Samir K. Gupta, Joseph A. Eustace, Jonathan A. Winston, Ivy I. Boydstun, Tejinder S. Ahuja, Rudolph A. Rodriguez, Karen T. Tashima, Michelle Roland, Nora Franceschini, Frank J. Palella, Jeffrey L. Lennox, Paul E. Klotman, Sharon A. Nachman, Stephen D. Hall, and Lynda A. Szczech Divisions of Infectious Diseases and Clinical Pharmacology, Department of Medicine, Indiana University School of Medicine, Indianapolis; Division of Nephrology, Johns Hopkins University, School of Medicine and Department of Epidemiology, Bloomberg School of Public Health, Baltimore, Maryland; Division of Nephrology, Department of Medicine, Mount Sinai School of Medicine, New York, and Division of Nephrology and Hypertension and Division of Infectious Diseases, Department of Pediatrics, State University of New York, Stony Brook; Division of Nephrology, Department of Medicine, University of Texas Medical Branch, Galveston; Division of Nephrology, Department of Medicine, San Francisco General Hospital and Positive Health Program at San Francisco General Hospital and the UCSF AIDS Research Institute, Department of Medicine, University of California at San Francisco; Division of Infectious Diseases, Department of Medicine, The Miriam Hospital, Brown Medical School, Providence, Rhode Island; Division of Nephrology and Hypertension, Department of Medicine, University of North Carolina at Chapel Hill, and Duke Clinical Research Institute and the Division of Nephrology, Department of Medicine, Duke University Medical Center, Durham, North Carolina; Division of Infectious Diseases, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois; and Grady Infectious Disease Program, Division of Infectious Diseases, Department of Medicine, Emory University, Atlanta, Georgia

/pdf/guidelines-for-the-management-of-chronic-kidney-disease-in-a6jmdl9h71.pdf

Guidelines for the Management of Chronic Kidney Disease in HIV-Infected Patients: Recommendations of the HIV Medicine Association of the Infectious Diseases Society of America

Primary HIV-1 infection causes extensive immune activation, during which CD4+ T cell activation supports massive HIV-1 production. We tested the safety and the immune-modulating effects of combining cyclosporin A (CsA) treatment with highly active antiretroviral therapy (HAART) during primary HIV-1 infection. Nine adults with primary HIV-1 infection were treated with CsA along with HAART. At week 8, all patients discontinued CsA but maintained HAART. Viral replication was suppressed to a comparable extent in the CsA + HAART cohort and in 29 control patients whose primary infection was treated with HAART alone. CsA restored normal CD4+ T cell levels, both in terms of percentage and absolute numbers. The increase in CD4+ T cells was apparent within a week and persisted throughout the study period. CsA was not detrimental to virus-specific CD8+ or CD4+ T cell responses. At week 48, the proportion of IFN-γ–secreting CD4+ and CD4+CCR7– T cells was significantly higher in the CsA + HAART cohort than in the HAART-alone cohort. In conclusion, rapid shutdown of T cell activation in the early phases of primary HIV-1 infection can have long-term beneficial effects and establish a more favorable immunologic set-point. Appropriate, immune-based therapeutic interventions may represent a valuable complement to HAART for treating HIV infection.

/pdf/treatment-of-primary-hiv-1-infection-with-cyclosporin-a-3qfcqc034z.pdf

Treatment of primary HIV-1 infection with cyclosporin A coupled with highly active antiretroviral therapy

Regulation of human immunodeficiency virus type 1 and cytokine gene expression in myeloid cells by NF-kappa B/Rel transcription factors.

Publisher Summary The powerful immunosuppressive activity of ciclosporin (CS), which is apparently restricted at the cellular level of certain T lymphocytes, is recognized as a breakthrough in immunopharmacology. CS is a potent inhibitor of chronic or immune-mediated inflammatory reactions, but has no effect in models of acute inflammation. Its importance for exploring the pathogenesis and treatment of some acute and chronic inflammatory diseases, generally grouped as suspected autoimmune.diseases, is clearly emerging in the clinic. The use of CS in the treatment of several such diseases has revealed its potential to counteract the imbalance of the immune system by improving the condition of both experimental animals and patients. After a difficult learning process in which the efficacy and the side effects of the drug were explored, CS has proved to be of permanent clinical value and has, in consequence, revitalized the field of organ transplantation. In contrast to classical immunosuppressants, CS exerts a specific action on lymphocytes but is not detrimental to the functions of phagocytes or hemopoietic stem cells. Besides being an immunosuppressive drug, CS is also widely used as an experimental probe in basic research. While evidence for this concept is compelling, various phenomena in vivo are not readily explained by this model. This review shows that in vitro several pathways can be used to induce gene transcription in lymphocytes. Whether the alternative pathways, that is, those bypassing the T-cell receptor, are also relevant in vivo remains another question. However, only the pathways involving mobilization of intracellular calcium are CS-sensitive.

In Vivo Pharmacological Effects of Ciclosporin and Some Analogues

The effects of the immunosuppressive drugs cyclosporin A and FK 506 were studied on cells chronically infected with human immunodeficiency virus type 1 (HIV-1) as well as on uninfected and newly infected cells When cells chronically infected with HIV-1 or with HIV-2 were cocultivated with uninfected cells in the presence of cyclosporin A or FK 506 there was a delay in the formation of syncytia and of cytopathic effects This inhibitory effect was not due to decreased membrane expression of CD4 In addition, there was an approximately 100-fold reduction in the yield of infectious HIV-1 when the infected cells were grown in the presence of these drugs, a finding consistent with other evidence of decreased HIV expression Both drugs were found to inhibit the growth of chronically infected cells at concentrations that did not inhibit the growth of the uninfected cells These results, demonstrating that cyclosporin A and FK 506 interfere with HIV production and selectively inhibit the growth of infected cells, suggest that they may be useful in the treatment of this infection and indicate further cellular targets for antiviral agents

Inhibition of human immunodeficiency virus and growth of infected T cells by the immunosuppressive drugs cyclosporin A and FK 506

Effects of cyclosporin on T-cell subsets in human immunodeficiency virus disease

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Effects of cyclosporin on T-cell subsets in human immunodeficiency virus disease