Degeneration of oxidative muscle fibers in HTLV-1 tax transgenic mice

• Published in: The American journal of pathology Vol. 135; no. 6; pp. 1025 - 1033
• Main Authors: Nerenberg, MI, Wiley, CA
• Format: Journal Article
• Language: English
• Published: Bethesda, MD ASIP 01-12-1989; American Society for Investigative Pathology
• Subjects: AIDS/HIV; Animals; Biological and medical sciences; Blotting, Northern; Blotting, Western; Fundamental and applied biological sciences. Psychology; Gene Expression Regulation; Histocytochemistry; Human T-lymphotropic virus 1; Immunochemistry; Immunologic Techniques; Mice; Mice, Transgenic - genetics; Microbiology; Microscopy, Electron; Muscles - metabolism; Muscles - pathology; Muscles - ultrastructure; Oxidation-Reduction; Replicative cycle, interference, host-virus relations, pathogenicity, miscellaneous strains; Trans-Activators - metabolism; Trans-Activators - physiology; Virology; Immunohistochemistry; Rodentia; Retroviridae; Transgenic animal; Virus; Pathogenicity; Vertebrata; Striated muscle disease; Mammalia; Gene; Mouse; Atrophia; Immunoblotting assay; Trans acting regulatory factor; HTLV-I virus
• ISSN: 0002-9440; 1525-2191

The HTLV-1 tax gene under control of the HTLV-1 long terminal repeat (LTR) was introduced into transgenic mice. Previously tax protein expression in the muscle and peripheral nerves of three independent mouse lines was reported. Here the localization of this transgenic protein at a cellular and subcellular level is described. Tax protein was expressed in oxidative muscle fibers that developed severe progressive atrophy. It localized to the cytoplasma where it was associated with structures resembling degenerating Z bands. This pattern of muscle fiber involvement is similar to that observed in human retroviral associated myopathy. This transgenic mouse model suggests that preferential expression of the HTLV-1 viral promoter in oxidative muscle fibers may explain the productive infection of these fibers in HTLV-1 myopathy.