The virus that causes AIDS may undergo changes in the genital tract rendering HIV-1 in semen different than HIV-1 in the blood, according to researchers from the University of North Carolina at Chapel Hill, the Edward Jenner Institute for Vaccine Research (United Kingdom), and the Baylor Pediatric Center of Excellence (Malawi). The research, published August 19 in the open-access journal PLoS Pathogens, advances our understanding of HIV-1 replication in the male genital tract.
Worldwide, much of the transmission of HIV-1 is through sexual contact, men being the transmitting partner in a majority of cases. The nature of the virus in the male genital tract is of central importance to understanding the transmission process and the selective pressures that may impact the transmitted virus. Ultimately, a vaccine or microbicide must block the transmitted virus.
The researchers examined the gene encoding the major surface protein of HIV-1 (the Env protein) in the viral populations in paired blood plasma and semen samples to determine any differences in the virus at the site of transmission, i.e., semen.
"In some men, the virus population in semen was similar to that in the blood, suggesting that virus was being imported from the blood into the genital tract and not being generated locally in the genital tract," said author Ronald Swanstrom, PhD. "However, we found two mechanisms that significantly altered the virus population in the semen, showing that virus can grow in the seminal tract in two different ways."
In one way, one or more viruses grow rapidly in the seminal tract over a short period such that the viral population in semen is relatively homogeneous (compared to the complex population in the blood). In the other way, the virus replicates in T cells in the seminal tract over a long period, creating a separate population of virus in semen that is both complex and distinct from the virus in the blood.
"While it remains unknown how these differences change the biology of the virus or if these changes are important for the transmission process, it is clear that the virus in the blood does not always represent the virus at the site of transmission," said author Dr. Jeffrey Anderson.
"Making molecular clones of these compartmentalized viral env genes is an important next step that will allow us to study these differences," said author Dr. Li-Hua Ping.
Volunteers participating in this study were attending the Kamuzu Central Hospital and the UNC Project in Lilongwe, Malawi.
FINANCIAL DISCLOSURE: This work was supported by the Center for HIV/AIDS Vaccine Immunology (NIH award U01 AI067854) and by an NIH award to MSC (R37 DK049381). We also acknowledge the efforts of the UNC CFAR Virology Core (NIH award P30 AI50410). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
COMPETING INTERESTS: The authors have declared that no competing interests exist.
PLEASE ADD THIS LINK TO THE PUBLISHED ARTICLE IN ONLINE VERSIONS OF YOUR REPORT: http://dx.plos.org/10.1371/journal.ppat.1001053 (link will go live upon embargo lift)
CITATION: Anderson JA, Ping L-H, Dibben O, Jabara CB, Arney L, et al. (2010) HIV-1 Populations in Semen Arise through Multiple Mechanisms. PLoS Pathog 6(8): e1001053. doi:10.1371/journal.ppat.1001053
PRESS-ONLY PDF: http://www.plos.org/press/plpa-06-08-19-swanstrom.pdf
CONTACT:
Dr. Ronald Swanstrom
University of North Carolina at Chapel Hill
risunc@med.unc.edu
Journal
PLoS Pathogens