Transcriptional Regulation of Latent Feline Immunodeficiency Virus in Peripheral CD4+ T-lymphocytes 英文参考文献.docVIP

Viruses 2012, 4, 878-888; doi:10.3390/v4050878 OPEN ACCESS viruses ISSN 1999-4915 /journal/viruses Brief Report Transcriptional Regulation of Latent Feline Immunodeficiency Virus in Peripheral CD4+ T-lymphocytes Samantha J. McDonnel 1,*, Ellen E. Sparger 2, Paul A. Luciw 3 and Brian G. Murphy 1 1 Department of Pathology, Microbiology Immunology, School of Veterinary Medicine, University of California, Davis, 4206 Vet Med 3A, Davis, CA 95616, USA; E-Mail: bmurphy@ 2 Department of Medicine and Epidemiology, School of Veterinary Medicine, University of California, 3115 Tupper Hall, Davis, CA 95616, USA; E-Mail: eesparger@ 3 Department of Pathology and Laboratory Medicine, Center for Comparative Medicine, University of California, Davis, County Road 98 and Hutchison Drive, Davis, CA 95616, USA; E-Mail: paluciw@ * Author to whom correspondence should be addressed; E-Mail: sjmcdonnel@; Tel.: +1-530-752-9011; Fax: +1-530-752-3349. Received: 23 April 2012; in revised form: 12 May 2012 / Accepted: 15 May 2012 / Published: 23 May 2012 Abstract: Feline immunodeficiency virus (FIV), the lentivirus of domestic cats responsible for feline AIDS, establishes a latent infection in peripheral blood CD4+ T-cells approximately eight months after experimental inoculation. In this study, cats experimentally infected with the FIV-C strain in the asymptomatic phase demonstrated an estimated viral load of 1 infected cell per approximately 103 CD4+ T-cells, with about 1 copy of viral DNA per cell. Approximately 1 in 10 proviral copies was capable of transcription in the asymptomatic phase. The latent FIV proviral promoter was associated with deacetylated, methylated histones, which is consistent with a condensed chromatin structure. In contrast, the transcriptionally active FIV promoter was associated with histone acetylation and demethylation. In addition, RNA polymerase II