Sodium dodecyl sulfate-polyacrylamide gel electrophoresis and mass spectrometry were used to analyze the structural proteins of the occlusion-derived virus (ODV) of Helicoverpa armigera single nucleocapsid nucleopolyhedrovirus (HearNPV), a group II NPV. Twenty-three structural proteins of HearNPV ODV were identified, 21 of which have been reported previously as structural proteins or ODV-associated proteins in other baculoviruses. These include polyhedrin, P78/83, P49, ODV-E18, ODV-EC27, ODV-E56, P74, LEF-3, HA66 (AC66), DNA polymerase, GP41, VP39, P33, ODV-E25, helicase, P6.9, ODV/BV-C42, VP80, ODV-EC43, ODV-E66, and PIF-1. Two proteins encoded by HearNPV ORF44 (ha44) and ORF100 (ha100) were discovered as ODV-associated proteins for the first time. ha44 encodes a protein of 378 aa with a predicted mass of 42.8 kDa. ha100 encodes a protein of 510 aa with a predicted mass of 58.1 kDa and is a homologue of the gene for poly(ADP-ribose) glycohydrolase (parg). Western blot analysis and immunoelectron microscopy confirmed that HA44 is associated with the nucleocapsid and HA100 is associated with both the nucleocapsid and the envelope of HearNPV ODV. HA44 is conserved in group II NPVs and granuloviruses but does not exist in group I NPVs, while HA100 is conserved only in group II NPVs.

Rubella virus (RV) is a highly transmissible pathogenic agent that causes the disease rubella. Maternal RV infection during early pregnancy causes the death of the fetus or congenital rubella syndrome in infants. However, the cellular receptor for RV has not yet been identified. In this study, we found that the myelin oligodendrocyte glycoprotein (MOG) specifically bound to the E1 envelope glycoprotein of RV, and an antibody against MOG could block RV infection. Most importantly, we also showed that ectopic expression of MOG on the cell surface of 293T cells rendered this nonpermissive cell line permissive for RV entry and replication. Thus, this study has identified a cellular receptor for RV and suggests that blocking the MOG attachment site of RV may be a strategy for molecular intervention of RV infection.Rubella virus (RV) is the only known member of the genus Rubivirus in the Togaviridae family and is the pathogenic agent of the disease rubella (6). RV consists of a positive-sense, single-stranded RNA genome enclosed in a quasispherical capsid and an envelope in which the two type I membrane glycoproteins, E2 and E1, are embedded as a heterodimeric spike complex (3). The clinical symptoms of RV infections acquired postnatally are usually mild, but maternal infection during the first 8 weeks after the last menstrual period results in chronic nonlytic infection in nearly all fetuses, with almost all infected fetuses developing congenital defects which entail a range of serious incurable illnesses, including cardiac, cerebral, ophthalmic, and auditory defects (18,34,37). RV is transmitted from person to person via respiratory aerosols, and humans are the only known natural hosts (18).Despite the pathogenicity of RV, little is known about the detailed mechanism of its entry into host cells. Research showed that similar to alphaviruses, RV enters cells via the endocytic pathway at physiological pH (17, 31). In the endosome vacuole, exposure of RV E1 and E2 glycoproteins to a pH of 6.0 or less induces a conformational change within the glycoproteins and leads to the fusion of the viral envelope to the endosomal membrane (16). Following this, the RV capsid protein undergoes a structural change; uncoating occurs in the endosome, allowing the release of viral genomic RNA into the cytoplasm (23).The recognition of specific receptors on the cell plasma membrane by proteins on the virus surface is necessary for virus attachment and subsequent infection (2). So far, two types of potential cell surface receptors for the alphaviruses in the Togaviridae family have been identified. Venezuelan equine encephalitis (VEE) virus uses laminin-binding protein (13). Semliki Forest virus (SFV) requires cholesterol in the host cell or a liposomal membrane for entry into target cells (26). Although RV and the alphaviruses possess similar characteristics in genomic organization and structural protein expression (8), their genomes share low levels of sequence homology, and their replication cycle kinetics are also different (40). Cell...

Using monofactorial and multivariate logistic regression analyses, the correlation of perioperative risk factors with postoperative pulmonary complications (PPCs) within 1 month after orthotopic liver transplantation (OLT) was investigated. Data on 107 patients (median age 46.8 years, 72% male) with end-stage liver disease who received OLT were retrospectively analysed. The incidence of PPCs was 60.7%. Overall mortality was 13.1% and pulmonary causes accounted for 85.7% of deaths. Mortality was 18.5% and 4.8% for patients with and without pulmonary complications, respectively. Independent risk factors for PPCs were a preoperative model for end-stage liver disease (MELD) score > or =25, intraoperative fluid transfusion volume > 10 1 and intraoperative blood transfusion volume > 4 l. A fluid balance of < or = -300 ml for > or =2 days of the first 3 days after surgery was protective. Other variables studied did not predict PPCs. It was concluded that improving the patient's preoperative medical condition, restricting intraoperative transfusion volumes and maintaining a negative fluid balance in the first 3 days after operation may decrease PPCs.