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. Author manuscript; available in PMC: 2014 Feb 5.
Published in final edited form as: Curr HIV Res. 2012 Apr;10(3):195–201. doi: 10.2174/157016212800618174

Figure 2. Mechanisms by which co-infections increase HIV-1 transmission and/or pathogenesis at mucosal immune sites.

Figure 2

Periodontal pathogens, including P. gingivalis, can infect tissues of the gingival and tonsils. These pathogens have been shown to exert direct effects on the mucosal epithelial cell and indirect effects on the local mucosal immune environment that can aid in HIV-1 transmission and spread after oral-genital exposures. The sexually transmitted infections, C. trachomatis, N. gonorrhea and HSV can also infect oropharyngeal tissues but investigations on their effects on HIV-1 transmission at these sites has not been well-described. Sexually transmitted co-infections with N. gonorrhea, C. trachomatis, T. vaginalis and HSV-2 and the presence of bacterial vaginosis are associated with increased transmission of HIV-1 across the female genital tract and/or increased HIV-1 viremia. The mechanisms causing these increases are variable and pathogen specific, although common mechanisms include epithelial disruption and local recruitment of target immune cells to the subepithelial tissues.