Abstract

BackgroundHIV-infected cells in semen facilitate viral transmission. We studied the establishment of HIV reservoirs in semen and blood during PHI, along with systemic immune activation and the impact of early cART.MethodsPatients in the ANRS-147-OPTIPRIM trial received two years of early cART. Nineteen patients of the trial were analyzed, out of which 8 had acute PHI (WB ≤1 Ab). We quantified total cell-associated (ca) HIV-DNA in blood and semen and HIV-RNA in blood and semen plasma samples, collected during PHI and at 24 months of treatment.ResultsAt enrollment, HIV-RNA load was higher in blood than in semen (median 5.66 vs 4.22 log10 cp/mL, p<0.0001). Semen HIV-RNA load correlated strongly with blood HIV-RNA load (r = 0.81, p = 0.02, the CD4 cell count (r = -0.98, p<0.0001), and the CD4/CD8 ratio (r = -0.85, p<0.01) in acute infection but not in later stages of PHI. Median blood and seminal cellular HIV-DNA levels were 3.59 and 0.31 log10cp/106 cells, respectively. HIV-DNA load peaked in semen later than in blood and then correlated with blood IP10 level (r = 0.62, p = 0.04). HIV-RNA was undetectable in blood and semen after two years of effective cART. Semen HIV-DNA load declined similarly, except in one patient who had persistently high IP-10 and IL-6 levels and used recreational drugs.ConclusionsHIV reservoir cells are found in semen during PHI, with gradual compartmentalization. Its size was linked to the plasma IP-10 level. Early treatment purges both the virus and infected cells, reducing the high risk of transmission during PHI.Clinical trials registrationNCT01033760

Highlights

  • HIV reservoir cells are found in semen during primary HIV infection (PHI), with gradual compartmentalization

  • Its size was linked to the plasma IP-10 level

  • Viral reservoirs are established during primary HIV infection (PHI) [1], a transient stage associated with a high risk of viral transmission and responsible for up to 50% of all new infections in some areas [2, 3]

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Summary

Introduction

Viral reservoirs are established during primary HIV infection (PHI) [1], a transient stage associated with a high risk of viral transmission and responsible for up to 50% of all new infections in some areas [2, 3]. The risk of sexual HIV-1 transmission correlates with HIV-1 RNA load in genital secretions, which contain both free virions and infected cells [6]. Profound dysregulation of inflammatory cytokine networks in blood and semen, creating a proinflammatory environment, may facilitate HIV-1 replication and transmission [9, 10]. HIV-infected cells in semen facilitate viral transmission. We studied the establishment of HIV reservoirs in semen and blood during PHI, along with systemic immune activation and the impact of early cART

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