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Prevalence of HIV-1 Dual Infection in Long-Term Nonprogressor–Elite Controllers

Pernas, María PhD*; Casado, Concepción PhD*; Sandonis, Virginia PhD*; Arcones, Carolina BSc*; Rodríguez, Carmen PhD; Ruiz-Mateos, Ezequiel PhD; Ramírez de Arellano, Eva PhD§; Rallón, Norma PhD; Del Val, Margarita PhD§,¶; Grau, Eulalia BSc#; López-Vazquez, Mariola PhD; Leal, Manuel MD; Del Romero, Jorge MD; López Galíndez, Cecilio PhD*

JAIDS Journal of Acquired Immune Deficiency Syndromes: November 1st, 2013 - Volume 64 - Issue 3 - p 225–231
doi: 10.1097/QAI.0b013e31829bdc85
Basic and Translational Science

Introduction: Human immunodeficiency virus type 1 (HIV-1) dual infection (DI) in long-term nonprogressor–elite controller patients (LTNP-EC) has been described only in sporadic cases and then, consequences in disease progression are not clearly established. To fill-up this limited knowledge, we analyzed, for the first time, the prevalence, host genetic polymorphisms, and clinical consequences of HIV-1 DI in a group of LTNP-EC.

Methods: For DI detection, nucleotide sequences in env gene from viruses from 20 LTNP-EC were analyzed by maximum likelihood. Epidemiological and clinical parameters and host factors of patients were also studied.

Results: DI was detected in 4 (20%) of the 20 LTNP-EC, of which 3 maintained the elite controller status. CD4+ T-cell counts were not different between single and DI patients although higher CD8+ T-cell counts were observed in DI patients, and, consequently, the CD4+/CD8+ ratios were lower in LTNP-EC DI patients.

Conclusions: Prevalence of HIV-1 DIs in LTNP-EC is similar to other groups of HIV-1 patients; in addition, DI was not associated with loss of disease control in the patients. These DI LTNP-EC patients showed, in comparison with single infected patients, higher numbers of CD8+ T cells and lower CD4+/CD8+ ratios.

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*Servicio de Virología Molecular, Centro Nacional de Microbiología (CNM), Instituto de Salud Carlos III, Madrid, Spain;

Centro Sanitario Sandoval, Instituto de Investigación Sanitaria del Hospital Clínico San Carlos (IdISSC), Madrid, Spain;

Laboratory of Immunovirology, Biomedicine Institute of Seville, Clinic Unit of Infectious Diseases, Microbiology and Preventive Medicine, Virgen del Rocío University Hospital, IBiS/CSIC/SAS/University of Seville, Seville, Spain;

§Unidad de Inmunología Viral, Centro Nacional de Microbiología (CNM), Instituto de Salud Carlos III, Madrid, Spain;

Enfermedades Infecciosas, Hospital Carlos III, Comunidad Autónoma de Madrid, Madrid, Spain;

Centro de Biología Molecular Severo Ochoa, CSIC/Universidad Autónoma de Madrid, Madrid, Spain; and

#IrsiCaixa Foundation, Hospital Universitari Germans Trias i Pujol, Universitat Autònoma de Barcelona, Badalona, Spain.

Correspondence to: Dr Cecilio López-Galíndez, PhD, Servicio de Virología Molecular, Centro Nacional de Microbiología (CNM), Instituto de Salud Carlos III, Majadahonda, Madrid 28220, Spain (e-mail:

Work in Centro Nacional de Microbiología is supported by grants (SAF 2007-61036, 2010-17226, and 2010-18917) from MICINN Spain, by grants (36558/06, 36641/07, 36779/08, 360766/09) from Fundación para la investigación y prevención del SIDA en España (FIPSE), Spain, and by RETIC de Investigación en SIDA (RD06/006/0033 and RD06/006/0036). The authors M.P., C.A., and E.R.A. were supported by the RETIC de Investigación en SIDA (RD06/006/0036 and RD06/006/0033) of the Fondo de Investigaciones Sanitarias (FIS). Partially funded by the RETIC of Instituto de Salud Carlos III (RD12/0017-RIS). E.R.M. was supported by Fondo de Investigacion Sanitaria (contract P08/00172) and RETICS (RD12/0017/0029). The HIV BioBank, integrated in the Spanish AIDS Research Network, is supported by Instituto de Salud Carlos III, Spanish Health Ministry (grant no RD06/0006/0035), and Fundación para la investigación y prevención del SIDA en España (FIPSE).

The authors have no conflicts of interest to disclose.

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Received February 22, 2013

Accepted May 14, 2013

© 2013 by Lippincott Williams & Wilkins