寻找病毒免疫力

敌对情绪和仇视心理。

Construction and Immunogenicity of Associated DNA Vaccine of PRRS and PCV-2 Disease

[ Objective ] The aim of the study was to construct associated DNA vaccine of PRRS （Porcine reproductive and respiratory syndrome） and PCV-2 （Porcine circovirus type 2） disease and study its immunogenicity. [ Method] In_ this study, the ORF5 gene of PRRSV isolated in Liaoning was cloned into plRES-neo expression vector, and the neo gene of plRES-neo expression vector was substituted by the ORF2 gene of the PCV-2 Mongolia strain to construct the recombinant expression vector. The expression in BHK cells was detected through Western blot and IFA. Then the ELISA antibody level and the number of spleen T lymphocytes were detected after Balb/c mice were immunized with this DNA vaccine. E Result] The recombinant plasmid plRES-ORF2-ORF5 was constructed successfully and could express the target proteins in BHK cells, as indicated by Western blot and IFA. There was no significant difference in ELISA antibody between plRES-ORF2-ORF5 immunized group and inactived vaccine immunized groups, while the number of spleen T lymphocytes induced by DNA vaccine was higher than that induced by inactived vaccine. [ Conclusion] The recombinant plasmid plRES-ORF2-ORF5 should induce good humoral immune response and cellular immune response in mice, providing the conditions for better prevention and control of PRRS and PCV-2 disease.

Interaction of hepatitis C virus with the type I interferon system

Hepatitis C virus （HCV） needs to tightly manipulate host defences in order to establish infection. The innate immune response slows down viral replication by activating cytokines such as the type Ⅰ interferons （IFN-α/ β）, which trigger the synthesis of antiviral proteins and modulate the adaptive immune system. HCV has therefore developed a number of countermeasures to stay ahead of the IFN system. Here, I will attempt to summarize the current state of research regarding IFN responses against HCV and the viral escape strategies. Particular emphasis will be put on the newly discovered mechanisms HCV employs to avoid the induction of IFN in infected cells.

Cytomegalovirus enteritis mimicking Crohn's disease in a lupus nephritis patient:A case report

Cytomegalovirus(CMV)infection of the gastrointestinal (GI)tract has been reported in both immunocompetent and,more frequently,in immunocompromised patients.We describe a case of a 19-year-old male who developed CMV infection of the terminal ileum while receiving immunosuppression for lupus nephritis. This was a distinctly unusual site of infection which clinically mimicked Crohn's ileitis.We note that reports of terminal ileal CMV infection have been infrequent. Despite a complicated hospital course,ganciclovir therapy was effective in resolving his symptoms and normalizing his ileal mucosa.This report highlights the importance of accurate histological diagnosis and clinical follow-up of lupus patients with GI symptoms undergoing intense immunosuppression.

Mononuclear phagocyte system in hepatitis C virus infection

The mononuclear phagocyte system （MPS）, which con-sists of monocytes, dendritic cells （DCs）, and macro-phages, plays a vital role in the innate immune defense against pathogens. Hepatitis C virus （HCV） is effcient in evading the host immunity, thereby facilitating its devel-opment into chronic infection. Chronic HCV infection is the leading cause of end-stage liver diseases, liver cirrhosis, and hepatocellular carcinoma. Acquired im-mune response was regarded as the key factor to era-dicate HCV. However, innate immunity can regulate the acquired immune response. Innate immunity-derived cytokines shape the adaptive immunity by regulating T-cell differentiation, which determines the outcome of acute HCV infection. Inhibition of HCV-specific T-cell responses is one of the most important strategies for im-mune system evasion. It is meaningful to illustrate the role of innate immune response in HCV infection. With the MPS being the important factor in innate immunity, therefore, understanding the role of the MPS in HCV infection will shed light on the pathophysiology of chronic HCV infection. In this review, we outline the impact of HCV infection on the MPS and cytokine production. We discuss how HCV is detected by the MPS and describe the function and impairment of MPS components in HCV infection.

Hepatitis C infected patients need vitamin D3 supplementation in the era of direct acting antivirals treatment

It has been reported that the serum level of vitamin D3(Vit D3) could affect the natural course of chronic hepatitis C(CH-C) and the response to treatment with pegylated interferon(Peg-IFN) and ribavirin. Although several mechanisms for the favorable effects of Vit D3 supplementation were reported, the total effect of Vit D3 supplementation remains unclear. Previously, we reported that supplementation with 1(OH)Vit D3 could enhance the Th1 response inducing not only a favorable immune response for viral eradication but also HCC control. Recently, the main treatment of CH-C should be direct acting antivirals(DAAs) without PegIFN. Peg-IFN is a strong immune-modulator. Therefore, an immunological analysis should be carried out to understand the effect of Vit D3 after treatment of DAAs without Peg-IFN. The induction of a favorable immune response by adding Vit D3 might be able to suppress the hepatocarcinogenesis after achieving SVR, especially in children and elderly patients with severe fibrosis lacking sufficient amounts of VitD 3.

The effect of human papilloma virus type 16 E7 protein expression on growth of RMA cells in vitro and in vivo

Objective： The aim of this study was to study the effect of human papilloma virus （HPV） type 16 E7 protein ex- pression on growth of RMA cells in vitro and in vivo. Methods： The recombination vector pcDNA3.1-E7 carrying wild type HPV 16 E7 was identified by sequencing. The recombination vector pcDNA3.1-E7 was transfected into mouse lymphadenoma cell line RMA by liposome, and the monoclonal cells transfected stably were obtained by antibiotics G418 sieving and limiting dilution assay. RT-PCR method was used to detect the expression of HPV 16 E7 mRNA in RMA-E7 cells. The growth of RMA cells and RMA-E7 cells cultured in vitro was tested by Cell Count Kit-8. RMA-E7 cells and RMA cells were subcutaneously inoculated in syngeneic mice respectively, the tumor size was measured by sliding caliper twice a week, and the E7 protein expression in tumor tissue of mice was detected by Western blot after tumor formation. The kinetics of cytolytic activity of E7 specific T cells in tumor-bearing mice was measured by LDH kit. Results： Sequencing of recombination vector showed the target gene which was inserted into the recombinant was correct, and RMA-E7 cells expressing E7 protein stably were obtained by limited dilution assay. There were no obvious differences in morphous and growth velocity between RMA cells and RMA-E7 cells in vitro. RMA-E7 cells grew in syngeneic mice were significantly slower than RMA cells. The E7 protein was ex- pressed stronger in RMA-E7 cells in vivo than in vitro. The cytolytic ability of ET-specific CTL was activated at the early stage, reached the maximum at the middle stage, and lost at the end stage. RMA-E7 cells isolated from the tumor-bearing mice were more resistant to E7-specific CTL killing than RMA-E7 cells cultured in vitro. Conclusion： The E7 protein expression has no obvious influence on growth of RMA-E7 cells in vitro, and can suppress growth of RMA-E7 cells in vivo. The activity curve of E7 specific CTL approximately presents ＂bell＂ shape. The RMA-E7 cells grew in vivo had a high expression levels of E7 protein, and more resistant to E7-specific CTL killing than those cultured in vitro. The E7 protein expression in vivo not only initiates immune activation, but also induces immune tolerance.

Activation and counteraction of antiviral innate immunity by KSHV: an update

The innate immune responses triggering production of type 1 interferons and inflammatory cytokines constitute a nonspecific innate resistance that eliminates invading pathogens including viruses. The acti- vation of innate immune signaling through pattern recognition receptors （PRRs） is by sensing pathogen- associated molecular patterns derived from viruses. According to their distribution within cells, PRRs are classified into three types of receptors： membrane, cytoplasmic, and nuclear. Kaposi＇s sarcoma- associated herpesvirus （I（SHV）, a large DNA virus, replicates in the nucleus. Its genome is protected by capsid proteins during transport in the cytosol. Multiple PRRs are involved in KSHV recognition. To suc- cessfully establish latent infection, KSHV has evolved to manipulate different aspects of the host antiviral innate immune responses. This review presents recent advances in our understanding about the activation of the innate immune signaling in response to infection of KSHV. It also reviews the evasion strate- gies used by KSHV to subvert host innate immune detection for establishing a persistent infection.

Roles of IκB kinase ε in the innate immune defense and beyond

IκB kinase ε(IKKε) is a non-canonical IκB kinase that is extensively studied in the context of innate immune response. Recently, significant progress has been made in understanding the role of IKKεin interferon(IFN) signaling. In addition to its roles in innate immunity, recent studies also demonstrate that IKKε is a key regulator of the adaptive immune response. Specifically, IKKεfunctions as a negative feedback kinase to curtail CD8 T cell response, implying that it can be a potential therapeutic target to boost antiviral and antitumor T cell immunity. In this review, we highlight the roles of IKKε in regulating IFN signaling and T cell immunity, and discuss a few imminent questions that remain to be answered.

DYNAMICS BEHAVIOR OF MUTATION DURING REPRODUCTION ON HIV-1 DRUG RESISTANCE

To study the transition dynamics of resistant-type human immunodeficiency virus 1 （HIV-1） in highly active antiretroviral therapy （HAART） and the affect of neutral mutation in the evolution of HIV-1, a mathematical model is proposed when mutation occurs mainly during reproduction. The derived results show that the resistant-type will certainly colonize in patients once mutation occurs. Furthermore, a neutral mutation is closely related to the colonized pattern of resistant-type HIV-1 quasispecies and there are some changes in the pattern of transmission dynamics when mutation occurs mainly during reproduction or in the absence of reproduction, which may lead to significant strategies for predicting or checking HIV-1 drug resistance in HAART.