Abstract
HIV-1 is present in anatomical compartments and bodily fluids. Most transmissions occur through sexual acts, making virus in semen the proximal source in male donors. We find three distinct relationships in comparing viral RNA populations between blood and semen in men with chronic HIV-1 infection, and we propose that the viral populations in semen arise by multiple mechanisms including: direct import of virus, oligoclonal amplification within the seminal tract, or compartmentalization. In addition, we find significant enrichment of six out of nineteen cytokines and chemokines in semen of both HIV-infected and uninfected men, and another seven further enriched in infected individuals. The enrichment of cytokines involved in innate immunity in the seminal tract, complemented with chemokines in infected men, creates an environment conducive to T cell activation and viral replication. These studies define different relationships between virus in blood and semen that can significantly alter the composition of the viral population at the source that is most proximal to the transmitted virus.
Highlights
Sexual transmission of the human immunodeficiency virus type 1 (HIV-1) is the most common mode of transmission worldwide
Blood and semen samples were obtained from twelve HIV-1-negative men without sexually transmitted infections (STI) from North Carolina and from 6 men from Malawi to serve as a control for the cytokine and chemokines analyses
We used viral RNA extracted from blood plasma and seminal plasma to generate cDNAs to use as a template in the single genome amplification (SGA) protocol of the viral env gene [34,35,36]
Summary
Sexual transmission of the human immunodeficiency virus type 1 (HIV-1) is the most common mode of transmission worldwide. Genital secretions are the most proximal source of the transmitted virus. An understanding of the virus at these sites is central to understanding the transmission event and the nature of the transmitted virus. Virus enters the male genital tract during primary infection [1,2,3,4,5]. During primary infection the viral RNA load is elevated in both the blood and the semen [1,3]. Factors that induce inflammation in the seminal tract, such as sexually transmitted infections (STI), can raise the level of virus in semen [13], and this may contribute to the transmission of HIV-1 by the sexual route [14]. The endogenous semen-derived enhancer of virus infection (SEVI), a fragment of prostatic acid phosphatase, has been shown to increase infectious viral titers in vitro by several orders of magnitude [15]
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