Trichomonas vaginalis adhesion protein 65 (TvAP65) modulates parasite pathogenicity by interacting with host cell proteins

Zhang, Zhenchao; Song, Xiaoxiao; Deng, Yangyang; Li, Yuhua; Li, Fakun; Sheng, Wanxin; Tian, Xiaowei; Yang, Zhenke; Mei, Xuefang; Wang, Shuai

doi:10.1016/j.actatropica.2023.106996

Cited by 4 publications

(4 citation statements)

References 57 publications

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“…Adhesion of T. vaginalis to vaginal epithelial cells (VECs) is complex. Surface proteins (AP65, AP51, AP33, and AP23) appear to interact with host cells through ligand–receptor type interactions [ 9 ]. The AP65 protein was identified as part of researchers’ efforts to determine which factors play a key role in adhesion.…”

Section: Discussionmentioning

confidence: 99%

“…The AP65 protein was identified as part of researchers’ efforts to determine which factors play a key role in adhesion. Moreover, AP65/BNIP3 interaction causes T. vaginalis to adhere to host cells and become pathogenic, and this protein is introduced as a basis for preventing and treating trichomoniasis [ 9 ]. The α-actinin protein is used to diagnose trichomoniasis and is an abundant immunogen in the serum of patients with this infection.…”

Section: Discussionmentioning

confidence: 99%

“…In researchers’ efforts to determine what factors play a key role in adhesion, the AP65 protein was identified. In addition, the AP65/BNIP3 interaction causes T. vaginalis to adhere to host cells and become pathogenic, and this protein is being introduced as a basis for the prevention and treatment of trichomoniasis [ 9 ]. The amoeba-like morphology induced by α-actinin is essential for pathogenicity and phagocytosis [ 2 ].…”

Section: Introductionmentioning

confidence: 99%

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Introduction of protein vaccine candidate based on AP65, AP33, and α-actinin proteins against Trichomonas vaginalis parasite: an immunoinformatics design

Ghasemi Nezhad,

Karmostaji,

Sarkoohi

et al. 2024

Parasites Vectors

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Background Trichomonas vaginalis is the most common nonviral sexually transmitted disease (STI) worldwide. Vaccination is generally considered to be one of the most effective methods of preventing infectious diseases. Using AP65, AP33 and α-actinin proteins, this research aims to develop a protein vaccine against Trichomonas vaginalis. Methods Based on the B-cell and T-cell epitope prediction servers, the most antigenic epitopes were selected, and with the necessary evaluations, epitope-rich domains of three proteins, AP65, AP33, and α-actinin, were selected and linked. Subsequently, the ability of the vaccine to interact with toll-like receptors 2 and 4 (TLR2 and TLR4) was assessed. The stability of the interactions was also studied by molecular dynamics for a duration of 100 nanoseconds. Results The designed protein consists of 780 amino acids with a molecular weight of 85247.31 daltons. The results of the interaction of the vaccine candidate with TLR2 and TLR4 of the immune system also showed that there are strong interactions between the vaccine candidate protein with TLR2 (-890.7 kcal mol-1) and TLR4 (-967.3 kcal mol-1). All parameters studied to evaluate the stability of the protein structure and the protein-TLR2 and protein-TLR4 complexes showed that the structure of the vaccine candidate protein is stable alone and in complex with the immune system receptors. Investigation of the ability of the designed protein to induce an immune response using the C-ImmSim web server also showed that the designed protein is capable of stimulating B- and T-cell lymphocytes to produce the necessary cytokines and antibodies against Trichomonas vaginalis. Conclusions Overall, our vaccine may have potential protection against Trichomonas vaginalis. However, for experimental in vivo and in vitro studies, it may be a good vaccine candidate. Graphical Abstract

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Introduction of protein vaccine candidate based on AP65, AP33, and α-actinin proteins against Trichomonas vaginalis parasite: an immunoinformatics design

Ghasemi Nezhad,

Karmostaji,

Sarkoohi

et al. 2024

Parasites Vectors

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“…Thus, adhesion proteins play a pivotal role in the interaction with host cells, exemplified by TvAP65 and TvAP33, which inhibit host cell proliferation and can induce apoptosis. Blocking this protein has been shown to reduce its pathogenicity [8][9][10]. There is an association between cluster formation in strains with higher adhesive capacity; however, the mechanisms behind this phenomenon are relatively understudied [11].…”

Section: Introductionmentioning

confidence: 99%

Trichomonas vaginalis: Monolayer and Cluster Formation—Ultrastructural Aspects Using High-Resolution Scanning Electron Microscopy

Ortiz,

Verdan,

Fortes

et al. 2023

Pathogens

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Trichomonas vaginalis is an extracellular protozoan parasite that causes human trichomoniasis, a sexually transmitted infection (STI) that affects approximately 270 million people worldwide. The phenomenon of T. vaginalis adhesion to inert substrates has been described in several reports. Still, very few studies on cluster formation have been conducted, and more detailed analyses of the contact regions between the parasites’ membranes in these aggregate formations have not been carried out. The present study aims to show that T. vaginalis forms a tight monolayer, similar to an epithelium, with parasites firmly adhered to the culture flask bottom by interdigitations and in the absence of host cells. In addition, we analyzed and compared the formation of the clusters, focusing on parasite aggregates that float in the culture flasks. We employed various imaging techniques, including high-resolution scanning electron microscopy, transmission electron microscopy, cytochemistry, TEM tomography, and dye injection. We analyzed whether the monolayer behaves as an epithelium, analyzing cell junctions, cell communication, and ultrastructural aspects, and concluded that monolayer formation differs from cluster formation in many aspects. The monolayers form strong adhesion, whereas the clusters have fragile attachments. We did not find fusion or the passage of molecules between neighbor-attached cells; there is no need for different strains to form filopodia, cytonemes, and extracellular vesicles during cluster and monolayer formation.

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TvAP65 inTrichomonas vaginalisPromotes HPV Infection by Interacting with Host Molecules

Mei,

Sheng,

Zhang

et al. 2024

Preprint

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Cervical cancer induced by human papillomavirus (HPV) infection poses a serious threat to women's health. Studies have shown that Trichomonas vaginalis (T. vaginalis), which is widely prevalent globally, can facilitate HPV infection. However, the underlying mechanism remains unclear. This study found that T. vaginalis significantly enhanced HPV infection in HaCaT cells and mouse vaginas through in vivo and in vitro experiments, and promoted the expression of HPV membrane receptor molecules CD151 and HSPG2. The HPV infection rate and CD151/HSPG2 expression levels were significantly decreased after reducing the expression of T. vaginalis adhesion protein 65 (TvAP65). In contrast, both HPV infection rates and CD151/HSPG2 expression were significantly increased in HaCaT cells over-expressing TvAP65. When both TvAP65 in T. vaginalis and CD151/HSPG2 in HaCaT cells were knocked down simultaneously, the infection rate of HPV in HaCaT cells was further reduced. These results suggest that TvAP65 promotes HPV infection by up-regulating the expression of CD151 and HSPG2. Furthermore, this study knocked down the 12 interacting molecules of TvAP65 in HaCaT cells one by one, and found that the HPV infection rate was significantly reduced after T. vaginalis infected HaCaT cells with low expression of FTH1, SPCS1, ATP5MC3, ITGB7, PMEPA1 or REEP5. Among them, SPCS1 played the most significant role. Simultaneous knockdown of TvAP65 and SPCS1 further significantly down-regulated the infection rate of HPV in HaCaT cells. Moreover, this molecule also down-regulated the promoting effect of T. vaginalis on HSPG2/CD151 expression. These results imply that SPCS1 plays an important role in T. vaginalis promoting HSPG2/CD151 expression and HPV infection. This study not only further proved that T. vaginalis can promote HPV infection but also explores the molecular mechanism by which TvAP65, through its interaction with SPCS1, up-regulates the expression of HSPG2 and CD151, thereby facilitating HPV infection. This provides a theoretical basis for clarifying the mechanism of co-infection between T. vaginalis and HPV. Keyword Trichomonas vaginalis, Human papillomavirus, adhesion protein 65, HPV membrane receptor molecules, co-infection

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Trichomonas vaginalis adhesion protein 65 (TvAP65) modulates parasite pathogenicity by interacting with host cell proteins

Cited by 4 publications

References 57 publications

Introduction of protein vaccine candidate based on AP65, AP33, and α-actinin proteins against Trichomonas vaginalis parasite: an immunoinformatics design

Introduction of protein vaccine candidate based on AP65, AP33, and α-actinin proteins against Trichomonas vaginalis parasite: an immunoinformatics design

Trichomonas vaginalis: Monolayer and Cluster Formation—Ultrastructural Aspects Using High-Resolution Scanning Electron Microscopy

TvAP65 inTrichomonas vaginalisPromotes HPV Infection by Interacting with Host Molecules

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