Li W.,Institute For Viral Dis Control And Prev |
Li W.,Shandong University |
Li W.,Jining Medical University |
Cao Y.,Institute For Viral Dis Control And Prev |
And 13 more authors.
Vector-Borne and Zoonotic Diseases | Year: 2014
Tahyna virus (TAHV) was first isolated from mosquitoes collected in the suburbs of Geermu city in the Qinghai-Tibet Plateau of China in 2007. Since then, TAHV antibodies have been detected in local livestock in Geermu, Qinghai. To determine whether the disease caused by TAHV was present in local residents, an investigation was conducted in the summer of 2009. During this investigation, ward inspections were conducted in rural clinics, and clinical information and specimens were collected from patients who complained mainly of acute fever. The collected samples were tested by serological and molecular methods. The results showed that four samples were positive for TAHV immunoglobulin M and had four-fold or higher levels of TAHV-neutralizing antibody titers between convalescent-phase and acute-phase, and that TAHV nucleotide sequences were detected in two acute sera. Clinical features of TAHV infection commonly included fever, accounting for 100%. Among all other symptoms, the one with the highest frequency was pharyngitis (80%), followed by malaise, inappetence, arthralgia, headache, and drowsiness. Follow-up surveys revealed that all cases recovered in 2-5 days after onset, and no serious or deadly cases were observed. This is the first time that the disease caused by TAHV infection has been reported in China. TAHV infection is another known mosquito-borne arboviral disease in China. © Copyright 2014, Mary Ann Liebert, Inc. 2014.
Zhu W.,Institute For Viral Dis Control And Prev |
Wang L.,Institute For Viral Dis Control And Prev |
Yang Y.,Institute For Viral Dis Control And Prev |
Jia J.,Uppsala University |
And 5 more authors.
PLoS ONE | Year: 2010
Cell culture-adapted strains of Sindbis virus (SINV) initially attach to cells by the ability to interact with heparan sulfate (HS) through selective mutation for positively charged amino acid (aa) scattered in E2 glycoprotein (W. B. Klimstra, K. D. Ryman, and R. E. Johnston, J. Virol. 72: 7357-7366, 1998). Here we have further confirmed that interaction of E2 protein with HS is crucial for cellular infection of SINV based on the reverse genetic system of XJ-160 virus, a Sindbis-like virus (SINLV). Both SINV YN87448 and SINLV XJ-160 displayed similar infectivity on BHK-21, Vero, or C6/36 cells, but XJ-160 failed to infect mouse embryonic fibroblast (MEF) cells. The molecular mechanisms underlying the selective infectivity of XJ-160 were approached by substituting the E1, E2, or both genes of XJ-160 with that of YN87448, and the chimeric virus was denominated as XJ-160/E1, XJ-160/E2, or XJ-160/E1E2, respectively. In contrast to the parental XJ-160, all chimeric viruses became infectious to wild-type MEF cells (MEF-wt). While MEF-Ext-/- cells, producing shortened HS chains, were resistant not only to XJ-160, but also to YN87448 as well as the chimeric viruses, indicating that the inability of XJ-160 to infect MEF-wt cells likely due to its incompetent discrimination of cellular HS. Treatment with heparin or HS-degrading enzyme resulted in a substantial decrease in plaque formation by YN87448, XJ-160/E2, and XJ-160/E1E2, but had marginal effect on XJ-160 and XJ-160/E1, suggesting that E2 glycoprotein from YN87448 plays a more important role than does E1 in mediating cellular HS-related cell infection. In addition, the peptide containing 145-150 aa from E2 gene of YN87448 specifically bound to heparin, while the corresponding peptide from the E2 gene of XJ-160 essentially showed no binding to heparin. As a new dataset, these results clearly confirm an essential role of E2 glycoprotein, especially the domain of 145-150 aa, in SINV cellular infection through the interaction with HS. © 2010 Zhu et al.