Host differences in influenza-specific CD4 T cell and B cell responses are modulated by viral strain and route of immunization.

The antibody response to influenza infection is largely dependent on CD4 T cell help for B cells. Cognate signals and secreted factors provided by CD4 T cells drive B cell activation and regulate antibody isotype switching for optimal antiviral activity. Recently, we analyzed HLA-DR1 transgenic (DR1) mice and C57BL/10 (B10) mice after infection with influenza virus A/New Caledonia/20/99 (NC) and defined epitopes recognized by virus-specific CD4 T cells.

Influenza virus variation in susceptibility to inactivation by pomegranate polyphenols is determined by envelope glycoproteins.

Pomegranates have high levels of polyphenols (PPs) and may be a rich source of compounds with antiviral activity. We evaluated the direct anti-influenza activity of three commercially available pomegranate extracts: pomegranate juice (PJ), a concentrated liquid extract (POMxl), and a 93% PP powder extract (POMxp). The acidity of PJ and POMxl solutions contributed to rapid anti-influenza activity, but this was not a factor with POMxp.

Quantitative analysis of influenza virus-specific B cell memory generated by different routes of inactivated virus vaccination.

We consider both Ab-secreting cell (ASC) and memory B cell (B(Mem)) populations in a quantitative analysis of virus-specific B cell memory generated by intramuscular or intranasal vaccination of mice with inactivated influenza virus. After both forms of vaccination, the memory phase was characterized by localization of ASCs in the bone marrow and dispersion of B(Mem) to organized lymphoid tissues. The stronger IgG response to intramuscular vaccination correlated with larger numbers of IgG ASCs in the bone marrow and IgG B(Mem).

Inhibitory effect of small interfering RNA specific for a novel candidate target in PB1 gene of influenza A virus.

Influenza, mainly caused by influenza virus, is becoming one of the major concerns in the world. Limitation in vaccines necessitates the urgent development of new therapeutic options against this virus. In the present study, we designed small interfering RNA (siRNA) targeting overlapping gene of PB1 and PB1-F2 gene of the influenza A virus and investigated its effect against influenza A virus infection.

Potent inhibition of human influenza H5N1 virus by oligonucleotides derived by SELEX.

New therapeutics are urgently needed for the treatment of pandemic influenza caused by H5N1 influenza virus mutants. Aptamer was a promising candidate for treatment and prophylaxis of influenza virus infections. In this study, systemic evolution of ligands through exponential enrichment (SELEX) was used to screen DNA aptamers targeted to recombinant HA1 proteins of the H5N1 influenza virus.

[Construction and immunogenicity study of DNA vaccine expressing human H5N1 influenza virus hemagglutinin].

Based on the first isolated human H5N1 influenza virus strain A/Anhui/1/2005 in China, HA and HA1 genes were amplified and cloned into the eukaryotic expression vector pStar. The recombinant plasmids pStar-HA and pStar-HA1 were transfected into COS7 cells. Western blot and IFA showed that the two recombinant DNA plasmids were successfully expressed in eukaryotic cells.

Construction and delivery of gene therapy vector containing soluble TNFalpha receptor-IgGFc fusion gene for the treatment of allergic rhinitis.

Tumor necrosis factor alpha plays primary role in the pathogenesis of inflammatory diseases. TNFalpha is essential for antigen-specific IgE production and for the induction of Th2-type cytokines. The lack of TNFalpha inhibited the development of allergic rhinitis.

[Expression of sTNFR-IgGFc fusion gene in endothelial cell and its application in gene therapy for rheumatoid arthritis].

Tumor necrosis factor alpha (TNFalpha) is a pro-inflammatory cytokine, acting as a regulator of inflammation and immunity. TNFalpha plays a critical role in the pathogenesis of rheumatoid arthritis. Blocking of TNFa activity suppressed inflammatory tissue damage.