The Open Virology Journal最新文献_第6页

Detection and Genotyping of Human Papillomavirus DNA in Formalin-Fixed Paraffin-Embedded Specimens with the HPV Direct Flow CHIP System. 利用 HPV Direct Flow CHIP 系统检测福尔马林固定石蜡包埋标本中的人类乳头瘤病毒 DNA 并进行基因分型。

The Open Virology Journal Pub Date : 2013-10-18 eCollection Date: 2013-01-01 DOI: 10.2174/1874357920130927004

Elsa Herraez-Hernandez, Ovidiu Preda, Sonia Alonso, Rosario Serrano Pardo, Asuncion Olmo

引用次数: 0

Application of maldi-tof mass spectrometry in clinical virology: a review. maldi-tof质谱法在临床病毒学中的应用综述。

The Open Virology Journal Pub Date : 2013-09-27 eCollection Date: 2013-01-01 DOI: 10.2174/1874357920130927003

Fernando Cobo

引用次数: 67

A case report of crimean congo hemorrhagic Fever in ostriches in iran. 一份关于伊朗鸵鸟 "克里米亚-刚果出血热 "的病例报告。

The Open Virology Journal Pub Date : 2013-08-22 eCollection Date: 2013-01-01 DOI: 10.2174/1874357901307010081

Ehsan Mostafavi, Sadegh Chinikar, Maryam Moradi, Neda Bayat, Mohsen Meshkat, Mohammad Khalili Fard, Seyyed Mojtaba Ghiasi

{"title":"A case report of crimean congo hemorrhagic Fever in ostriches in iran.","authors":"Ehsan Mostafavi, Sadegh Chinikar, Maryam Moradi, Neda Bayat, Mohsen Meshkat, Mohammad Khalili Fard, Seyyed Mojtaba Ghiasi","doi":"10.2174/1874357901307010081","DOIUrl":"10.2174/1874357901307010081","url":null,"abstract":"Crimean Congo hemorrhagic fever (CCHF) is a viral zoonosis, which is usually transmitted via tick bites or close contact with infected blood or tissue. This disease can cause a case fatality rate of up to 25%-30% in humans. CCHF Infection in birds is less documented. An ostrich can reproduce viruses and can also play the role of a mechanical vector, by transporting infected ticks without becoming ill. In March 2007, three butchers and one worker in an ostrich farm were infected with CCHF in central part of Iran. Considering the role ostriches play in transmitting the disease, serum samples from five ostriches of that farm were taken and sent to the laboratory for CCHF ELISA tests. The result of the IgG test was positive for one (20%) of the ostriches. At the same time, serum samples of eight sheep from the same farm were sent for IgG testing, two (25%) of which were positive. This was the first report of CCHF infection of an ostrich in Iran and tracing CCHF IgG against this ostrich and the afore-mentioned sheep may have revealed that the disease in the worker was the cause of transmission of this disease from these animals or their ticks. ","PeriodicalId":23111,"journal":{"name":"The Open Virology Journal","volume":"7 ","pages":"81-3"},"PeriodicalIF":0.0,"publicationDate":"2013-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/0b/2e/TOVJ-7-81.PMC3763622.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31717251","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

T-Cell Signaling in HIV-1 Infection. HIV-1感染中的t细胞信号传导

The Open Virology Journal Pub Date : 2013-07-26 eCollection Date: 2013-01-01 DOI: 10.2174/1874357920130621001

Wasim Abbas, Georges Herbein

引用次数: 31

Inhibition of HIV-1 Replication by Secondary Metabolites From Endophytic Fungi of Desert Plants. 荒漠植物内生真菌次生代谢物对HIV-1复制的抑制作用

The Open Virology Journal Pub Date : 2013-07-26 eCollection Date: 2013-01-01 DOI: 10.2174/1874357920130624002

Brian P Wellensiek, Rajesh Ramakrishnan, Bharat P Bashyal, Yvette Eason, A A Leslie Gunatilaka, Nafees Ahmad

{"title":"Inhibition of HIV-1 Replication by Secondary Metabolites From Endophytic Fungi of Desert Plants.","authors":"Brian P Wellensiek, Rajesh Ramakrishnan, Bharat P Bashyal, Yvette Eason, A A Leslie Gunatilaka, Nafees Ahmad","doi":"10.2174/1874357920130624002","DOIUrl":"https://doi.org/10.2174/1874357920130624002","url":null,"abstract":"Most antiretroviral drugs currently in use to treat an HIV-1 infection are chemically synthesized and lead to the development of viral resistance, as well as cause severe toxicities. However, a largely unexplored source for HIV-1 drug discovery is endophytic fungi that live in a symbiotic relationship with plants. These fungi produce biologically active secondary metabolites, which are natural products that are beneficial to the host. We prepared several hundred extracts from endophytic fungi of desert plants and evaluated the inhibitory effects on HIV-1 replication of those extracts that showed less than 30% cytotoxicity in T-lymphocytes. Those extracts that inhibited viral replication were fractionated in order to isolate the compounds responsible for activity. Multiple rounds of fractionation and antiviral evaluation lead to the identification of four compounds, which almost completely impede HIV-1 replication. These studies demonstrate that metabolites from endophytic fungi of desert plants can serve as a viable source for identifying potent inhibitors of HIV-1 replication. ","PeriodicalId":23111,"journal":{"name":"The Open Virology Journal","volume":"7 ","pages":"72-80"},"PeriodicalIF":0.0,"publicationDate":"2013-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2174/1874357920130624002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31670552","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 26

Tropism Analysis of Two Coxsackie B5 Strains Reveals Virus Growth in Human Primary Pancreatic Islets but not in Exocrine Cell Clusters In Vitro. 两株柯萨奇B5病毒株的趋向性分析显示病毒在人原代胰岛中生长，但在体外外分泌细胞簇中不生长。

The Open Virology Journal Pub Date : 2013-04-05 Print Date: 2013-01-01 DOI: 10.2174/1874357901307010049

M Hodik, A Lukinius, O Korsgren, G Frisk

{"title":"Tropism Analysis of Two Coxsackie B5 Strains Reveals Virus Growth in Human Primary Pancreatic Islets but not in Exocrine Cell Clusters In Vitro.","authors":"M Hodik, A Lukinius, O Korsgren, G Frisk","doi":"10.2174/1874357901307010049","DOIUrl":"https://doi.org/10.2174/1874357901307010049","url":null,"abstract":"Human Enteroviruses (HEVs) have been implicated in human pancreatic diseases such as pancreatitis and type 1 diabetes (T1D). Human studies are sparse or inconclusive and our aim was to investigate the tropism of two strains of Coxsackie B virus 5 (CBV-5) in vitro to primary human pancreatic cells. Virus replication was measured with TCID50 titrations of aliquots of the culture medium at different time points post inoculation. The presence of virus particles or virus proteins within the pancreatic cells was studied with immunohistochemistry (IHC) and electron microscopy (EM). None of the strains replicated in the human exocrine cell clusters, in contrast, both strains replicated in the endocrine islets of Langerhans. Virus particles were found exclusively in the endocrine cells, often in close association with insulin granules. In conclusion, CBV-5 can replicate in human endocrine cells but not in human exocrine cells, thus they might not be the cause of pancreatitis in humans. The association of virus with insulin granules might reflect the use of these as replication scaffolds.","PeriodicalId":23111,"journal":{"name":"The Open Virology Journal","volume":"7 ","pages":"49-56"},"PeriodicalIF":0.0,"publicationDate":"2013-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/8f/0c/TOVJ-7-49.PMC3657700.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31471680","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 21

Role of Filopodia in HSV-1 Entry into Zebrafish 3-O-Sulfotransferase-3-Expressing Cells. 丝状足在HSV-1进入表达3- o -硫转移酶-3的斑马鱼细胞中的作用

The Open Virology Journal Pub Date : 2013-04-05 Print Date: 2013-01-01 DOI: 10.2174/1874357901307010041

Samiksha Choudhary, Lorrie Burnham, Jeffrey M Thompson, Deepak Shukla, Vaibhav Tiwari

{"title":"Role of Filopodia in HSV-1 Entry into Zebrafish 3-O-Sulfotransferase-3-Expressing Cells.","authors":"Samiksha Choudhary, Lorrie Burnham, Jeffrey M Thompson, Deepak Shukla, Vaibhav Tiwari","doi":"10.2174/1874357901307010041","DOIUrl":"https://doi.org/10.2174/1874357901307010041","url":null,"abstract":"Background: Heparan sulfate proteoglycans (HSPGs) modified by zebrafish (ZF) encoded glucosaminyl 3-O sulfotransferase-3 (3-OST-3) generate a receptor for herpes simplex virus type-1 (HSV-1) entry and spread. In order to elucidate the mechanism by which HSV-1 enters into ZF-3-OST-3 cells, we investigated the mode of viral entry.Results: Under high resolution scanning electron microscopy (SEM), actin cytoskeleton changes were observed by a dramatic increase in the number of filopodia formed during early interactions of HSV-1 with the target cells. While the increase in number was common among all the infected cells, the highest numbers of filopodia was observed in cells expressing the 3-OST-3 modified form of heparan sulfate (HS) encoded either by human or ZF. The levels of viral infection and filopodia induction were reduced with the actin polymerization inhibitors, Cytochalasin-D and Lantriculin B, suggesting an important role for actin reorganization during ZF-3-OST-3 mediated HSV-1 entry. Supporting an interesting possibility of filopodia usage during HSV-1 spread, pre-treatment of cytochalasin D in ZF-3-OST-3 cells drastically reduced virus glycoprotein induced cell fusion.Conclusions: Taken together, our results provide new evidence on the involvement of filopodia during HSV-1 infection of ZF-3-OST-3 cells and confirm a role for modified heparan sulfate in cytoskeleton rearrangement during HSV-1 entry.","PeriodicalId":23111,"journal":{"name":"The Open Virology Journal","volume":"7 ","pages":"41-8"},"PeriodicalIF":0.0,"publicationDate":"2013-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/49/82/TOVJ-7-41.PMC3648776.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31425051","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 12

Hepatitis C Virus Envelope Protein E1 Binds PERK and Represses the Unfolded Protein Response. 丙型肝炎病毒包膜蛋白E1结合PERK并抑制未折叠蛋白反应。

The Open Virology Journal Pub Date : 2013-03-22 Print Date: 2013-01-01 DOI: 10.2174/1874357901307010037

Philip A Egan, Michal Sobkowiak, Shiu-Wan Chan

{"title":"Hepatitis C Virus Envelope Protein E1 Binds PERK and Represses the Unfolded Protein Response.","authors":"Philip A Egan, Michal Sobkowiak, Shiu-Wan Chan","doi":"10.2174/1874357901307010037","DOIUrl":"https://doi.org/10.2174/1874357901307010037","url":null,"abstract":"Unfolded protein response (UPR) is a cellular adaptive response which functions to reduce stress caused by misfolded proteins in the endoplasmic reticulum (ER). We and others have previously shown that infection with hepatitis C virus (HCV) or expression of the viral proteins can trigger the UPR. HCV is a single-stranded positive-sense RNA virus causing chronic diseases in humans. Its genome encodes two envelope proteins E1 and E2 that mature in the ER to form non-covalently bound native complex and disulphide-bonded aggregates. Apart from the ER targeting proteins, cytosolic forms have been documented. We have previously shown that the ER-targeting E1 and E2 are capable of eliciting the UPR whereas others have shown that the cytosolic-targeting E2 can bind to the ER stress kinase PERK to dampen the UPR. In this report, we further show that the other envelope protein E1, in its cytosolic form, can also bind PERK and dampen the UPR. Using GST-pulldown assay, we show that E1 binds to the cytoplasmic domain of PERK, suggesting interaction of E1 and PERK takes place in the cytoplasm. Using reporter gene assay and Western blotting, we show that cytosolic E1 can repress UPR-induced BiP and CHOP promoter activity and reduce UPR-induced CHOP expression level. Altogether these results suggest opposing functions of ER- and cytosolic forms of HCV envelope proteins depending on their subcellular localization.","PeriodicalId":23111,"journal":{"name":"The Open Virology Journal","volume":"7 ","pages":"37-40"},"PeriodicalIF":0.0,"publicationDate":"2013-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/c8/fc/TOVJ-7-37.PMC3648774.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31425050","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 11

An Influenza Virus M2 Protein Specific Chimeric Antigen Receptor Modulates Influenza A/WSN/33 H1N1 Infection In Vivo. 流感病毒M2蛋白特异性嵌合抗原受体在体内调节甲型流感/WSN/ 33h1n1感染

The Open Virology Journal Pub Date : 2013-01-01 Epub Date: 2013-02-25 DOI: 10.2174/1874357901307010028

Simon J Talbot, Natalie F Blair, Niolette McGill, Yvonne Ligertwood, Bernadette M Dutia, Ingo Johannessen

{"title":"An Influenza Virus M2 Protein Specific Chimeric Antigen Receptor Modulates Influenza A/WSN/33 H1N1 Infection In Vivo.","authors":"Simon J Talbot, Natalie F Blair, Niolette McGill, Yvonne Ligertwood, Bernadette M Dutia, Ingo Johannessen","doi":"10.2174/1874357901307010028","DOIUrl":"https://doi.org/10.2174/1874357901307010028","url":null,"abstract":"A potential target for the development of universal vaccine strategies against Influenza A is the M2 protein - a membrane protein with a highly conserved extracellular domain. In this study we developed engineered T-cell receptors, by fusing M2-specific antibody sequences with T-cell receptor transmembrane and signaling domains to target influenza infected cells. When expressed on T-cells, these novel T-cell receptors (chimeric antigen receptors - CARs) are able to recognize specific antigens on the surface of target cells via an MHC-independent mechanism. Using an existing monoclonal antibody (14C2) specific for the M2 ectodomain (M2e), we generated an M2-specific CAR. We tested the specificity of this M2 CAR in vitro by measuring the activation of T-cells in response to M2-specific peptides or M2-expressing cell lines. Both Jurkat T-cells and peripheral blood mononuclear cells expressing the M2-specific CAR responded to specific antigen stimulation by upregulating NFAT and producing γ-interferon. To test whether the M2-specific CAR are effective at recognizing influenza infected cells in vivo we used an established BALB/c murine infection model. At day 4 post-infection, when M2 CAR expressing splenocytes could be detected in the lung, the Influenza A/WSN/33 virus titre was around 50% of that in control mice. Although the lung virus titre later increased in the treated group, virus was cleared in both groups of mice by day 8. The results provide support for the development of M2e as a target for cell mediated immunotherapy.","PeriodicalId":23111,"journal":{"name":"The Open Virology Journal","volume":"7 ","pages":"28-36"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/c5/e5/TOVJ-7-28.PMC3594705.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31399388","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 9

The Tanapoxvirus 142R Protein is a Serine-Threonine Kinase that Phosphorylates the Tumor Suppressor p53. Tanapoxvirus 142R蛋白是一种丝氨酸-苏氨酸激酶，可磷酸化肿瘤抑制因子p53。

The Open Virology Journal Pub Date : 2013-01-01 Epub Date: 2013-01-21 DOI: 10.2174/1874357901307010001

Krystal N Seibert, Karim Essani, Bruce E Bejcek

{"title":"The Tanapoxvirus 142R Protein is a Serine-Threonine Kinase that Phosphorylates the Tumor Suppressor p53.","authors":"Krystal N Seibert, Karim Essani, Bruce E Bejcek","doi":"10.2174/1874357901307010001","DOIUrl":"https://doi.org/10.2174/1874357901307010001","url":null,"abstract":"To effectively respond to viral infections, mammals rely on the innate and adaptive immune systems. Additionally, host cellular responses, such as apoptosis also play a vital role in the host defense mechanisms. To accomplish a successful replicative strategy in vivo, animal viruses have evolved a variety of molecular mechanisms that interfere with host responses. Poxviruses in particular, represents a prime example of where animal viruses encode a wide variety of proteins necessary for replication and subversion of the host's immune and single cell responses. Several proteins that inhibit host immmunomodulatory cytokines and apoptosis of infected cells have been characterized in vaccinia virus (VV). Here, we describe the identification of a protein encoded by the tanapox virus genome (142R open reading frame) that is orthologous to the B1R protein from VV. We demonstrate that like B1R, TPV142R encodes a serine threonine kinase that can phosphorylate the tumor suppressor p53 and therefore has the potential for inhibiting apoptosis of infected cells.","PeriodicalId":23111,"journal":{"name":"The Open Virology Journal","volume":"7 ","pages":"1-4"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/af/77/TOVJ-7-1.PMC3553498.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31285719","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0