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Publication Date



UM campus only

Degree Type


Degree Name

Master of Science (MS)


Microbiology and Immunology (Medicine)

Date of Defense


First Committee Member

Savita Pahwa

Second Committee Member

Lisa R. W. Plano

Third Committee Member

Kenneth A. Fields


The bacterium Chlamydia trachomatis as well as the Human Immunodeficiency virus-1 (HIV-1) are sexually transmitted pathogens; both can infect monocytes/ macrophages and have an obligate intracellular replication cycle. It has been hypothesized that sexually transmitted infections (STIs), including genital Chlamydia, enhance HIV-1 transmission; yet, the underlying biological mechanisms remain unclear. The pathogen¡¯s common biology makes it possible that C. trachomatis and HIV mutually affect each other¡¯s replication cycle during monocyte/macrophage co-infection. To test this hypothesis we used two different bacteria strains in an in vitro HIV co-infection model: Latently virus-infected U1 promonocytes were either inoculated with C. trachomatis serovar D or serovar L2. It was found that serovar D, but not the LGV serovar L2, quickly and significantly reactivates integrated HIV-1 provirus. This reactivation depends on viable bacteria but seemingly neither on a microbial pathogen-associated molecular pattern (PAMP) nor on de novo gene expression by C. trachomatis. Hence, it could be triggered by a preformed protein that the bacterium translocates into the human cell. Because virus production occurs in Chlamydia-infected as well as Chlamydia-free cells and cannot be induced by conditioned culture medium, we propose a cell contact-dependent signal to U1 bystander cells. The HIV reactivation mechanism involves NF-kappaB activation but is independent of eukaryotic de novo protein translation. In summary, the findings might describe a novel Chlamydia-mediated HIV-1 reactivation mechanism from latently infected cells.


Diseases; Microorganism