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Blood, 1 May 2002, Vol. 99, No. 9, pp. 3119-3128
CHEMOKINES
Increased expression of the inflammatory chemokine CXC
chemokine ligand 9/monokine induced by interferon- in lymphoid
tissues of rhesus macaques during simian immunodeficiency virus
infection and acquired immunodeficiency syndrome
Todd A. Reinhart,
Beth A. Fallert,
Melanie E. Pfeifer,
Sonali Sanghavi,
Saverio Capuano III,
Premeela Rajakumar,
Michael Murphey-Corb,
Richard Day,
Craig L. Fuller, and
Todd M Schaefer
From the Departments of Infectious Diseases and
Microbiology, Molecular Genetics and Biochemistry, and Biostatistics,
University of Pittsburgh, Pittsburgh, PA.
Chemokines are important mediators of cell trafficking during
immune inductive and effector activities, and dysregulation of their
expression might contribute to the pathogenesis of human immunodeficiency virus type 1 and the related simian immunodeficiency virus (SIV). To understand better the effects of SIV infection on
lymphoid tissues in rhesus macaques, we examined chemokine messenger
RNA (mRNA) expression patterns by using DNA filter array hybridization.
Of the 34 chemokines examined, the interferon  (IFN-)-inducible
chemokine CXC chemokine ligand 9/monokine induced by interferon-
(CXCL9/Mig) was one of the most highly up-regulated chemokines in
rhesus macaque spleen tissue early after infection with pathogenic SIV.
The relative levels of expression of CXCL9/Mig mRNA in spleen and lymph
nodes were significantly increased after infection with SIV in both
quantitative image capture and analysis and real-time reverse
transcriptase-polymerase chain reaction assays. In addition, in situ
hybridization for CXCL9/Mig mRNA revealed that the patterns of
expression were altered after SIV infection. Associated with the
increased expression of CXCL9/Mig were increased numbers of IFN-
mRNA-positive cells in tissues and reduced percentages of CXC
chemokine receptor (CXCR) 3+/CD3+ and
CXCR3+/CD8+ lymphocytes in peripheral
blood. We propose that SIV replication in vivo
initiates IFN--driven positive-feedback loops in lymphoid tissues that disrupt the trafficking of effector T lymphocytes and lead to chronic local inflammation, thereby contributing
to immunopathogenesis.
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