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.
*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: firstname.lastname@example.org).
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.
Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal's Web site (www.jaids.com).
Received February 22, 2013
Accepted May 14, 2013