Induction of innate immunity and its perturbation by influenza viruses

Influenza A viruses (IAV) are highly contagious pathogens causing dreadful losses to human and animal, around the globe. IAVs first interact with the host through epithelial cells, and the viral RNA containing a 5'-triphosphate group is thought to be the critical trigger for activation of effective innate immunity via pattern recognition receptors-dependent signaling pathways. These induced immune responses establish the antiviral state of the host for effective suppression of viral replication and enhancing viral clearance. However, IAVs have evolved a variety of mechanisms by which they can invade host cells, circumvent the host immune responses, and use the machineries of host cells to synthesize and transport their own components, which help them to establish a successful infection and replication. In this review, we will highlight the molecular mechanisms of how IAV infection stimulates the host innate immune system and strategies by which IAV evades host responses.

Advances of Researches on Anti-phage Mechanisms of Host / 病毒学报

Phages also known as bacteria viruses, are recognized as the most abundant and diverse microbes. This diversity is adapting to the selective pressures such as the prevalence of the phage resistance mechanisms of bacteria. Phages invade and lyse bacterial through six steps (adsorption, injection, replication, transcription translation, assemble, release). Bacteria evolve to many anti-phage mechanisms to avoid phage infection and lysis. This paper focus on a variety of anti-phage mechanisms of bacteria.

Research into the Pathogenicity of Enterovirus 71 / 病毒学报

Enterovirus 71 (EV71) is a major causative agent of hand, foot and mouth disease (HFMD). belongs to family Picornaviridae, genus Enterovirus, species A. EV71 infection usually affects subjects aged <5 years. HFMD caused by EV71 infection is usually mild in children. However, in some cases EV71 infection can lead to severe neurogenic disease and even death. EV71 infection has caused epidemic worldwide (especially in the Asia Pacific). HFMD caused by EV71 has become a major public-health prol lem across the Asia Pacific. In EV71 infection, the pathogenesis is determined by viral and host factor, Here, we review research on host susceptibility and how EV71 suppresses immune and intracellular ri

Molecular mechanism of SCARB2-mediated attachment and uncoating of EV71

Unlike the well-established picture for the entry of enveloped viruses, the mechanism of cellular entry of non-enveloped eukaryotic viruses remains largely mysterious. Picornaviruses are representative models for such viruses, and initiate this entry process by their functional receptors. Here we present the structural and functional studies of SCARB2, a functional receptor of the important human enterovirus 71 (EV71). SCARB2 is responsible for attachment as well as uncoating of EV71. Differences in the structures of SCARB2 under neutral and acidic conditions reveal that SCARB2 undergoes a pivotal pH-dependent conformational change which opens a lipid-transfer tunnel to mediate the expulsion of a hydrophobic pocket factor from the virion, a pre-requisite for uncoating. We have also identified the key residues essential for attachment to SCARB2, identifying the canyon region of EV71 as mediating the receptor interaction. Together these results provide a clear understanding of cellular attachment and initiation of uncoating for enteroviruses.

Screening of dengue II virus-binding molecules from Aedes albopictus C6/36 cells / 南方医科大学学报

<p><b>OBJECTIVE</b>To screen the molecules binding dengue II virus expressed in Aedes albopictus C6/36 cells and characterize their biological functions.</p><p><b>METHODS</b>Aedes albopictus C6/36 cells were infected with dengue II virus, and the virus were collected and purified. The total and membrane proteins of C6/36 cells were extracted and analyzed using 12% SDS-polyacrylamide gel (PAGE). After electrophoresis, the proteins were transferred to a nitrocellulose membrane, and virus overlay protein-binding assay (VOPBA) was carried out using an anti-dengue virus 1-4 monoclonal antibody.</p><p><b>RESULTS</b>Two specific bands of 67 000 and 30 000 occurred after VOPBA of the proteins from the cells incubated with the virus, while the negative control group did not show these specific bands.</p><p><b>CONCLUSION</b>Two putative dengue virus receptor molecules of 67 000 and 30000 have been obtained from C6/36 cells using VOPBA, and their functional identification is in progress.</p>

Comparative study of synonymous codon usage variations between the nucleocapsid and spike genes of coronavirus, and C-type lectin domain genes of human and mouse

Coronaviruses (CoVs) are single-stranded RNA viruses which contain the largest RNA genomes, and severe acute respiratory syndrome coronavirus (SARS-CoV), a newly found group 2 CoV, emerged as infectious disease with high mortality rate. In this study, we compared the synonymous codon usage patterns between the nucleocapsid and spike genes of CoVs, and C-type lectin domain (CTLD) genes of human and mouse on the codon basis. Findings indicate that the nucleocapsid genes of CoVs were affected from the synonymous codon usage bias than spike genes, and the CTLDs of human and mouse partially overlapped with the nucleocapsid genes of CoVs. In addition, we observed that CTLDs which showed the similar relative synonymous codon usage (RSCU) patterns with CoVs were commonly derived from the human chromosome 12, and mouse chromosome 6 and 12, suggesting that there might be a specific genomic region or chromosomes which show a more similar synonymous codon usage pattern with viral genes. Our findings contribute to developing the codon-optimization method in DNA vaccines, and further study is needed to determine a specific correlation between the codon usage patterns and the chromosomal locations in higher organisms.