IMR Press / FBL / Volume 13 / Issue 8 / DOI: 10.2741/2886

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

HIV-1 transgenic expression in mice induces selective atrophy of fast-glycolytic skeletal muscle fibers
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1 Program on Differentiation and Cancer, Centre for Genomic Regulation (CRG), UPF/PRBB, Centro de Investigacion Biomedica en Red sobre Enfermedades Neurodegenerativas, 08003 Barcelona, Spain
2 Mount Sinai School of Medicine, New York, New York 10029, USA

*Author to whom correspondence should be addressed.

Academic Editor: Vicente Andres

Front. Biosci. (Landmark Ed) 2008, 13(8), 2797–2805;
Published: 1 January 2008

Human immunodeficiency virus (HIV)-induced wasting syndrome, characterized by weakness and severe loss of muscle mass, is a common condition of patients with advanced acquired immunodeficiency syndrome (AIDS). The homozygous HIV-1 transgenic mouse line Tg26 reproduces the wasting syndrome of AIDS patients, thus constituting a valid animal model to characterize the muscle phenotype induced by HIV infection. In this study, we identified a selective atrophy of fast-glycolytic myofibers in skeletal muscles of homozygous HIV-1 transgenic mice, whereas the more oxidative fiber types are spared. In agreement with this, muscles enriched in fast-glycolytic myofibers such as the extensor digitorum longus and gastrocnemius, but not those rich in oxidative fibers such as the soleus, exhibited a reduced muscle size in homozygous HIV-1 transgenic mice compared to their littermate control counterparts. Additionally, muscles of heterozygous HIV-1 transgenic mice displayed increased inflammation and blunted myofiber growth in an injury-induced muscle regeneration process. Since no myogenic intrinsic defect was observed in satellite cells from the transgenic mice, these results support the notion of an inflammation-mediated, fiber-type-specific inhibition of muscle growth in the presence of the HIV-1 transgene.

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