Giuseppe Nunnari, MD; Luciano Nigro, MD; Filippo Palermo, ScD; Massimo Attanasio, PhD; Annemarie Berger, MD; Hans W. Doerr, MD; Roger J. Pomerantz, MD; Bruno Cacopardo, MD
Acknowledgments: The authors thank the patients from the University of Catania clinics. They also thank Brenda O. Gordon and Rita Victor at the Center for Human Virology and Biodefense, Thomas Jefferson University, for excellent secretarial assistance and Drs. Carlo Vancheri and Valerio Tomaselli from the Chest Disease Unit of the Department of Internal Medicine and Medical Specialties at the University of Catania for providing some of the laboratory reagents.
Grant Support: By academic funds from the Institute of Infectious Diseases, University of Catania; the Center for Human Virology and Biodefense, Thomas Jefferson University; and the Institute of Medical Virology, Johann Wolfgang Goethe University.
Potential Financial Conflicts of Interest: None disclosed.
Requests for Single Reprints: Giuseppe Nunnari, MD, Jefferson Alumni Hall, Thomas Jefferson University, 1020 Locust Street, Suite 329, Philadelphia, PA 19107; e-mail, email@example.com.
Current Author Addresses: Drs. Nunnari and Pomerantz: Jefferson Alumni Hall, Thomas Jefferson University, 1020 Locust Street, Suite 329, Philadelphia, PA 19107.
Drs. Nigro, Palermo, and Cacopardo: Unit of Infectious Diseases, University of Catania, Via Passo Gravina 185, 95125 Catania, Italy.
Drs. Berger and Doerr: Institute fur Medizinische Virologie, Paul-Ehrlich Strasse 40, 60596 Frankfurt, Germany.
Dr. Attanasio: Dipartimento dei Metodi Quantitativi per le Scienze Umane, University of Palermo, Viale delle Scienze, 90128 Palermo, Italy.
Author Contributions: Conception and design: G. Nunnari, L. Nigro, H.W. Doerr, R.J. Pomerantz, B. Cacopardo.
Analysis and interpretation of the data: G. Nunnari, L Nigro, F. Palermo, R.J. Pomerantz, B. Cacopardo.
Drafting of the article: G. Nunnari, R.J. Pomerantz, B. Cacopardo.
Critical revision of the article for important intellectual content: G. Nunnari, R.J. Pomerantz, B. Cacopardo.
Final approval of the article: G. Nunnari, R.J. Pomerantz, B. Cacopardo.
Statistical expertise: F. Palermo, M. Attanasio.
Obtaining of funding: B. Cacopardo.
Administrative, technical, or logistic support: A. Berger, H.W. Doerr.
Collection and assembly of data: G. Nunnari, L. Nigro, F. Palermo, A. Berger, H.W. Doerr, B. Cacopardo.
Progression to AIDS is slower in persons infected with both HIV-1 and GB virus C (GBV-C), also known as hepatitis G virus.
To compare clinical, virologic, and immunologic variables in HIV-1seropositive patients with and without GBV-C co-infection.
Subanalysis of a prospective cohort study.
Institute of Infectious Diseases, University of Catania, Catania, Italy.
80 asymptomatic HIV-1seropositive patients.
GBV-C RNA level; plasma HIV-1 viral load; CD4+ cell counts; and serum levels of interleukin (IL)-2, IL-4, IL-10, and IL-12.
At the start of the study, plasma GBV-C RNA was detected in 17 patients (21%). During follow-up, IL-2 and IL-12 levels decreased significantly (P = 0.005 and P = 0.01, respectively) and IL-4 and IL-10 levels increased significantly (P = 0.01 and P = 0.004, respectively) in the GBV-Cnegative group but did not change substantially in the GBV-Cpositive group. Each measured variable differed significantly between GBV-Cpositive and GBV-Cnegative groups during follow-up (P < 0.001 for IL-12, IL-4, and IL-10; P = 0.002 for IL-2).
GB virus C may immunologically interfere with progression of HIV-1 infection to AIDS by maintaining an intact T-helper 1 cytokine profile.
Nunnari G, Nigro L, Palermo F, et al. Slower Progression of HIV-1 Infection in Persons with GB Virus C Co-Infection Correlates with an Intact T-Helper 1 Cytokine Profile. Ann Intern Med. 2003;139:26–30. doi: https://doi.org/10.7326/0003-4819-139-1-200307010-00009
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Published: Ann Intern Med. 2003;139(1):26-30.
Gastroenterology/Hepatology, HIV, Infectious Disease, Viral Hepatitis.
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