Human immunodeficiency virus type I as a target for gene therapy

Gottfreðsson, Magnús

doi:10.2741/a218

Cited by 8 publications

(31 citation statements)

References 180 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This part, also known as the fusion-peptide, mediates the fusion between the viral and host membranes. The Env protein is also capable of mediating fusion between infected and non-infected cells by a process known as syncytium formation [4,7,8]. …”

Section: Introductionmentioning

confidence: 99%

“…The amino acid sequence corresponds to the so-called connection domain of RT, in particular a tryptophan-rich 19-mer sequence corresponding to residues 389–407, which efficiently inhibits viral replication [30]. Likewise, strategies based on intracellular expression of sFvs [7,18] and RNA aptamers [31-33] targeted against the RT enzyme are potent inhibitors of HIV-1 replication. The aptamers all recognize the same template-primer-binding cleft on RT.…”

Section: Introductionmentioning

confidence: 99%

“…This transfer of viral DNA is mediated by a nuclear localization signal present in the Vpr protein. Furthermore, it has been shown that Vpr is involved in arresting HIV-infected cells in the G2 phase of the cell cycle, where the virus production has been shown to reach a maximum level [4-7]. Integration of proviral DNA is mediated by the viral IN enzyme by a process that requires the host protein integrase interactor 1 (INI1 / hSNF5).…”

Section: Introductionmentioning

confidence: 99%

“…IN consists of an N-terminal zinc finger domain, a catalytic core domain, and a C-terminal domain that is important for binding HIV-1 LTR DNA [39,40]. It has two enzymatic functions; DNA cleavage and insertion of the provirus into the genome of the host [4,7]. IN recognizes short inverted repeats (att sites) at both ends of the proviral DNA and cleaves an AT overhang at the 5' end.…”

Section: Introductionmentioning

confidence: 99%

“…Transcriptional regulation of HIV-1 gene expression is controlled by co-operative and cell-specific interactions between several host cells transcription factors, including AP-1, NF-κB, NF-AT, NF-IL-6, CREB, IRF, Sp1, LEF-1/TCF-1α, Ets-1 and USF, and the viral Tat protein [5,7,43]. The Tat protein recognizes a stem-loop structure, the trans-activation responsive element region (TAR), located in the 5'-end of the primary transcript (R region).…”

Section: Introductionmentioning

confidence: 99%

See 4 more Smart Citations

Molecular strategies to inhibit HIV-1 replication

2005

View full text Add to dashboard Cite

The human immunodeficiency virus type 1 (HIV-1) is the primary cause of the acquired immunodeficiency syndrome (AIDS), which is a slow, progressive and degenerative disease of the human immune system. The pathogenesis of HIV-1 is complex and characterized by the interplay of both viral and host factors. An intense global research effort into understanding the individual steps of the viral replication cycle and the dynamics during an infection has inspired researchers in the development of a wide spectrum of antiviral strategies. Practically every stage in the viral life cycle and every viral gene product is a potential target. In addition, several strategies are targeting host proteins that play an essential role in the viral life cycle. This review summarizes the main genetic approaches taken in such antiviral strategies.

show abstract

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Molecular strategies to inhibit HIV-1 replication

2005

View full text Add to dashboard Cite

show abstract

Gene Therapy in HIV‐Infected Cells to Decrease Viral Impact by Using an Alternative Delivery Method

et al. 2010

View full text Add to dashboard Cite

The ability of dendrimer 2G-[Si{O(CH(2))(2)N(Me)(2) (+)(CH(2))(2)NMe(3) (+)(I(-))(2)}](8) (NN16) to transfect a wide range of cell types, as well as the possible biomedical application in direct or indirect inhibition of HIV replication, was investigated. Cells implicated in HIV infection such as primary peripheral blood mononuclear cells (PBMC) and immortalized suspension cells (lymphocytes), primary macrophages and dendritic cells, and immortalized adherent cells (astrocytes and trophoblasts) were analyzed. Dendrimer toxicity was evaluated by mitochondrial activity, cell membrane rupture, release of lactate dehydrogenase, erythrocyte hemolysis, and the effect on global gene expression profiles using whole-genome human microarrays. Cellular uptake of genetic material was determined using flow cytometry and confocal microscopy. Transfection efficiency and gene knockdown was investigated using dendrimer-delivered antisense oligonucleotides and small interfering RNA (siRNA). Very little cytotoxicity was detected in a variety of cells relevant to HIV infection and erythrocytes after NN16 dendrimer treatment. Imaging of cellular uptake showed high transfection efficiency of genetic material in all cells tested. Interestingly, NN16 further enhanced the reduction of HIV protein 24 antigen release by antisense oligonucleotides due to improved transfection efficiency. Finally, the dendrimer complexed with siRNA exhibited therapeutic potential by specifically inhibiting cyclooxygenase-2 gene expression in HIV-infected nervous system cells. NN16 dendrimers demonstrated the ability to transfect genetic material into a vast array of cells relevant to HIV pathology, combining high efficacy with low toxicity. These results suggest that NN16 dendrimers have the potential to be used as a versatile non-viral vector for gene therapy against HIV infection.

show abstract

Animal Models in Virology

Bryant

2008

Sourcebook of Models for Biomedical Research

View full text Add to dashboard Cite

The knowledge we have gained from the study of many diseases that affect humans comes from the study of disease processes in different animal species, and this has enhanced our understanding of the pathogenesis of the disease in humans. The American Medical Association says almost every advance in medical science in the twentieth century, from antibiotics and vaccines to antidepressant drugs and organ transplants, has been achieved either directly or indirectly through the use of animals as models of disease. In this chapter a brief overview of the uses of animal models for research on human viral diseases is presented.

show abstract

Human immunodeficiency virus type I as a target for gene therapy

Cited by 8 publications

References 180 publications

Molecular strategies to inhibit HIV-1 replication

Molecular strategies to inhibit HIV-1 replication

Gene Therapy in HIV‐Infected Cells to Decrease Viral Impact by Using an Alternative Delivery Method

Animal Models in Virology

Contact Info

Product

Resources

About