The 15th International Symposium on Human Chlamydial Infections (ISHCI) was convened at the Menger hotel in San Antonio, Texas, June 19–24, 2022. This was the first in-person international meeting on Chlamydia since the start of the COVID pandemic and Julius Schachter's passing. Despite these tragedies we regained our strength and gathered in the Alamo city for commemorating Dr Schachter's many contributions to the Chlamydia field. The meeting has been renamed “The Julius Schachter-International Symposium on Human Chlamydial Infections (JS-ISHCI).
Julius Schachter was among the first to recognize Chlamydia trachomatis as a common infectious agent that causes sexually transmitted disease. He also reported the first case of chlamydia-induced pneumonia in infants, which triggered screening and intervention programs to prevent pulmonary infection of newborns. By 1981, he and his team members, including Jeanne Moncada, isolated C. trachomatis from nasopharyngeal and rectal swabs from children in a trachoma-endemic area, which led to the proposal of a multicenter trial using oral azithromycin to eliminate blinding trachoma. Julius also significantly improved the laboratory diagnosis of human chlamydial infections by using less invasive urine and vaginal swab sampling, making patient self-collection possible for the diagnosis and treatment of asymptomatic infections. Besides his own research on C. trachomatis human infections, Julius was deeply involved in the organization and production of every ISHCI. Since the first meeting in 1962 at Lake Placid, the ISHCI has remained a highly respected quadrennial symposium for all chlamydial researchers to exchange scientific findings and ideas and explore collaboration opportunities.
The meeting began by commemorating the members of the Chlamydia family who recently passed away, including Joseph Igietseme (USA), Byron Batteiger (USA), Pekka Saikku and Maija Leinonen (Finland). Two living legends were recognized: Dr. Sheila West (USA) for her contributions to trachoma research and Dr. Robert C. Brunham (Canada) for his contributions to both clinical and basic research of sexually transmitted chlamydial infections.
As revealed in the Supplemental Material (https://links.lww.com/OLQ/A888), a very robust scientific program was developed for the symposium, which started with the clinical challenges caused by chlamydial infections in both human genital and ocular tissues. Most of the week was used to reveal new findings on diagnostics and the mechanisms of chlamydial biology and its interactions with host cells, as well as host responses. Finally, the program ended with presentations on how to use what we have learnt about Chlamydia and model systems, particularly animal models, to promote the development of vaccines for protecting humans from chlamydial infections and diseases. The program was organized into 7 research tracks with a keynote lecture for introducing each track.
The success of the 15th JS-ISHCI was because of the collective efforts by everyone in the chlamydia community. The International Scientific Committee together with other scientists formed a review board, which carefully reviewed the abstracts and made constructive suggestions, ensuring the high scientific quality of the symposium. The local organizing committee members effectively worked together with others in the community to ensure that every step was executed according to the plan. The steering committee provided strong logistical guidance and ensured financial support. Important contributions to the success of the symposium came from the ~100 attendees.
As revealed in the presentations and during the discussions at the 15th JS-ISHCI, the Chlamydia field has made significant progresses in both research and clinical applications since last meeting in the Netherlands in 2018. We have learned more about Chlamydia genetics, making the manipulation of the chlamydial genome more efficient for supporting subsequent functional studies. The combination of Chlamydia mutants with in vitro and in vivo research models has allowed us to gain new insights into the intricate molecular networks between Chlamydia and its host at the molecular, cellular and tissue levels. Both new chlamydial mechanisms and host response patterns unique to chlamydial infections have been identified. The exciting findings may motivate more biologists to take advantage of the unique chlamydial evolutionary niches to uncover host mechanisms that are otherwise difficult to discover. More importantly, the basic research achievements will help address the clinical challenges of human chlamydial infections. One of the clinical challenges is to understand why some C. trachomatis–infected women can spontaneously clear infection within 2 weeks1 and remain resistant to subsequent infections2 while others allow persistent C. trachomatis infection. Although clinical studies have identified some correlates,3,4 the mechanisms remain largely unknown. At the conference, a mouse model-based study reported a cGAS-STING signaling-dependent mechanism for inhibiting C. trachomatis infection in the lower genial tract,5 which has not only validated previous in vitro observations on chlamydial activation of the cGAS-STING pathway6,7 but also provided the urgently needed mechanistic information for designing new clinical studies. This and other exciting findings have been published in the symposium proceedings.8 Many attendees have realized that a fundamental understanding of Chlamydia and its interactions with its natural hosts in the context of mucosal microbiome may hold the key for designing an effective and safe Chlamydia vaccine. The intimate format of the meeting successfully served as a platform for attendees to exchange ideas, establish collaborations, develop out of the box thinking and strategize synergistic research plans, all of which will enable the field as a whole to make new discoveries in chlamydial research in the coming 4 years. Hopefully, when we meet again at the 16th, we may be closer to an effective vaccine for protecting humans from chlamydial infections and diseases.
REFERENCES
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2. Geisler WM, Lensing SY, Press CG, et al. Spontaneous resolution of genital
Chlamydia trachomatis infection in women and protection from reinfection. J Infect Dis 2013; 207:1850–1856.
3. Bakshi RK, Gupta K, Jordan SJ, et al. An adaptive
Chlamydia trachomatis-specific IFN-γ-producing CD4
+ T cell response is associated with protection against chlamydia reinfection in women. Front Immunol 2018; 9:1981.
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Chlamydia trachomatis infection compared to women who do not clear; A pilot study. Front Cell Infect Microbiol 2021; 11:615770.
5. Su X, Xu H, French M, et al. Evidence for cGAS-STING signaling in the female genital tract resistance to
Chlamydia trachomatis infection. Infect Immun 2022; 90:e0067021.
6. Zhang Y, Yeruva L, Marinov A, et al. The DNA sensor, cyclic GMP-AMP synthase, is essential for induction of IFN-β during
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7. Barker JR, Koestler BJ, Carpenter VK, et al. STING-dependent recognition of cyclic di-AMP mediates type I interferon responses during
Chlamydia trachomatis infection. MBio 2013; 4:e00018–e00013.
8. Zhong G, Brunham R, Chernesky M, Clarke I, Darville T, JC de Vires H, Gaydos C, Greub G, W. Hook E III, Mabey D, Moncada J, Morre S, Paavonen J, Stary A, Valdivia R, Van Der Pol B, West S. 2022. Proceedings of the Julius Schachter Fifteenth International Symposium on Human Chlamydial Infections UT Print, University of Texas Health Science Center at San Antonio; June 19–24, 2022.
