Gene therapy can also be used to treat life-threatening infections where no other treatment is available. In this case, genetic information is specifically introduced into infected cells with a view to prevent the effective replication of the target pathogen. In this section we describe some of the approaches that have been adopted in the treatment of the most prevalent infectious diseases.
Human immunodeficiency virus (HIV) is the causative agent of acquired immunodeficiency syndrome (AIDS) [1]. According to the report from World Health Organization (WHO), in 2009, there were 33.3 million people living with HIV/AIDS, with 2.6 million new infections and 1.8 million deaths due to AIDS (http://www.who.int/hiv/data/2009_global_summary.png). HIV infection affects a large area and spreads actively ever since it was identified, with a significant number of AIDS deaths occurring in Sub-Saharan Africa [Greener R (2002) AIDS and macroeconomic impact. In S, Forsyth (ed) State of the Art: AIDS and Economics IAEN: pp. 49-55].
A number of different enzymes and molecules are involved in the maintenance of reduction-oxidation reaction (redox) balance in tissues. The three mammalian dismutases, cytosolic CuZnSOD (SOD1), mitochondrial MnSOD (SOD2), and extracellular superoxide dismutase (SOD3) are among the most important redox enzymes. They differ by the cellular localization and therefore have slightly different regulation of expression and therapeutic effects in tissue damage recovery suggesting distinct targets for gene therapy. In the current review I focus on the regulation of SOD3 gene expression in tissues and on the effect of SOD3 transgene on signal transduction.
Prolonged ischemic insult can cause irreversible tissue injuries. Despite advances in medical and surgical therapies, myocardial infarction and stroke, both consequences of ischemic insults, remain to be the top two causes of morbidity and mortality in the Western world, with survivals usually carrying permanent disabilities. Treatments that help restoring blood flow to ischemic area remain to be one of the most important therapeutic goals. Enhancing the innate angiogenesis by exogenous delivery of angiogenic factors lessens the ischemic injury. However, uncontrolled angiogenic gene expression can cause some unwanted side effects. In this mini-review, we describe two systems that can be used to mediate hypoxia-inducible and tissue-specific gene expression.
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