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Reuters Health Information (2006-08-11): HIV impairs CD8 T cell responsiveness to other pathogens


HIV impairs CD8 T cell responsiveness to other pathogens

Last Updated: 2006-08-11 10:08:40 -0400 (Reuters Health)

NEW YORK (Reuters Health) - Patients co-infected with hepatitis C virus (HCV) and HIV show a reduced responsiveness of CD8 T cells to stimulation by CD28 cells compared with patients infected with HCV alone.

"HIV infection appears to have a global effect on the activation or differentiation state of CD8 T cells response to other pathogens, reflected here by reduced responsiveness to CD28 stimulation," lead author Dr. Donald D. Anthony of Case Western Reserve University in Cleveland, Ohio, said in correspondence with Reuters Health.

Dr. Anthony and colleagues measured CD4- and CD8-specific interferon-gamma responses to HCV peptide pools in the presence and absence of CD28 costimulation in three groups: 14 patients with HCV infection, 15 patients chronically infected with HCV and HIV, and 10 healthy subjects.

Dr. Anthony reports in the June 1st issue of The Journal of Infectious Diseases that anti-CD28 agonist "increased the breadth and cumulative frequency of HCV-specific CD8 responses only in patients with HCV mono-infection." In addition, only those with HCV/HIV co-infection had lower proportions of CD8 cells that expressed CD28.

This reduced responsiveness by CD8 cells to CD28 stimulation is similar to that seen in patients with HIV mono-infection.

"Current work is aimed at clarifying the mechanism of reduced responsiveness to CD28 co-stimulation" in patients with HIV infection that accompanies HCV infection, Dr. Anthony said.

"These results may provide one mechanism by which HIV impairs the host ability to optimally respond to non-HIV pathogens, including HCV," eventually leading to a possible therapeutic strategy, he commented.

Co-investigator on the study, Dr. Benigno Rodriguez, also at Case Western Reserve University, told Reuters Heath that "current studies by our group and others are looking at immune-based therapies that may inhibit some of the mechanisms through which HIV suppresses normal immune responses, such as generalized immune activation."

J Infect Dis 2006;194:391-400.

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