Virus Adaptation and Treatment最新文献_第4页

The management of Herpes Simplex virus infections in HIV infected patients: Current issues and the role of cidofovir HIV感染患者单纯疱疹病毒感染的管理:当前问题和西多福韦的作用

Virus Adaptation and Treatment Pub Date : 2011-06-14 DOI: 10.2147/VAAT.S12984

Ethel Nakakawa, S. Reynolds

引用次数: 2

Clinical utility and long-term use of atazanavir in the treatment of HIV-1 infection 阿扎那韦治疗HIV-1感染的临床应用和长期使用

Virus Adaptation and Treatment Pub Date : 2011-03-25 DOI: 10.2147/VAAT.S15680

T. Rampling, M. Nelson

{"title":"Clinical utility and long-term use of atazanavir in the treatment of HIV-1 infection","authors":"T. Rampling, M. Nelson","doi":"10.2147/VAAT.S15680","DOIUrl":"https://doi.org/10.2147/VAAT.S15680","url":null,"abstract":"Correspondence: Thomas Rampling Chelsea and westminster Hospital NHS Foundation Trust, 369 Fulham Road, London Sw10 9NH, UK email tommy rampling@hotmail.com Abstract: The protease inhibitor atazanavir (ATV) now forms an integral component of many combination antiretroviral regimens. It has been shown to have a favorable side effect profile, and it does not negatively affect plasma lipids as some other protease inhibitors can. ATV also has a long half-life, which allows for a once-daily dosing schedule. Coadministration of ATV with low-dose ritonavir (RTV) potentiates the effect of ATV (“RTV boosting”), allowing for lower doses of ATV than those prescribed without RTV. ATV boosted with RTV (ATV/r) has shown noninferiority to RTV-boosted lopinavir (LPV/r), and it has been shown to be effective as a simplification strategy in switch studies. ATV/r-based regimens have also shown promise as a rescue strategy for patients failing other regimens. Several important adverse events and drug interactions have been identified, and care must be taken when administering ATV with other medications. The most commonly reported adverse effect is unconjugated hyperbilirubinemia, which occurs as a result of the metabolic pathway by which it is excreted. Resistance to ATV has been described in both treatment-experienced and treatment-naïve patients.","PeriodicalId":337688,"journal":{"name":"Virus Adaptation and Treatment","volume":"33 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2011-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"128125322","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: 2

Boceprevir in the treatment of chronic hepatitis C virus infection 博昔普韦治疗慢性丙型肝炎病毒感染

Virus Adaptation and Treatment Pub Date : 2011-02-22 DOI: 10.2147/VAAT.S9677

M. Berenguer, F. López-Labrador

引用次数: 4

A paradigm linking herpesvirus immediate-early gene expression apoptosis and myalgic encephalomyelitis chronic fatigue syndrome 疱疹病毒即时-早期基因表达凋亡与肌痛性脑脊髓炎慢性疲劳综合征的关系

Virus Adaptation and Treatment Pub Date : 2011-02-21 DOI: 10.2147/VAAT.S15105

A. Lerner, S. Beqaj

{"title":"A paradigm linking herpesvirus immediate-early gene expression apoptosis and myalgic encephalomyelitis chronic fatigue syndrome","authors":"A. Lerner, S. Beqaj","doi":"10.2147/VAAT.S15105","DOIUrl":"https://doi.org/10.2147/VAAT.S15105","url":null,"abstract":"correspondence: A Martin Lerner 32804 Pierce rd, Beverly hills, Mi 48025, UsA Tel +1 248 540 9866 Fax +1 248 540 0139 email amartinlerner@yahoo.com Abstract: There is no accepted science to relate herpesviruses (Epstein–Barr virus [EBV], human cytomegalovirus [HCMV], and human herpesvirus 6 [HHV6]) as causes of myalgic encephalomyelitis (ME)/chronic fatigue syndrome (CFS). ME/CFS patients have elevated serum immunoglobulin (Ig)G serum antibody titers to EBV, HCMV, and HHV6, but there is no herpesvirus DNA-emia, herpesvirus antigenemia, or uniformly elevated IgM serum antibody titers to the complete virions. We propose that herpesvirus EBV, HCMV, and HHV6 immediate-early gene expression in ME/CFS patients leads to host cell dysregulation and host cell apoptosis without lytic herpesvirus replication. Specific antiviral nucleosides, which alleviate ME/CFS, namely valacyclovir for EBV ME/CFS and valganciclovir for HCMV/ HHV6 ME/CFS, inhibit herpesvirus DNA polymerases and/or thymidine kinase functions, thus inhibiting lytic virus replication. New host cell recruitment thus ceases. In the absence of new herpesvirus, nonpermissive herpesvirus replication stops, and ME/CFS recovery ensues.","PeriodicalId":337688,"journal":{"name":"Virus Adaptation and Treatment","volume":"33 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2011-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"120856007","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: 9

Acyclovir and hydrocortisone cream for the early treatment of recurrent cold sores 阿昔洛韦氢化可的松乳膏用于复发性唇疱疹的早期治疗

Virus Adaptation and Treatment Pub Date : 2011-01-11 DOI: 10.2147/VAAT.S7748

Carrie A Sailer, S. Spruance, C. Hull

引用次数: 5

Viral vectors for cystic fibrosis gene therapy: What does the future hold? 囊性纤维化基因治疗的病毒载体:前景如何?

Virus Adaptation and Treatment Pub Date : 2010-12-13 DOI: 10.2147/VAAT.S8887

U. Griesenbach, M. Inoue, M. Hasegawa, E. Alton

{"title":"Viral vectors for cystic fibrosis gene therapy: What does the future hold?","authors":"U. Griesenbach, M. Inoue, M. Hasegawa, E. Alton","doi":"10.2147/VAAT.S8887","DOIUrl":"https://doi.org/10.2147/VAAT.S8887","url":null,"abstract":"Correspondence: Uta Griesenbach Department of Gene Therapy, Faculty of Medicine at the National Heart and Lung institute, imperial College London, Manresa Road, London Sw3 6LR, UK Tel +44 207 351 8339 Fax +44 207 351 8340 email u.griesenbach@imperial.ac.uk Abstract: Gene transfer to the airway epithelium has been more difficult than originally anticipated, largely because of significant extraand intracellular barriers in the lung. In general, viral vectors are more adapted to overcoming these barriers than nonviral gene transfer agents and are, therefore, more efficient in transferring genes into recipient cells. Viral vectors derived from adenovirus, adeno-associated virus, and Sendai virus, which all have a natural tropism for the airway epithelium, have been evaluated for cystic fibrosis (CF) gene therapy. Although these vectors transduce airway epithelial cells efficiently, gene expression is transient and repeated administration is inefficient. They are, therefore, unlikely to be suitable for CF gene therapy. More recently, lentiviruses (LV) have been assessed for lung gene transfer. In contrast to retroviruses, they transduce nondividing cells and randomly integrate into the genome. However, LVs do not have a natural tropism for the lung, and a significant amount of effort has been put into pseudotyping these vectors with proteins suitable for airway gene transfer. Several studies have shown that LV-mediated transduction leads to persistent gene expression (for the lifetime of the animal) in the airways and, importantly, repeated administration is feasible. Thus, appropriately pseudotyped LV vectors are promising candidates for CF gene therapy. Here, we will review preclinical and clinical research related to viral CF gene therapy.","PeriodicalId":337688,"journal":{"name":"Virus Adaptation and Treatment","volume":"101 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2010-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"124785993","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: 12

Antibody targeting of TSG101 on influenza-infected cells 针对流感感染细胞的TSG101抗体

Virus Adaptation and Treatment Pub Date : 2010-11-09 DOI: 10.2147/VAAT.S13506

A. Bonavia, Leyla S. Diaz, D. Santos, Josephine Cassella, Zena Fesseha, Douty Bamba, B. Sui, Wu-Bo Li, Roxanne D. Duan, Li-mei Chen, R. Donis, Michael Goldblatt, M. Kinch

{"title":"Antibody targeting of TSG101 on influenza-infected cells","authors":"A. Bonavia, Leyla S. Diaz, D. Santos, Josephine Cassella, Zena Fesseha, Douty Bamba, B. Sui, Wu-Bo Li, Roxanne D. Duan, Li-mei Chen, R. Donis, Michael Goldblatt, M. Kinch","doi":"10.2147/VAAT.S13506","DOIUrl":"https://doi.org/10.2147/VAAT.S13506","url":null,"abstract":"Influenza remains a significant cause of morbidity and mortality worldwide. Although vaccination programs and conventional antiviral therapies can reduce disease burden, increasing resistance to conventional therapies renders much of the population susceptible to infection. The present study focuses on an important host protein target, tumor susceptibility gene 101 (TSG101), which is functionally exploited (hijacked) by certain enveloped viruses to facilitate viral budding and release. We find that influenza viruses depend on TSG101 for progeny virion morphogenesis in infected host cells. Antibody-binding studies revealed that TSG101 is exposed at the surface of influenza-infected cells but remains intracellular in uninfected cells. Using recombinant TSG101 and influenza M1 protein, we demonstrated a direct interaction between these proteins involving the ubiquitin E2 variant domain of TSG101. These findings identify an interaction between TSG101 and M1 protein in infected cells. Furthermore, a monoclonal antibody directed against TSG101 reduced virus yields in cell-based assessment of influenza virus infection, underscoring the potential of the TSG101-M1 interaction as a possible antivi- ral therapeutic target. The display of TSG101 at the surface of infected cells, combined with evidence that TSG101 antibodies reduce virus yields, suggest that TSG101 plays an essential role in the budding process of influenza virus. Our findings may also suggest potential oppor- tunities for influenza treatment and prevention by using monoclonal antibody therapeutics to interfere with virus replication.","PeriodicalId":337688,"journal":{"name":"Virus Adaptation and Treatment","volume":"212 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2010-11-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"129231579","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: 3

An update on the management of glandular fever (infectious mononucleosis) and its sequelae caused by Epstein–Barr virus (HHV-4): new and emerging treatment strategies Epstein-Barr病毒(HHV-4)引起的腺热(传染性单核细胞增多症)及其后遗症的最新管理:新的和正在出现的治疗策略

Virus Adaptation and Treatment Pub Date : 2010-09-23 DOI: 10.2147/VAAT.S6749

A. Lerner, S. Beqaj, K. Gill, J. Edington, J. Fitzgerald, R. Deeter

{"title":"An update on the management of glandular fever (infectious mononucleosis) and its sequelae caused by Epstein–Barr virus (HHV-4): new and emerging treatment strategies","authors":"A. Lerner, S. Beqaj, K. Gill, J. Edington, J. Fitzgerald, R. Deeter","doi":"10.2147/VAAT.S6749","DOIUrl":"https://doi.org/10.2147/VAAT.S6749","url":null,"abstract":"Correspondence: A Martin Lerner 32804 Pierce Rd, Beverly Hills, MI 48025, USA Tel +1 248 540 9866 Fax +1 248 540 0139 Email amartinlerner@yahoo.com Purpose: Beginning in 1993 at a single chronic fatigue syndrome (CFS) treatment center, we began studies that demonstrate Epstein–Barr virus (EBV) nonpermissive replication. In the most recent study performed, EBV nonpermissive replication is the cause of 28.3% of 106 consecutive CFS cases, and is etiologic with human cytomegalovirus (HCMV) and/or human herpes virus 6 (HHV-6) as a coinfection in an additional 52.8% of CFS cases. Therefore, EBV is causally involved in 81% of cases of CFS. Further, EBV CFS is effectively treated with long-term valacyclovir. Coinfection HCMV and HHV-6 CFS requires valganciclovir with valacyclovir. Patients and results: The validated Energy Index Point Score (EIPS) monitors severity of CFS illness and its recovery. A specific CFS diagnostic panel identifies EBV CFS subsets. Four separate EBV CFS therapeutic studies of several hundred CFS patients describe valacyclovir administration and long-term patient recovery. With valacyclovir, serum EBV titers (EBV, early antigen (diffuse); EBV, viral capsid antigen, immunoglobulin M); 24-hour electrocardiography Holter monitors; and cardiac dynamic studies improve. Conclusion: Nonpermissive EBV infection is causal in a significant proportion of CFS cases. EBV CFS is safely and effectively treated with long-term valacyclovir.","PeriodicalId":337688,"journal":{"name":"Virus Adaptation and Treatment","volume":"352 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2010-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"123406845","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: 10

p38 and STAT3 activation by vGPCR in KSHV-infected cells 用vGPCR激活kshv感染细胞的p38和STAT3

Virus Adaptation and Treatment Pub Date : 2010-09-06 DOI: 10.2147/VAAT.S13434

Mingli Liu, Shanchun Guo

{"title":"p38 and STAT3 activation by vGPCR in KSHV-infected cells","authors":"Mingli Liu, Shanchun Guo","doi":"10.2147/VAAT.S13434","DOIUrl":"https://doi.org/10.2147/VAAT.S13434","url":null,"abstract":"Correspondence: Mingli Liu Department of Microbiology, Immunology and Biochemistry, Morehouse School of Medicine, 720 Westview Drive SW, Atlanta, GA 30310, USA Tel +1 404 752 1850 Fax +1 404 752 1179 Email mliu@msm.edu Abstract: The molecular mechanism whereby viral G protein-coupled receptor (vGPCR) signaling regulates vascular endothelial growth factor (VEGF) expression in Kaposi sarcoma (KS) formation remains incompletely defined. mECK36 cells, generated by transfection of mouse bone marrow endothelial cells with Kaposi’s sarcoma-associated herpesviruses (KSHV) bacterial artificial chromosome (KSHVBac36), have been reported to be angiogenic, tumorigenic, and suitable for demonstrating a nonredundant role for vGPCR in KSHV-mediated tumorigenesis. In this report we used mECK36 and the cells composed of wild-type KSHVBac36 or the cells without vGPCR, namely vGPCR-null KSHVBac36 mutant, to dissect the molecular mechanisms of VEGF secretion induced by vGPCR in the context of KSHV infection. We found that vGPCR activates VEGF transcription via p38 MAPK and STAT3 in mECK36 and mECK36-derived cell models. We also found that in cells containing KSHV genome, STAT3 is tyrosine-phosphorylated and translocated into the nucleus, transactivating the target VEGF gene by binding to the specific DNA element TT (N 4–5 ) AA in a strictly vGPCR-dependent manner. Moreover, treatment of mECK36-derived cells with AG490 or a dominant negative STAT3 DNA vector showed strong inhibitory effects on vGPCR-induced VEGF promoter activity. In addition, vGPCR can upregulate STAT3 mRNA levels. Taken together, our findings show that vGPCR plays a nonredundant role in STAT3 activation in KSHV infected cells and that this activation plays an important role in the connection of the viral oncogene vGPCR and VEGF upregulation. Our results indicate the broad signaling activating capacity of vGPCR in the context of KSHV infection and suggest that the STAT3 pathway could be targeted for preventing KSHV-mediated angiogenesis in KS.","PeriodicalId":337688,"journal":{"name":"Virus Adaptation and Treatment","volume":"23 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2010-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"116930396","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: 3

Small molecule inhibitors of the SARS-CoV Nsp15 endoribonuclease SARS-CoV Nsp15核糖核酸内切酶的小分子抑制剂

Virus Adaptation and Treatment Pub Date : 2010-09-06 DOI: 10.2147/VAAT.S12733

J. Ortíz-Alcántara, K. Bhardwaj, S. Palaninathan, M. Frieman, R. Baric, C. Kao

{"title":"Small molecule inhibitors of the SARS-CoV Nsp15 endoribonuclease","authors":"J. Ortíz-Alcántara, K. Bhardwaj, S. Palaninathan, M. Frieman, R. Baric, C. Kao","doi":"10.2147/VAAT.S12733","DOIUrl":"https://doi.org/10.2147/VAAT.S12733","url":null,"abstract":": The severe acute respiratory syndrome (SARS) virus encodes several unusual RNA processing enzymes, including Nsp15, an endoribonuclease that preferentially cleaves 3’ of uridylates through a ribonuclease A (RNase A)-like mechanism. Crystal structures of Nsp15 confirmed that the Nsp15 active site is structurally similar to that of RNase A. These similarities and our molecular docking analysis lead us to hypothesize that previously characterized RNase A inhibitors will also inhibit the SARS-CoV Nsp15. Benzopurpurin B, C-467929, C-473872, N-306711, N-65828, N-103019 and congo red were tested for effects on Nsp15 endoribonuclease activity. A fluorescence assay revealed that the IC 50 values for inhibiting endoribonuclease activity were between 0.2 µ M and 40 µ M. These compounds were demonstrated to bind SARS-CoV Nsp15 by a differential scanning fluorimetry assay. Benzopurpurin B also inhibited the endoribonuclease activities of the Nsp15 orthologs from two other coronaviruses: mouse hepatitis virus (MHV) and infectious bronchitis virus (IBV). Benzopurpurin B, C-473872, and congo red reduced infectivity of MHV in L2 cells by 8- to 26- fold. The more effective drugs caused a decrease in MHV RNA accumulation. All three compounds reduced the infectivity of the SARS-CoV in Vero cells.","PeriodicalId":337688,"journal":{"name":"Virus Adaptation and Treatment","volume":"245 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2010-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"122699395","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: 29