). Furthermore, the average survival time of the treatment group (46.9 ± 5.6 days) was longer than that of the control group (28.9 ± 4.7 days). Most symptoms of patients in the treatment group improved significantly. Additionally, 52.9% of patients who received T-705 had a >100-fold viral load reduction, compared with only 16.7% of patients in the control group. CONCLUSIONS: Treatment of EVD with T-705 was associated with prolonged survival and markedly reduced viral load, which makes a compelling case for further randomized controlled trials of T-705 for treating EVD.

VEGFR2 Gene Polymorphism Correlates with Deep Venous Thrombosis Risk in Chinese Han Population.

OBJECTIVE: To investigate the correlations between three vascular endothelial growth factor 2 (VEGFR2) gene polymorphisms, +1192C>T, +1719T>A, and -604T>C, and deep venous thrombosis (DVT) in Chinese Han population. METHODS: We conducted a case-control study, between September 2009 and September 2012, in a Chinese Han population with onset of lower extremity DVT. A total of 135 patients were enrolled in the case group and 156 healthy individuals in the control group. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was used to detect the genotype and allele frequencies of the VEGFR2 gene polymorphisms +1192C>T, +1719T>A, and -604T>C. Haplotype analyses were conducted with SHEsis program. Logistic regression was used to detect the risk factors of DVT. Outpatient review and telephone follow-up were conducted to analyze the long-term treatment of DVT patients. RESULTS: The allele and genotype frequencies of -604T>C VEGFR2 polymorphism exhibited significant differences between the case and control groups (both p < 0.05). Haplotype analyses showed remarkable differences between the case and control groups in the distribution frequency of TAC and CTT haplotypes in the VEGFR2 gene (both p < 0.05). Logistic regression analysis showed independent correlation between the incidence of DVT and TAC haplotype in the VEGFR2 gene (p < 0.05). In addition, the TAC haplotype may be a risk factor for DVT treatment failure. CONCLUSION: Our findings suggest that the VEGFR2 gene -604T>C polymorphism and TAC haplotype are associated with DVT, and the TAC haplotype might affect the efficacy of long-term treatment of DVT patients.

Ebola Virus Outbreak Investigation, Sierra Leone, September 28-November 11, 2014.

During 2014-2015, an outbreak of Ebola virus disease (EVD) swept across parts of West Africa. The China Mobile Laboratory Testing Team was dispatched to support response efforts; during September 28-November 11, 2014, they conducted PCR testing on samples from 1,635 suspected EVD patients. Of those patients, 50.4% were positive, of whom 84.6% lived within a 3-km zone along main roads connecting rural towns and densely populated cities. The median time from symptom onset to testing was 5 days. At testing, 75.7% of the confirmed patients had fever, and 94.1% reported at least 1 gastrointestinal symptom; all symptoms, except rash and hemorrhage, were more frequent in confirmed than nonconfirmed patients. Virus loads were significantly higher in EVD patients with fever, diarrhea, fatigue, or headache. The case-fatality rate was lower among patients 15-44 years of age and with virus loads of <100,000 RNA copies/mL. These findings are key for optimizing EVD control and treatment measures.