Infectious agents and disease最新文献_第8页

Poxviral modifiers of cytokine responses to infection. 细胞因子对感染反应的痘病毒修饰因子。

Infectious agents and disease Pub Date : 1994-04-01

D J Pickup

{"title":"Poxviral modifiers of cytokine responses to infection.","authors":"D J Pickup","doi":"","DOIUrl":"","url":null,"abstract":"Poxviruses include some of the most virulent of all human pathogens. In part, the virulence of these viruses stems from their abilities to counter host defenses against infection. A family of cytokine-response modifiers encoded by the poxviruses contribute to these countermeasures. The poxviral cytokine-response modifiers appear to affect cytokine responses in at least four different ways: (a) by inhibiting the synthesis and release of cytokines from infected cells; (b) by interfering with the interaction between a cytokine and its receptor; (c) by inhibiting cytokine signal transmission; and (d) by synthesizing virus-encoded cytokines that antagonize the effects of host cytokines mediating antiviral processes. Known poxviral, cytokine-response modifiers include CrmA, an inhibitor of the interleukin-1 beta converting enzyme; several secreted soluble receptors for tumor necrosis factor, interleukin-1, and interferon-gamma; and poxvirus-encoded growth factors resembling epidermal growth factor. Collectively, these and other as yet unidentified cytokine-response modifiers contribute to the inhibition of a variety of nonspecific and virus-specific immune defenses against virus infection. Information gained on the mechanisms used by poxviruses to modify cytokine-mediated processes should assist the development of novel therapies for a variety of diseases.","PeriodicalId":77176,"journal":{"name":"Infectious agents and disease","volume":"3 2-3","pages":"116-27"},"PeriodicalIF":0.0,"publicationDate":"1994-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18812911","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Coronavirus: how a large RNA viral genome is replicated and transcribed. 冠状病毒:大RNA病毒基因组如何复制和转录。

Infectious agents and disease Pub Date : 1994-04-01

M M Lai, C L Liao, Y J Lin, X Zhang

引用次数: 0

Cis-acting signals and trans-acting factors involved in influenza virus RNA synthesis. 参与流感病毒RNA合成的顺式作用信号和反式作用因子。

Infectious agents and disease Pub Date : 1994-04-01

R E O'Neill, P Palese

引用次数: 0

Epstein-Barr virus protein LMP2A regulates reactivation from latency by negatively regulating tyrosine kinases involved in sIg-mediated signal transduction. Epstein-Barr病毒蛋白LMP2A通过负调控参与sig介导的信号转导的酪氨酸激酶来调节潜伏期的再激活。

Infectious agents and disease Pub Date : 1994-04-01

C L Miller, J H Lee, E Kieff, A L Burkhardt, J B Bolen, R Longnecker

{"title":"Epstein-Barr virus protein LMP2A regulates reactivation from latency by negatively regulating tyrosine kinases involved in sIg-mediated signal transduction.","authors":"C L Miller, J H Lee, E Kieff, A L Burkhardt, J B Bolen, R Longnecker","doi":"","DOIUrl":"","url":null,"abstract":"Like other herpesviruses, Epstein-Barr Virus (EBV) persists in its host through an ability to establish latent infection with episodic reactivations. In latent infection EBV expresses an integral membrane protein LMP2A that regulates reactivation from latency. LMP2A is constitutively tyrosine phosphorylated and is associated with lyn and syk tyrosine kinases. The activity of lyn is substantially reduced. In EBV-infected cells in which LMP2A is expressed, crosslinking of sIg fails to trigger the protein tyrosine kinase signal cascade, tyrosine phosphorylation of cell proteins does not change, second messengers are not generated, and lytic EBV infection is not induced. In contrast, crosslinking of sIg on cells infected with EBV recombinants with null mutations in LMP2A results in transient tyrosine phosphorylation of lyn, syk, phospholipase C gamma 2 and phosphatidylinositol-3' kinase, transiently increased intracellular free calcium, and reactivation of lytic EBV infection. These studies describe a novel molecular regulator of herpesvirus latency and focus attention on the importance of transmembrane signal transduction in herpes virus reactivation from latency. They support the working hypothesis that the identification of ligand-receptor interactions that can result in the induction of reactivation will provide an important inroad toward the delineation of the molecular mechanism, which govern herpesvirus reactivation from latency.","PeriodicalId":77176,"journal":{"name":"Infectious agents and disease","volume":"3 2-3","pages":"128-36"},"PeriodicalIF":0.0,"publicationDate":"1994-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18812912","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Immune recognition of viral antigens. 病毒抗原的免疫识别。

Infectious agents and disease Pub Date : 1994-04-01

I A Wilson, R L Stanfield, D A Jewell, J B Ghiara, D H Fremont, E A Stura

{"title":"Immune recognition of viral antigens.","authors":"I A Wilson, R L Stanfield, D A Jewell, J B Ghiara, D H Fremont, E A Stura","doi":"","DOIUrl":"","url":null,"abstract":"The response exhibited by the immune system to viral and other foreign antigens consists of antibody-mediated and T cell-mediated immunity. Structural and molecular biological studies have shown that the antibody response is tailored to provide exquisite specificity by generating binding pockets that are complementary in shape as well as in charge to the antigen. On the other hand, the cellular response uses T-cell receptors (TCRs) and the major histocompatibility complex (MHC) antigens. Structural information on the TCRs is not yet available, but the crystal structures of several MHC class I molecules have shown how one MHC molecule can bind many different peptide sequences that share only the common anchor residue positions that determine allele specificity. MHC class I interactions with the peptide backbone at the N and C termini explain the high specificity of the binding groove for peptide ligands and suggest a universal mode of recognition for peptides to MHC class I molecules. Peptide-MHC class II interactions are less well understood, although recent structural work has shown important differences in the binding clefts of MHC class I and II that lead to longer peptides being bound to class II molecules. Detailed analysis at the molecular level has indicated that conformational changes in both antibodies and MHC molecules occur upon antigen binding.(ABSTRACT TRUNCATED AT 250 WORDS)","PeriodicalId":77176,"journal":{"name":"Infectious agents and disease","volume":"3 2-3","pages":"155-62"},"PeriodicalIF":0.0,"publicationDate":"1994-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18812913","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Properties of an HSV-1 regulatory protein that appears to impair host cell splicing. 似乎损害宿主细胞剪接的HSV-1调节蛋白的特性。

Infectious agents and disease Pub Date : 1994-04-01

R M Sandri-Goldin

{"title":"Properties of an HSV-1 regulatory protein that appears to impair host cell splicing.","authors":"R M Sandri-Goldin","doi":"","DOIUrl":"","url":null,"abstract":"The herpes simplex virus type 1 (HSV-1) immediate early (alpha) protein ICP27 is an essential regulatory protein that appears to be involved in a number of different processes during lytic viral infection. Viral mutants defective in ICP27 have a variety of phenotypes that include defects in the shutoff of host protein synthesis, overexpression of some immediate early and early genes, reduced levels of DNA replication, and severely reduced levels of late gene products. ICP27 has been shown to act posttranscriptionally in the performance of some of its regulatory roles. It affects mRNA processing at the level of both polyadenylation and splicing. During polyadenylation, ICP27 appears to stimulate 3' RNA processing at selected poly(A) sites. The opposite effect, occurs on host cell splicing, that is, during HSV-1 infection, an inhibition in host cell splicing was found that required ICP27 expression. This impairment of splicing contributes to the shutoff of host protein synthesis by decreasing levels of spliced cellular mRNAs available for translation. A redistribution of splicing factors regulated by ICP27 has also been seen. Mutational analysis has shown that the C-terminal repressor region of the protein is required for the effects seen on splicing, whereas the activator region, encompassing the C-terminal half of the protein is required for the effects on 3' processing and the induction of late gene expression during viral infection. A highly basic arginine-rich region in the N-terminal half of the protein is required for nuclear localization of ICP27. Details on the mechanisms by which ICP27 contributes to these regulatory processes have been poorly defined to date.","PeriodicalId":77176,"journal":{"name":"Infectious agents and disease","volume":"3 2-3","pages":"59-67"},"PeriodicalIF":0.0,"publicationDate":"1994-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18812917","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

RNA-sequence-mediated gene regulation in HIV-1. rna序列介导的HIV-1基因调控。

Infectious agents and disease Pub Date : 1994-04-01

B R Cullen

引用次数: 0

Prion protein and the scrapie agent: in vitro studies in infected neuroblastoma cells. 朊蛋白和瘙痒剂:感染神经母细胞瘤细胞的体外研究。

Infectious agents and disease Pub Date : 1994-04-01

S A Priola, B Caughey, G J Raymond, B Chesebro

{"title":"Prion protein and the scrapie agent: in vitro studies in infected neuroblastoma cells.","authors":"S A Priola, B Caughey, G J Raymond, B Chesebro","doi":"","DOIUrl":"","url":null,"abstract":"The mouse neuroblastoma cell line N2a was persistently infected with the Chandler strain of the mouse scrapie agent. Although the infection did not spread to infect > 1% of the cells, clones were established that had from 50 to 100% infected cells. These clones expressed the abnormal protease-resistant form of prion protein (PrP), which is believed to mediate brain degeneration in animals with scrapie and bovine spongiform encephalopathy and in humans with kuru, Creutzfeldt-Jakob disease, and Gerstmann-Straussler-Scheinker syndrome. With this in vitro system, Congo red and several sulfated polysaccharides, including heparin and pentosan polysulfate, were found to inhibit accumulation of protease-resistant PrP. These results and additional data confirming PrP binding to heparin suggested a possible role for sulfated glycosaminoglycans in the generation of protease-resistant PrP during scrapie infection. Accumulation of protease-resistant PrP was also blocked in vitro by expression of foreign PrP molecules, indicating that PrP from different species might compete for common substrates in this process. These results using scrapie-infected cell lines provide new opportunities for development of drugs capable of blocking the brain degeneration caused by scrapie and other transmissible spongiform encephalopathies.","PeriodicalId":77176,"journal":{"name":"Infectious agents and disease","volume":"3 2-3","pages":"54-8"},"PeriodicalIF":0.0,"publicationDate":"1994-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18811621","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Current frontiers in virology. 病毒学的最新前沿。

Infectious agents and disease Pub Date : 1994-04-01

B Roizman, P G Spear

引用次数: 0

Regulation of TNF-mediated cell death and inflammation by human adenoviruses. 人腺病毒对tnf介导的细胞死亡和炎症的调控。

Infectious agents and disease Pub Date : 1994-04-01

L R Gooding

引用次数: 0