Abstract
The G2-S16 polyanionic carbosilane dendrimer is a promising microbicide that inhibits HSV-2 infection in vitro and in vivo in mice models. This G2-S16 dendrimer inhibits HSV-2 infection even in the presence of semen. Murine models, such as BALB/c female mice, are generally used to characterize host-pathogen interactions within the vaginal tract. However, the composition of endogenous vaginal flora remains largely undefined with modern microbiome analyses. It is important to note that the G2-S16 dendrimer does not change healthy mouse vaginal microbiome where Pseudomonas (10.2–79.1%) and Janthinobacterium (0.7–13%) are the more abundant genera. The HSV-2 vaginally infected female mice showed a significant microbiome alteration because an increase of Staphylococcus (up to 98.8%) and Escherichia (30.76%) levels were observed becoming these bacteria the predominant genera. BALB/c female mice vaginally-treated with the G2-S16 dendrimer and infected with the HSV-2 maintained a healthy vaginal microbiome similar to uninfected female mice. Summarizing, the G2-S16 polyanionic carbosilane dendrimer inhibits the HSV-2 infection in the presence of semen and prevents the alteration of mice female vaginal microbiome.
Highlights
A safe and effective microbicide to prevent sexual transmission infections (STIs) such as HSV-2 is still needed
It is important to note that microbicides that have been proven to inhibit STIs had failed in different clinical trials [1,2], most probably because these microbicides failed to prevent semen-exposed infection [3] as well as they interfere with the microbiota of healthy individuals, increasing the HSV-2 infection or generating bacterial vaginosis (BV)
When HSV-2 was incubated with SP and treated with G2-S16 dendrimer, this dendrimer inhibited increased infection with the same behavior, which in the absence of semen, inhibited >99% of HSV-2 infection (Figure 2)
Summary
A safe and effective microbicide to prevent sexual transmission infections (STIs) such as HSV-2 is still needed. It is important to note that microbicides that have been proven to inhibit STIs had failed in different clinical trials [1,2], most probably because these microbicides failed to prevent semen-exposed infection [3] as well as they interfere with the microbiota of healthy individuals, increasing the HSV-2 infection or generating bacterial vaginosis (BV). TFV and many other microbicide candidates failed due to the microbiome impairment that may lead to the BV and subsequent increasing the risk of STIs. it is urgently needed to research the relationship between leading microbicides and changes in vaginal microbiome structure and diversity
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