ABSTRACT
Background & objectives: Studies have shown that certain flaviviruses influence susceptibility of mosquitoes by inhibiting/enhancing replication of important flaviviruses. Hence, a study was designed to determine whether Bagaza virus (BAGV), a flavivirus isolated from Culex tritaeniorhynchus mosquitoes in India, alters susceptibility of Cx. tritaeniorhynchus and Cx. quinquefasciatus mosquitoes to Japanese encephalitis (JEV) and West Nile viruses (WNV). Methods: JEV and WNV infection in Cx. tritaeniorhynchus and Cx. quinquefasciatus mosquitoes in the presence of BAGV was carried out by intrathoracic (IT) inoculation and oral feeding methods. Mosquitoes were infected with BAGV and WNV/JEV either simultaneously or in a phased manner, in which mosquitoes were infected with BAGV by IT inoculation followed by super-infection with JEV/WNV after eight days post-infection (PI). JEV and WNV yield on 7th and 14th day PI after super-infection was determined by 50 per cent tissue culture infective dose (TCID50) method. Results: In Cx. tritaeniorhynchus mosquitoes, prior infection with BAGV significantly reduced JEV and WNV replication while in Cx. quinquefasciatus, BAGV influence was only seen with WNV. Reduction in virus titre was observed in IT inoculated and oral fed mosquitoes irrespective of the infection mode. JEV replication was also found reduced in Cx. tritaeniorhynchus mosquitoes persistently infected with BAGV at passage four. Interpretation & conclusions: BAGV infection in Cx. tritaeniorhynchus and Cx. quinquefasciatus mosquitoes altered their susceptibility to JEV and WNV producing low virus yield. However, the role of BAGV in inhibiting JEV/WNV replication in field mosquitoes needs further investigations
ABSTRACT
Objective To investigate the prevalence of hepatitis B virus (HBV) and hepatitis C virus (HCV) in human immunodeficiency virus (HIV)-positive patients infected by blood (with exception of intravenous drug users) and sexual transmission routes in China. Methods Three hundred and sixty-two cases of HIV positive patients from 13 acquired immune deficiency syndrome (AIDS) centers of China (those intravenous drug users were excluded) were analyzed retrospectively. The serological markers of HBV infection including HBsAg, anti-HBs, HBeAg, anti-Hbe, anti-HBc and anti-HCV antibodies were detected by the chemiluminescence immunoassay(CMIA) or enzyme-linked immunosorbent assay (ELISA). Numeration and measurement data were hnalyzed using chi square test and t test, respectively. Results Both HBV markers and HCV antibody were detected in 315 HIV postitive patients. Among them, fourteen cases were HBsAg positive, with the percentage of 4.4%. One hundred and fifty-eight cases (50. 2%) were anti-HCV antibody postive and 157 cases (49.8%) were negative. Only 2 cases (0.6%) were H1V, HBV, HCV co-infection. In the anti-HCV positive group, the percentage of blood and sexual transmission were 92 % and 4 %, respectively, with a predominant blood transmission; while in the anti-HCV negative group, the percentage of blood and sexual transmission were 11% and 66% respectively, dominating with sexual transmission. The duration of HIV infection, CD4+ T cell absolute numbers, alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels were all higher in the anti-HCV positive group than those in the anti-HCV negative group. Meanwhile, there were 2 cases (1.3%) of HBsAg positive in the anti-HCV positive group while 12 cases (7.6%) in the anti-HCV negative group, with a statistically significant difference (X2= 7.542, P<0.01). HBV DNA detection was performed in 10 HBsAg positive patients, four of them were HBV DNA positive but all were anti-HCV negative. Fifty-seven patients with anti-HCV positive received HCV RNA detection and 63.2% of them were positive. Conclusions HBV and HCV co-infection exists in HIV-infected Chinese patients, predominantly with HCV co-infection and by blood transmission. HCV infection may aggravate the liver injury of HIV infection and, at the same time, may have some mechanisms to interfere HBV replication.