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International Immunology Advance Access originally published online on December 13, 2005
International Immunology 2006 18(1):125-137; doi:10.1093/intimm/dxh355
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© The Japanese Society for Immunology. 2005. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

HIV-1 burden influences host response to co-infection with Neisseria gonorrhoeae in vitro

Monty Montano1,2, Matthew Rarick1, Paola Sebastiani3, Patrick Brinkmann1,2, Jerry Skefos1 and Russell Ericksen1

1 Department of Medicine, Section of Infectious Diseases, Center for HIV-1/AIDS Care and Research, Boston University School of Medicine, 2 Department of Immunology and Infectious Diseases, Harvard School of Public Health, 3 Department of Biostatistics, Boston University School of Public Health

Correspondence to: M. Montano; E-mail: mmontano{at}bu.edu

There is considerable evidence that co-infection with the sexually transmitted pathogen Neisseria gonorrhoeae (Gc) can increase the likelihood of both transmitting and acquiring HIV-1 worldwide. However, less information is available on how host immune response to co-infection differs with immune response to HIV-1 infection alone. To evaluate HIV-1 burden effects on host response to co-infection with Gc, we performed gene-expression profiling of human PBMCs infected over a broad range of viral titers (HIV-1 series) and upon exposure to a single infectious dose of Gc (HIV-1/Gc series). The transcriptional profiles differed substantially between each series (P < 0.0001). Major shifts in the transcriptional landscape were identified in contour plots based on fold stimulation and hierarchical clustering. Prominent regions of transcriptional activity were evaluated for statistical enrichment to identify up-regulated pathways associated with immune response, infection and T-cell stimulation. Notably, gene enrichment was dependent on HIV-1 burden and shifted during co-infection to reveal a disproportionate effect on lymphocyte signaling, apoptosis and proteasome activity. Further evaluation of these findings may help to better understand the role of viral burden in defining cellular contribution to host immune response upon co-infection with secondary sexually transmitted pathogens.

Keywords: bacteria, gene regulation, HIV-1, microarray

Transmitting editor: D. Tarlinton


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