The concept of targeting several proteins, at different stages of the chlamydial developmental cycle, is being explored. The recent ability to genetically manipulate Chlamydia may allow deletion or inactivation of key genes to understand their role in pathology [13]. For example, plasmid-free vaccine strains have shown protection against ocular infection in non-human primates,

without immunopathology [14]. Research must be translated to humans, and immunologic and host factors associated with transmission and acquisition should be explored using clearly defined clinical Idelalisib in vivo cohorts. The ultimate profile of a chlamydia vaccine remains to be determined. For example, a chlamydia vaccine that induces more rapid clearance of infection could have a notable impact on transmission, even if complete immunity against infection may be difficult to achieve [15]. A vaccine with limited protection against infection could also still

protect against upper genital tract disease. Of note, upper genital tract infections and disease are currently difficult to diagnose. Efforts to develop better diagnostic tests, including potential immunological biomarkers or radiological imaging strategies, http://www.selleckchem.com/products/Neratinib(HKI-272).html are essential not only for vaccine trials but also for elucidating chlamydial natural history and clinical care. Meeting participants recognized the increasing urgency of developing a vaccine against gonorrhea, because of rising gonococcal antimicrobial resistance globally [16]. The epidemiology of gonorrhea is fairly well understood in high-income countries, where gonorrhea infection is mostly limited to higher-risk core groups; out however, better epidemiologic data are needed in lower-income countries. More precise data on gonorrhea strains, contributions to complications such as PID and infertility, antimicrobial resistance, and co-infections will allow modeling to understand the global health and economic impact of gonorrhea, and how antimicrobial resistance will affect its spread. As reviewed by Jerse et al. in this issue, basic

and translational research has shown that N. gonorrhoeae has adapted to evade the host immune response through antigenic variation and immunosuppression, e.g., the induction of regulatory T-cells [17]. The high genetic variation of N. gonorrhoeae frustrated early vaccine efforts. Two vaccine approaches, killed whole cells and purified pilin, were tested in clinical trials over 30 years ago and were unsuccessful. Interest in gonorrhea vaccines has been limited ever since, despite major new technological advances such as use of proteomics and genome mining, which enabled development of vaccines against group B Neisseria meningitidis [18]. These technologies have uncovered several conserved peptides that may be potential antigens for vaccine development, including AniA, TbpAB, MtrE, and a peptide mimic of the 2C7 oligosaccharide epitope [17] and [19].