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1. FLT3L governs the development of partially overlapping hematopoietic lineages in humans and mice

Author

Momenilandi, Mana, Lévy, Romain, Sobrino, Steicy, Li, Jingwei, Lagresle-Peyrou, Chantal, Esmaeilzadeh, Hossein, Fayand, Antoine, Le Floc’h, Corentin, Guérin, Antoine, Della Mina, Erika, Shearer, Debra, Delmonte, Ottavia M., Yatim, Ahmad, Mulder, Kevin, Mancini, Mathieu, Rinchai, Darawan, Denis, Adeline, Neehus, Anna-Lena, Balogh, Karla, Brendle, Sarah, Rokni-Zadeh, Hassan, Changi-Ashtiani, Majid, Seeleuthner, Yoann, Deswarte, Caroline, Bessot, Boris, Cremades, Cassandre, Materna, Marie, Cederholm, Axel, Ogishi, Masato, Philippot, Quentin, Beganovic, Omer, Ackermann, Mania, Wuyts, Margareta, Khan, Taushif, Fouéré, Sébastien, Herms, Florian, Chanal, Johan, Palterer, Boaz, Bruneau, Julie, Molina, Thierry J., Leclerc-Mercier, Stéphanie, Prétet, Jean-Luc, Youssefian, Leila, Vahidnezhad, Hassan, Parvaneh, Nima, Claeys, Kristl G., Schrijvers, Rik, Luka, Marine, Pérot, Philippe, Fourgeaud, Jacques, Nourrisson, Céline, Poirier, Philippe, Jouanguy, Emmanuelle, Boisson-Dupuis, Stéphanie, Bustamante, Jacinta, Notarangelo, Luigi D., Christensen, Neil, Landegren, Nils, Abel, Laurent, Marr, Nico, Six, Emmanuelle, Langlais, David, Waterboer, Tim, Ginhoux, Florent, Ma, Cindy S., Tangye, Stuart G., Meyts, Isabelle, Lachmann, Nico, Hu, Jiafen, Shahrooei, Mohammad, Bossuyt, Xavier, Casanova, Jean-Laurent, and Béziat, Vivien

Published
2024
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2. Gender Difference in DNA Damage Induced by the Environmental Carcinogen Dibenzo[def,p]chrysene Individually and in Combination with Mouse Papillomavirus Infection in the Mouse Oral Cavity

Author

Chen, Kun-Ming, primary, Sun, Yuan-Wan, additional, Hu, Jiafen, additional, Balogh, Karla, additional, Gowda, Krishne, additional, Aliaga, Cesar, additional, Sun, Dongxiao, additional, Christensen, Neil, additional, Amin, Shantu, additional, and El-Bayoumy, Karam, additional

Published
2024
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5. Passive Immunization with a Single Monoclonal Neutralizing Antibody Protects against Cutaneous and Mucosal Mouse Papillomavirus Infections

Author

Brendle, Sarah A., primary, Li, Jingwei, additional, Cladel, Nancy M., additional, Balogh, Karla K., additional, Booth, Jennifer, additional, Shearer, Debra A., additional, Walter, Vonn, additional, Lu, Song, additional, Christensen, Neil D., additional, Covington, Danielle, additional, DeBroff, Jake, additional, Milici, Janice, additional, Zhu, Yusheng, additional, Viscidi, Raphael, additional, and Hu, Jiafen, additional

Published
2022
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11. Mouse Papillomavirus L1 and L2 Are Dispensable for Viral Infection and Persistence at Both Cutaneous and Mucosal Tissues

Author

Brendle, Sarah, primary, Li, Jingwei J., additional, Cladel, Nancy M., additional, Shearer, Debra A., additional, Budgeon, Lynn R., additional, Balogh, Karla K., additional, Atkins, Hannah, additional, Costa-Fujishima, Marina, additional, Lopez, Paul, additional, Christensen, Neil D., additional, Doorbar, John, additional, Murooka, Thomas T., additional, and Hu, Jiafen, additional

Published
2021
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12. Humans with inherited T cell CD28 deficiency are susceptible to skin papillomaviruses but are otherwise healthy

Author

Béziat, Vivien, primary, Rapaport, Franck, additional, Hu, Jiafen, additional, Titeux, Matthias, additional, Bonnet des Claustres, Mathilde, additional, Bourgey, Mathieu, additional, Griffin, Heather, additional, Bandet, Élise, additional, Ma, Cindy S., additional, Sherkat, Roya, additional, Rokni-Zadeh, Hassan, additional, Louis, David M., additional, Changi-Ashtiani, Majid, additional, Delmonte, Ottavia M., additional, Fukushima, Toshiaki, additional, Habib, Tanwir, additional, Guennoun, Andrea, additional, Khan, Taushif, additional, Bender, Noemi, additional, Rahman, Mahbuba, additional, About, Frédégonde, additional, Yang, Rui, additional, Rao, Geetha, additional, Rouzaud, Claire, additional, Li, Jingwei, additional, Shearer, Debra, additional, Balogh, Karla, additional, Al Ali, Fatima, additional, Ata, Manar, additional, Dabiri, Soroosh, additional, Momenilandi, Mana, additional, Nammour, Justine, additional, Alyanakian, Marie-Alexandra, additional, Leruez-Ville, Marianne, additional, Guenat, David, additional, Materna, Marie, additional, Marcot, Léa, additional, Vladikine, Natasha, additional, Soret, Christine, additional, Vahidnezhad, Hassan, additional, Youssefian, Leila, additional, Saeidian, Amir Hossein, additional, Uitto, Jouni, additional, Catherinot, Émilie, additional, Navabi, Shadi Sadat, additional, Zarhrate, Mohammed, additional, Woodley, David T., additional, Jeljeli, Mohamed, additional, Abraham, Thomas, additional, Belkaya, Serkan, additional, Lorenzo, Lazaro, additional, Rosain, Jérémie, additional, Bayat, Mousa, additional, Lanternier, Fanny, additional, Lortholary, Olivier, additional, Zakavi, Faramarz, additional, Gros, Philippe, additional, Orth, Gérard, additional, Abel, Laurent, additional, Prétet, Jean-Luc, additional, Fraitag, Sylvie, additional, Jouanguy, Emmanuelle, additional, Davis, Mark M., additional, Tangye, Stuart G., additional, Notarangelo, Luigi D., additional, Marr, Nico, additional, Waterboer, Tim, additional, Langlais, David, additional, Doorbar, John, additional, Hovnanian, Alain, additional, Christensen, Neil, additional, Bossuyt, Xavier, additional, Shahrooei, Mohammad, additional, and Casanova, Jean-Laurent, additional

Published
2021
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16. The environmental pollutant and tobacco smoke constituent dibenzo[def,p]chrysene is a co-factor for malignant progression of mouse oral papillomavirus infections

Author

Christensen, Neil D., primary, Chen, Kun-Ming, additional, Hu, Jiafen, additional, Stairs, Douglas B., additional, Sun, Yuan-Wan, additional, Aliaga, Cesar, additional, Balogh, Karla K., additional, Atkins, Hannah, additional, Shearer, Debra, additional, Li, Jingwei, additional, Brendle, Sarah A., additional, Gowda, Krishne, additional, Amin, Shantu, additional, Walter, Vonn, additional, Viscidi, Raphael, additional, and El-Bayoumy, Karam, additional

Published
2021
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18. Abstract LB-200: A cGMP-grade chimeric papillomavirus candidate vaccine (HPV16 RG1-VLP) confers long term cross-protection compared to a nonavalent hpv vaccine in a pre-clinical papillomavirus animal model

Author

Hu, Jiafen, primary, Balogh, Karla, additional, Matsui, Ken, additional, Tan, Huimin, additional, Olczak, Pola, additional, Buchman, George, additional, Howard, Brian, additional, White, Jonathan, additional, Kennedy, Michelle, additional, Sei, Shizuko, additional, Glaze, Elizabeth, additional, Brendle, Sarah, additional, Schellenbacher, Christina, additional, Kirnbauer, Reinhard, additional, Roden, Richard, additional, Shoemaker, Robert, additional, Christensen, Neil, additional, and Wang, Joshua Weiyuan, additional

Published
2019
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19. Papillomavirus can be transmitted through the blood and produce infections in blood recipients: Evidence from two animal models

Author

Cladel, Nancy M., primary, Jiang, Pengfei, additional, Li, Jingwei J., additional, Peng, Xuwen, additional, Cooper, Timothy K., additional, Majerciak, Vladimir, additional, Balogh, Karla K., additional, Meyer, Thomas J., additional, Brendle, Sarah A., additional, Budgeon, Lynn R., additional, Shearer, Debra A., additional, Munden, Regina, additional, Cam, Maggie, additional, Vallur, Raghavan, additional, Christensen, Neil D., additional, Zheng, Zhi-Ming, additional, and Hu, Jiafen, additional

Published
2019
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20. BET bromodomain inhibitors show anti-papillomavirus activity in vitro and block CRPV wart growth in vivo

Author

Morse, Mary A., primary, Balogh, Karla K., additional, Brendle, Sarah A., additional, Campbell, Colin A., additional, Chen, Mao X., additional, Furze, Rebecca C., additional, Harada, Isobel L., additional, Holyer, Ian D., additional, Kumar, Umesh, additional, Lee, Kevin, additional, Prinjha, Rab K., additional, Rüdiger, Martin, additional, Seal, Jonathan T., additional, Taylor, Simon, additional, Witherington, Jason, additional, and Christensen, Neil D., additional

Published
2018
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44. Mouse Papillomavirus L1 and L2 Are Dispensable for Viral Infection and Persistence at Both Cutaneous and Mucosal Tissues

Author

Brendle, Sarah, Li, Jingwei J., Cladel, Nancy M., Shearer, Debra A., Budgeon, Lynn R., Balogh, Karla K., Atkins, Hannah, Costa-Fujishima, Marina, Lopez, Paul, Christensen, Neil D., Doorbar, John, Murooka, Thomas T., and Hu, Jiafen

Subjects
L1 mutant, L2 mutant, ISH, qPCR, tumor growth, RCA, viral copy number, viral production, TEM, RNAscope, 3. Good health, mouse papillomavirus, IHC
Abstract

Papillomavirus L1 and L2, the major and minor capsid proteins, play significant roles in viral assembly, entry, and propagation. In the current study, we investigate the impact of L1 and L2 on viral life cycle and tumor growth with a newly established mouse papillomavirus (MmuPV1) infection model. MmuPV1 L1 knockout, L2 knockout, and L1 plus L2 knockout mutant genomes (designated as L1ATGko-4m, L2ATGko, and L1-L2ATGko respectively) were generated. The mutants were examined for their ability to generate lesions in athymic nude mice. Viral activities were examined by qPCR, immunohistochemistry (IHC), in situ hybridization (ISH), and transmission electron microscopy (TEM) analyses. We demonstrated that viral DNA replication and tumor growth occurred at both cutaneous and mucosal sites infected with each of the mutants. Infections involving L1ATGko-4m, L2ATGko, and L1-L2ATGko mutant genomes generally resulted in smaller tumor sizes compared to infection with the wild type. The L1 protein was absent in L1ATGko-4m and L1-L2ATGko mutant-treated tissues, even though viral transcripts and E4 protein expression were robust. Therefore, L1 is not essential for MmuPV1-induced tumor growth, and this finding parallels our previous observations in the rabbit papillomavirus model. Very few viral particles were detected in L2ATGko mutant-infected tissues. Interestingly, the localization of L1 in lesions induced by L2ATGko was primarily cytoplasmic rather than nuclear. The findings support the hypothesis that the L2 gene influences the expression, location, transport, and assembly of the L1 protein in vivo.

45. Mouse Papillomavirus L1 and L2 Are Dispensable for Viral Infection and Persistence at Both Cutaneous and Mucosal Tissues

Author

Brendle, Sarah, Li, Jingwei J, Cladel, Nancy M, Shearer, Debra A, Budgeon, Lynn R, Balogh, Karla K, Atkins, Hannah, Costa-Fujishima, Marina, Lopez, Paul, Christensen, Neil D, Doorbar, John, Murooka, Thomas T, and Hu, Jiafen

Subjects
L1 mutant, L2 mutant, viral copy number, Mice, Nude, Genome, Viral, Virus Replication, ISH, Mice, Animals, RNAscope, Papillomaviridae, Skin, Mucous Membrane, RCA, viral production, Oncogene Proteins, Viral, Cell Transformation, Viral, 3. Good health, mouse papillomavirus, qPCR, tumor growth, DNA, Viral, Mutation, TEM, Capsid Proteins, Female, IHC
Abstract

Papillomavirus L1 and L2, the major and minor capsid proteins, play significant roles in viral assembly, entry, and propagation. In the current study, we investigate the impact of L1 and L2 on viral life cycle and tumor growth with a newly established mouse papillomavirus (MmuPV1) infection model. MmuPV1 L1 knockout, L2 knockout, and L1 plus L2 knockout mutant genomes (designated as L1ATGko-4m, L2ATGko, and L1-L2ATGko respectively) were generated. The mutants were examined for their ability to generate lesions in athymic nude mice. Viral activities were examined by qPCR, immunohistochemistry (IHC), in situ hybridization (ISH), and transmission electron microscopy (TEM) analyses. We demonstrated that viral DNA replication and tumor growth occurred at both cutaneous and mucosal sites infected with each of the mutants. Infections involving L1ATGko-4m, L2ATGko, and L1-L2ATGko mutant genomes generally resulted in smaller tumor sizes compared to infection with the wild type. The L1 protein was absent in L1ATGko-4m and L1-L2ATGko mutant-treated tissues, even though viral transcripts and E4 protein expression were robust. Therefore, L1 is not essential for MmuPV1-induced tumor growth, and this finding parallels our previous observations in the rabbit papillomavirus model. Very few viral particles were detected in L2ATGko mutant-infected tissues. Interestingly, the localization of L1 in lesions induced by L2ATGko was primarily cytoplasmic rather than nuclear. The findings support the hypothesis that the L2 gene influences the expression, location, transport, and assembly of the L1 protein in vivo.

46. Vaccine generated immunity targets an HPV16 E7 HLA-A2.1-restricted CD8+ T cell epitope relocated to an early gene or a late gene of the cottontail rabbit papillomavirus (CRPV) genome in HLA-A2.1 transgenic rabbits

Author

Bounds, Callie E., Hu, Jiafen, Cladel, Nancy M., Balogh, Karla, and Christensen, Neil D.

Subjects
*IMMUNOGENETICS, *EPITOPES, *VIRAL vaccines, *PAPILLOMAVIRUSES, *HLA histocompatibility antigens, *T cells, *GENE expression, *GENOMES, *LABORATORY rabbits, *COTTONTAILS
Abstract

Abstract: The newly established HLA-A2.1 transgenic rabbit model has proven useful for testing the immunogenicity of well known and computer-predicted A2-restricted epitopes. In the current study we compared the protective immunity induced to a preferred HPV16 E7 A2-restricted epitope that has been relocated to positions within the CRPV E7 gene and the CRPV L2 gene. Epitope expression from both the E7 protein and the L2 protein resulted in increased protection against viral DNA challenge of the HLA-A2.1 transgenic rabbits as compared to control-vaccinated rabbit groups. These data indicate that proteins expressed at both early and late time points during a natural papillomavirus infection can be targeted by epitope-specific immunity and indicate this immunity is increased to early rather than late expressed proteins of papillomaviruses. This study also highlights the broad utility of the HLAA2.1 transgenic rabbit model for testing numerous immunological factors involved in vaccine generated protective immunity. [ABSTRACT FROM AUTHOR]

Published
2011
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47. Establishment of a Cottontail Rabbit Papillomavirus/HLA-A2.1 Transgenic Rabbit Model.

Author

Jiafen Hu, Xuwen Peng, Budgeon, Lynn R., Cladel, Nancy M., Balogh, Karla K., and Christensen, Neil D.

Subjects
*PAPILLOMAVIRUSES, *COTTONTAILS, *MAJOR histocompatibility complex, *TRANSGENES, *INFECTION, *EPITOPES
Abstract

Three transgenic rabbit lines that express a well-characterized human major histocompatibility complex class I (MHC-I) gene (HLA-A2.1) have been established. All three lines carry the HLA-A2.1 heavy chain and are able to pass the transgene to their offspring with both the outbred and the inbred EIII/JC genetic background. HLA-A2.1 colocalizes exclusively with rabbit MHC-I on the cell surfaces. These HLA-A2.1 transgenic rabbits demonstrated infection patterns similar to those found after cottontail rabbit papillomavirus (CRPV) challenge when compared with results in normal rabbits, although higher regression rates were found in HLA-A2.1 transgenic rabbits. Because the CRPV genome can accommodate significant modifications, the CRPV/HLA-A2.1 rabbit model has the potential to be used to screen HLA-A2.1-restricted immunogenic epitopes from human papillomaviruses in the context of in vivo papillomavirus infection. [ABSTRACT FROM AUTHOR]

Published
2007
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48. Monitoring mouse papillomavirus-associated cancer development using longitudinal Pap smear screening.

Author

Atkins HM, Uslu AA, Li JJ, Shearer DA, Brendle SA, Han C, Kozak M, Lopez P, Nayar D, Balogh KK, Abendroth C, Copper J, Cheng KC, Christensen ND, Zhu Y, Avril S, Burgener AD, Murooka TT, and Hu J

Subjects
Animals, Female, Mice, Early Detection of Cancer methods, Papillomaviridae genetics, Papillomaviridae isolation & purification, DNA, Viral genetics, Vaginal Smears, Humans, Longitudinal Studies, Papanicolaou Test, Papillomavirus Infections virology, Papillomavirus Infections diagnosis, Disease Models, Animal, Uterine Cervical Neoplasms virology, Uterine Cervical Neoplasms pathology
Abstract

A substantial percentage of the population remains at risk for cervical cancer due to pre-existing human papillomavirus (HPV) infections, despite prophylactic vaccines. Early diagnosis and treatment are crucial for better disease outcomes. The development of new treatments heavily relies on suitable preclinical model systems. Recently, we established a mouse papillomavirus (MmuPV1) model that is relevant to HPV genital pathogenesis. In the current study, we validated the use of Papanicolaou (Pap) smears, a valuable early diagnostic tool for detecting HPV cervical cancer, to monitor disease progression in the MmuPV1 mouse model. Biweekly cervicovaginal swabs were collected from the MmuPV1-infected mice for viral DNA quantitation and cytology assessment. The Pap smear slides were evaluated for signs of epithelial cell abnormalities using the 2014 Bethesda system criteria. Tissues from the infected mice were harvested at various times post-viral infection for additional histological and virological assays. Over time, increased viral replication was consistent with higher levels of viral DNA, and it coincided with an uptick in epithelial cell abnormalities with higher severity scores noted as early as 10 weeks after viral infection. The cytological results also correlated with the histological evaluation of tissues harvested simultaneously. Both immunocompromised and immunocompetent mice with squamous cell carcinoma (SCC) cytology also developed vaginal SCCs. Notably, samples from the MmuPV1-infected mice exhibited similar cellular abnormalities compared to the corresponding human samples at similar disease stages. Hence, Pap smear screening proves to be an effective tool for the longitudinal monitoring of disease progression in the MmuPV1 mouse model., Importance: Papanicolaou (Pap) smear has saved millions of women's lives as a valuable early screening tool for detecting human papillomavirus (HPV) cervical precancers and cancer. However, more than 200,000 women in the United States alone remain at risk for cervical cancer due to pre-existing HPV infection-induced precancers, as there are currently no effective treatments for HPV-associated precancers and cancers other than invasive procedures including a loop electrosurgical excision procedure (LEEP) to remove abnormal tissues. In the current study, we validated the use of Pap smears to monitor disease progression in our recently established mouse papillomavirus model. To the best of our knowledge, this is the first study that provides compelling evidence of applying Pap smears from cervicovaginal swabs to monitor disease progression in mice. This HPV-relevant cytology assay will enable us to develop and test novel antiviral and anti-tumor therapies using this model to eliminate HPV-associated diseases and cancers., Competing Interests: The authors declare no conflict of interest.

Published
2024
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49. Gender Difference in DNA Damage Induced by the Environmental Carcinogen Dibenzo[ def,p ]chrysene Individually and in Combination with Mouse Papillomavirus Infection in the Mouse Oral Cavity.

Author

Chen KM, Sun YW, Hu J, Balogh K, Gowda K, Aliaga C, Sun D, Christensen N, Amin S, and El-Bayoumy K

Abstract

Tobacco smoking and human papillomavirus infection are established etiological agents in the development of head and neck squamous cell carcinoma (HNSCC). The incidence and mortality of HNSCC are higher in men than women. To provide biochemical basis for sex differences, we tested the hypothesis that carcinogen treatment using dibenzo[ def,p ]chrysene, which is an environmental pollutant and tobacco smoke constituent, in the absence or presence of the mouse papillomavirus infection results in significantly higher levels of DNA damage in the oral cavity in male than in female mice. However, the results of the present investigation do not support our hypothesis since we found that females were more susceptible to carcinogen-induced covalent DNA damage than males independent of the viral infection. Since DNA damage represents only a single-step in the carcinogenesis process, additional factors may contribute to sex differences in humans., Competing Interests: The authors declare no competing financial interest., (© 2024 The Authors. Published by American Chemical Society.)

Published
2024
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