title: Inhibition of HIV-1-specific T-cells and increase of viral load during immunosuppressive treatment in an HIV-1 infected patient with Chlamydia trachomatis induced arthritis.
abstract: BACKGROUND
  Studies in HIV-1 infected long-term non-progressors could demonstrate a strong HIV-1-specific CTL response, but it is difficult to prove that this strong CTL response actually is the cause of the efficient control of HIV-1 and not the consequence of low HIV-1 replication in these patients.
  
  
  OBJECTIVE
  Studies of HIV-1-specific immunity and viral replication in patients undergoing immunosuppressive therapy provide important opportunities to understand the role of HIV-1-specific T-cells.
  
  
  RESULTS
  In this report we describe an HLA B27 positive patient with normal CD4 counts and a low viral load of 200 copies/ml without antiretroviral therapy who exhibited a very strong HIV-1-specific CTL response. He had to be treated with steroids, NSAIDS and hydroxchloroquine because of a severe inflammatory reactive arthritis triggered by an acute Chlamydia trachomatis infection. Analysis of HIV-1 specific T-cells by gamma-IFN-ELISPOT revealed a high frequency of HIV-1 gag-specific CTL both in blood and synovial fluid, whereas gag-specific CD4-cells could be detected only in the peripheral blood. Further analysis revealed that the gag-specific T-cells were predominantly targeting the HLA B27-restricted CTL epitope KRWIILGLNK (KK10). Immunosuppressive therapy by prednisone was associated with a moderate increase of HIV-1 viremia and a decrease both in the number and in the gamma-IFN production of KK10-specific CTL indicating that inhibition of CTL function contributed to the increase of viral load.
  
  
  CONCLUSIONS
  This study is suggesting that HIV-1 specific CTL play an important role in the control of HIV-1, at least in this patient. Inhibition of CTL function by immunosuppressive therapy with prednisone may enhance viral replication. In addition, we could demonstrate for the first time the migration of HIV-1 specific T-cells into the synovial fluid.
authors.affiliation: Immunodeficiency Center, Department of Medicine III, University Hospital Erlangen, Krankenhausstrasse 12, 91054 Erlangen, Germany. Thomas.Harrer@med3.imed.uni-erlangen.de
authors.forename: T
authors.initials: T
authors.lastname: Harrer
authors.forename: M
authors.initials: M
authors.lastname: Bäuerle
authors.forename: S
authors.initials: S
authors.lastname: Bergmann
authors.forename: K
authors.initials: K
authors.lastname: Eismann
authors.forename: E G
authors.initials: EG
authors.lastname: Harrer
mesh_terms: D000328:Adult; D016918:Arthritis, Reactive / Q000150:complications* / Q000188:drug therapy; D002690:Chlamydia Infections / Q000150:complications* / Q000188:drug therapy; D002692:Chlamydia trachomatis; D015658:HIV Infections / Q000150:complications* / Q000276:immunology / Q000821:virology; D015497:HIV-1 / Q000276:immunology; D006801:Humans; D007166:Immunosuppressive Agents / Q000009:adverse effects*; D008297:Male; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology*; D019562:Viral Load
chemical_list: D007166:Immunosuppressive Agents