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Chalmet et?al. recently reported that 11% of 63 transmission clusters identified in 539 recently diagnosed patients resulted from CXCR4 transmission, and concluded that CCR5 or CXCR4 infections resulted from a stochastic process [8]. We previously reported the frequency of X4-strains in patients included in the French ANRS PRIMO cohort at the time of primary HIV-1 infection (PHI) [2, 3]. We further described that 12.7% of the patients of our cohort were involved in clustered transmission chains and further contributed to the diffusion of the viral epidemic throughout the whole French territory [9]. Here our aim was to compare the frequency of X4 viruses in sexually HIV-infected patients included in the PRIMO cohort and involved or not in clustered transmissions. The study population comprised 555 sexually-infected Transducin patients enrolled in the PRIMO cohort between 2003 and 2010 at the time of PHI. PHI was defined by a western blot profile compatible with ongoing seroconversion (incomplete western blot with absence of antibodies to pol proteins) in most patients (94%), detectable plasma HIV RNA with a negative or weakly reactive ELISA (2%), or an interval of Staurosporine viruses, co-receptor usage was determined using a recombinant virus phenotypic entry assay [3, 11]. Finally, a population-based phylogenetic GSK126 approach based on viral RT sequences was used to identify clustered transmission events [9]. Phylogenetic interrelationships among viral sequences were estimated using neighbour-joining trees [12] and maximum likelihood methods with BioEdit and MEGA4 integrated molecular evolutionary genetic analysis software [13, 14]. The existence of clusters was ascertained using the statistical robustness of the maximum likelihood topologies assessed by high bootstrap values (>98%) with 1000 re-samplings and short branch lengths (genetic distances