Viral Escape of Mucosal Immunity in Sexually Transmitted Diseases

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Background

Mucosae of the female and male genital tracts are the portals of entry for sexually transmitted diseases (STDs) of viral, bacterial, fungal, and parasitic origin; 2.6 million cases of STDs are reported annually. The viruses implicated in sexually transmitted infections (STIs) include HSV, HIV, viral hepatitis, EBV, CMV, molluscum contagiosum, HHV-8, and HPVs. The emerging Monkeypox Virus has been recently isolated in semen as well. This route has the most rapidly rising incidence of new infections, especially among women, who are infected at higher rates than men. Thus, induction of innate and adaptive immune responses at the major portals of entry of these pathogens is important for protection against infection. However, during their co-evolution with the host, viruses have evolved strategies to counteract the immune control, promoting their survival and/or persistence. Past and ongoing attempts to create vaccines against sexually transmitted pathogens have met with varying success.

The mucosal surfaces are particularly vulnerable to infections but display a complex spectrum of innate and adaptive mechanisms to counteract pathogens. In turn, viruses have evolved to modulate the host’s immunity, resulting in successful infection. Host factors influence whether virus exposure leads to productive infection. These may include the physical barrier of the mucosa, the number of available target cells, altered mucosal microbiota, humoral response, and immune activation by genital inflammation established by other sexually transmitted infections. Also, genital fluids contain proteins that enhance viral infection, like semen-derived enhancers of virus infectivity (SEVI) and complement. The transmission risk is associated with the specific within-host barriers, which creates a selection bias with an advantage for viruses with higher between-host transmission potential. Important cells that exert opposing selection pressures are the different dendritic cell (DC) subsets localized in the mucosal tissues. A thorough understanding of how viruses engage in crosstalk with the host at these anatomic sites is still missing. The goal of this research topic is to shed light on the critical interactions of viruses with the genital mucosal immune system allowing the virus to escape from it, and ultimately complete its life cycle.

In this Research Topic, we aim at bringing together researchers from the immunological and virological fields to build up a wide and comprehensive landscape of the various aspects of mucosal immunity and viral escape mechanisms in the context of STDs. We welcome the submission of Review, Original Research, Perspective, Clinical Trial, and Case Report covering, but not limited to, the following sub-topics:

• Background and advances in the STDs research, focusing on local and/or systemic immune responses.
• Studies providing novel knowledge on immune responses in STDs with a special emphasis on local immune responses in the genital tract.
• The role of dendritic cells in eliciting the immune response and preventing viral escape.
• The strategies for prevention and control of STDs including novel therapeutics and vaccine development.

Keywords: STDs, Mucosae, Immune response, Viral escape, Vaccine, IgA, Dendritic cells

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