Key T-Cell Subset Loses Efficacy During Structured Treatment Interruptions

Researchers in Italy have reported that antiviral activity from a key T-cell subset is impaired during structured treatment interruptions (STIs) in HIV treatment.

According to Federico Martini and colleagues at Rome's Lazzaro Spallanzani National Institute of Infectious Diseases, "T cells expressing Vgamma9/Vdelta 2 display lytic and proliferative responses against human immunodeficiency virus (HIV) infected cells and release antiviral soluble factors." The researchers found that while antiretroviral therapy restores Vgamma9/Vdelta 2 T-cell function lost during infection, STIs negate this benefit. The researchers assessed gammadelta T-cell activity in HIV patients during STIs of highly active antiretroviral therapy. During the resulting rise in plasma viremia, the number of circulating gammadelta T cells dropped significantly.

Hardest hit during STIs were effector gammadelta T cells, resulting in T cell anergy, manifesting as a sharp reduction in gamma interferon production in response to viral antigens. Following reinitiation of HAART, gammadelta T-cell counts and antiviral activity rose to normal levels. "These observations indicate that Vgamma9/Vdelta2 T cells are activated early after active HIV replication but are rapidly lost when viremia is not controlled," the researchers concluded.

The full report, "Acute Human Immunodeficiency Virus Replication Causes a Rapid and Persistent Impairment of Vgamma9Vdelta2 T Cells in Chronically Infected Patients Undergoing Structured Treatment Interruption," was published in the September 15 issue of the Journal of Infectious Diseases (2002;186(6):847-850).

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