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Reconstitution of EBV Latent but Not Lytic Antigen-Specific CD4⁺ and CD8⁺ T Cells after HIV Treatment with Highly Active Antiretroviral Therapy ¹

Erwan Piriou^*, Christine A. Jansen^*, Karel van Dort^*, Iris De Cuyper^*, Nening M. Nanlohy^2,*, Joep M. A. Lange^,, Marinus H. J. van Oers, Frank Miedema^2,*, and Debbie van Baarle^3,*,

^* Department of Clinical Viro-Immunology, Sanquin Research at CLB and Landsteiner Laboratory, Academic Medical Center, University of Amsterdam, Department of Internal Medicine, Division of Infectious Diseases, Tropical Medicine and AIDS, Academic Medical Center, University of Amsterdam, Department of Human Retrovirology, Academic Medical Center, University of Amsterdam, and Department of Hematology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands

The incidence of (EBV-related) malignancies in HIV-infected subjects has declined since the introduction of highly active antiretroviral therapy (HAART). To investigate the effect of HAART on EBV infection, we performed a longitudinal analysis of the T cell response to both a latent and a lytic Ag and EBV viral load in 10 subjects from early in HIV infection up to 5 years after HAART. All individuals responded to HAART by a decline in HIV viral load, a restoration of total CD4⁺ T cell numbers, and a decline in T cell immune activation. Despite this, EBV load remained unaltered, even after 5 years of therapy, although a decline in both CD4⁺ and CD8⁺ T cells specific for the lytic EBV protein BZLF1 suggested a decreased EBV reactivation rate. In contrast, latent EBV Ag EBNA1-specific CD4⁺ and CD8⁺ T cell responses were restored after 5 years of treatment to levels comparable to healthy individuals. In two individuals who were treated by HAART late during HIV progression, a lymphoma developed shortly after initiation of HAART, despite restoration of EBV-specific CD4⁺ and CD8⁺ T cells. In conclusion, long-term HAART does not alter the EBV DNA load, but does lead to a restoration of EBNA1-specific T cell responses, which might allow better control of EBV-infected cells when applied early enough during HIV infection.