lentivirus

Lentivirus (lente-, Latin for “slow”) is a genus of viruses of the Retroviridae family, characterized by a long incubation period. Lentiviruses can deliver a significant amount of viral RNA into the DNA of the host cell and have the unique ability among retroviruses of being able to infect non-dividing cells, so they are one of the most efficient methods of a gene delivery vector.

Gene Therapy Using Lentivirus to Treat Wiskott-Aldrich Syndrome Promising (Science Daily)

Two Houston researchers from Baylor College of Medicine and Texas Children’s Hospital were part of an international team that developed a new gene therapy approach to treatment of Wiskott-Aldrich Syndrome, a fatal inherited form of immunodeficiency. The new research, led by researchers at the San Raffaele Telethon Institute for Gene Therapy in Milan, Italy was published in Science Express.

Within the first few hours of an HIV-1 infection, the virus enters both Langerhans cells (purple) and CD4+ T lymphocytes (not shown) residing in the vaginal epithelium. This TEM shows a Langerhans cell (purple) exiting an isolated epithelium to disseminate the HIV-1. A long cytoplasmic extension of the Langerhans cell remains anchored between basal keratinocytes and contains a large vacuole with one HIV-1BaL virion (red) inside. Viruses taken up by Langerhans cells are usually degraded in endosomal compartments to generate antigens for presenting to T cells. However, HIV may have a mechanism to slow down its degradation in intracellular compartments of dendritic cells, allowing the virion to survive and infect other cells of the immune system.

By Florian Hladik, Polachai Sakchalathorn, and Juliana M. McElrath, University of Washington

Human Imminodeficiency Virus.

Also known as: HIV


Associated with: Acquired immunodeficiency syndrome (AIDS)

Classification: Virus

Industry of interest: Healthcare

Microbiology: HIV is a lentivirus from the retrovirus family that can lead to acquired immunodeficiency syndrome (AIDS), a condition where the infected person’s immune system declines progressively. This leaves the individual open to many life-threatening opportunistic infections.

HIV’s Cousin Is Way Older Than We Thought

Turns out that monkeys may have been battling against viruses similar to HIV for a lot longer than we used to think.

A3G is an antiviral gene found in Old World monkeys that protects against these sorts of viral infections. In response, these viruses have developed a protein called Vif that inhibits the activity of A3G.

Virologists have traced back mutations in A3G that protect against Vif inhibition to five to six million years ago, which means that HIV-like viruses have been around a lot longer in non-human primates (like four million years longer…) than previously thought.

They published their findings Thursday in PLOS Pathogens.

Keep up the fight, monkeys!

(Image of simian immunodeficiency virus from Sriram Subramaniam and Donald Bliss/PLoS Pathogens)

False-colored TEM image of HIV virus particles (yellow and purple) budding from a human T cell (blue) in culture. T cells counter HIV transmission using a surprisingly simple trick: they tie the virions to the cell membrane with an intermembrane protein, appropriately named “tetherin.” When a virion buds from the cell surface, one tetherin domain inserts into the new viral membrane, while another domain stays embedded in the cell’s plasma membrane, preventing the virus particle from diffusing away.

By Klaus Boller, Paul-Ehrlich-Institute, Germany

Genforscher weltweit verlassen sich auf deutschen Mittelstand

Ein neuer Beitrag ist auf dem MIT-Blog erschienen: http://mit-blog.de/genforscher-weltweit-verlassen-sich-auf-deutschen-mittelstand/

SIRION Biotech katapultiert sich zum internationalen Partner akademischer wie industrieller Einrichtungen mit neuesten viralen Vektoren.

Virale Vektoren sind auf dem Vormarsch: einerseits für die Erforschung der Funktion von Genen und die Austestung neuartiger Substanzen an Zellmodellen, andererseits selbst als ‚Substanzen‘ für den Einsatz in der Gentherapie und bei neuartigen Impfstoffen. Forscher und Entwickler weltweit machen sich ihre einzigartige Eigenschaft zunutze, in tierische wie menschliche Zellen eindringen zu können, um dort genetische Veränderungen hervorzurufen, entweder temporär oder auf Dauer. So werden nicht nur die Funktionen von Genen besser verstanden, auch lassen sich gezielt Modelle menschlicher Zellen herleiten, um ihre Interaktion mit neuartigen Substanzen zu ergründen (cell based assay screening). Diese technischen Möglichkeiten werden zunehmend relevant beim gewollten Verzicht auf Tierversuche.

SIRION Biotech hat sich mit der Gründung in 2007 auf die Entwicklung und Anwendung viraler Vektoren (Adenovirus (AV), Lentivirus (LV) und AAV) für die genetische Modifikation von Zellen spezialisiert, sei es für Zwecke der Discovery, des Substanzscreenings oder auch direkt der Entwicklung von Gentherapien und Impfstoffen. Japan ist wichtigster Auslandsmarkt, gefolgt von Schweiz, USA und Israel; über die Hälfte des Geschäfts findet im Ausland statt. Das jährliche Wachstum seit Gründung beläuft sich auf 70%, 18 Mitarbeiter beschäftigt das Unternehmen bereits. Labors von Tokio, San Francisco, Tel-Aviv, Singapur und Kopenhagen verlassen sich für Ihre Forschung und Entwicklung auf virale Vektoren aus Martinsried. SIRIONs neueste Entwicklung ist ein patentierter Adenovirus Serotyp (Ad19a), welcher bereits in ersten klinischen Modellen für die Impfstoffentwicklung getestet wird.

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nOVO ARTIGO EM Soropositivo.Org Há vida com HIV HIV provoca ‘suicídio em massa’ de células de defesa Maioria dos linfócitos em pessoas com o vírus HIV morre por reação inflamatória Dois novos estudos desvendam esse processo e propõem uso de anti-inflamatório para combater a AIDS DÉBORA MISMETTI EDITORA DE “CI... http://soropositivo.org/hiv-provoca-suicidio-em-massa.html

nOVO aRTIGO FOI PUBLICADO EM http://soropositivo.org/hiv-provoca-suicidio-em-massa.html

HIV provoca ‘suicídio em massa’

HIV provoca ‘suicídio em massa’ de células de defesa Maioria dos linfócitos em pessoas com o vírus HIV morre por reação inflamatória Dois novos estudos desvendam esse processo e propõem uso de anti-inflamatório para combater a AIDS DÉBORA MISMETTI EDITORA DE “CI…

[Effects of Sam68 gene silence on proliferation of acute T lymphoblastic leukemia cell line Jurkat].

[Effects of Sam68 gene silence on proliferation of acute T lymphoblastic leukemia cell line Jurkat].

Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2014 Aug;22(4):894-8

Authors: Wang CJ, Xu H, Zhang HR, Wang J, Lin YN, Pang TX, Li QH

Abstract
This study was purposed to investigate the effect of Sam68 gene silence on proliferation of human acute T lymphoblastic leukemia cell line Jurkat. The sequence of shRNA targeting the site 531-552 of Sam68 mRNA was designed and chemically synthesized, then a single-vector lentiviral, Tet-inducible shRNA-Sam68 system (pLKO-Tet-On) was constructed; next the Jurkat cells were infected with lentivirus to create stable cell clones with regulatable Sam68 gene expression. The inhibitory efficiency of Sam68 gene was assayed by Real-time PCR and Western blot; the cell activity of Jurkat cells was detected with MTT assay; the change of colony forming potential of Jurkat cells was analyzed by colony forming test; the cell cycle distribution was tested by flow cytometry. The results indicated that the expression of Sam68 in experimental cells was statistically decreased as compared with that of the control cells; the cells activity and colony forming capacity of the Jurkat cells with Sam68 gene silence were significantly inhibited; with Sam68 gene silencing, the percentage of S phase cells was significantly increased, while the percentage of G2 phase cells was significantly decreased. It is concluded that the silencing Sam68 gene using shRNA interference can effectively inhibit the proliferation of human acute T lymphoblastic leukemia cell line Jurkat.

PMID: 25130799 [PubMed - in process]



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Intrastriatal GDNF gene transfer by inducible lentivirus vectors protects dopaminergic neurons in a rat model of parkinsonism.

PubMed:


Related Articles

Intrastriatal GDNF gene transfer by inducible lentivirus vectors protects dopaminergic neurons in a rat model of parkinsonism.

Exp Neurol. 2014 Nov;261:87-96 

Authors: Chen SS, Yang C, Hao F, Li C, Lu T, Zhao LR, Duan WM

Abstract
Glial cell line-derived neurotrophic factor (GDNF) has neuroprotective effects on dopaminergic (DA) neurons both in vivo and in vitro. However, substantial evidence has shown that a long-term overexpression of GDNF gene is often associated with side effects. We previously improved tetracycline (Tet)-On lentivirus system carrying human GDNF (hGDNF) gene, and demonstrated that hGDNF gene expression was tightly regulated and functional in vitro. Here we further examined the efficiency and neuroprotection of Tet-On lentivirus-mediated hGDNF gene regulation in neural progenitor cells (NPCs) and a rat model of parkinsonism. The results showed that hGDNF gene expression was tightly regulated in transduced NPCs. Doxycycline (Dox)-induced hGDNF protected DA neurons from 6-hydroxydopamine (6-OHDA)-induced toxicity in vitro. Intrastriatal injections of Tet-On lentivirus vectors resulted in dramatically increased levels of hGDNF protein in the striatum of rats with Dox-drinking water, when compared to lentivirus-injected and saline-injected rats with normal drinking water, respectively. In addition, hGDNF protected nigral DA neurons and striatal DA fibers, and attenuated d-amphetamine-induced rotational asymmetry in the 6-OHDA lesioned rats. To the best of our knowledge, this is the first report that hGDNF gene transfer by Tet-On lentivirus vectors is tightly regulated in rat brain, and Dox-induced hGDNF is functional in neuroprotection of nigral DA neurons in a rat model of parkinsonism.

PMID: 24997241 [PubMed - indexed for MEDLINE] http://dlvr.it/7sWQPX

Effects of TNF Secreting HEK Cells on B Lymphocytes' Apoptosis in Human Chronic Lymphocytic Leukemias.

Effects of TNF Secreting HEK Cells on B Lymphocytes’ Apoptosis in Human Chronic Lymphocytic Leukemias.

Asian Pac J Cancer Prev. 2014;15(22):9885-9

Authors: Valizadeh A, Ahmadzadeh A, Teimoori A, Khodadadi A, Saki G

Abstract
BACKGROUND: Tumor necrosis factor (TNF) related apoptosis-inducing ligand (TRAIL) is an antitumor candidate in cancer therapy. This study focused on effects of TRAIL, as a proapototic ligand that causes apoptosis, in B-CELL chronic lymphocytic leukemia cells (B-CLL) .
MATERIALS AND METHODS: A population of HEK 293 cells was transducted by lentivirus that these achieved ability for producing the TRAIL protein and then HEK 293 cells transducted were placed in the vicinity of CLL cells. After 24 hours of co-culture, apoptosis of CLL cells was assessed by annexin V staining.
RESULTS: The amount of Apoptosis was examined separately in four groups: 293 HEK TRAIL (16.17±1.04%); 293 HEK GFP (2.7±0.57%); WT 293 HEK (2±2.6%); and CLL cells (0.01±0.01%). Among the groups studied, the maximum amount of apoptosis was in the group that the vector encoding TRAIL was transducted. In this group, the mean level of soluble TRAIL in the culture medium was 253pg/ml; also flow cytometry analyzes showed that proapotosis in this group was 32.8±1.6%, which was higher than the other groups.
CONCLUSIONS: In this study, we have demonstrated that TNF secreted from HEK 293 cells are effective in death of CLL cells.

PMID: 25520123 [PubMed - in process]



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