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3. Potent neutralizing antibodies elicited by dengue vaccine in rhesus macaque target diverse epitopes

Author

Li, Leike, primary, Meng, Weixu, additional, Horton, Melanie, additional, DiStefano, Daniel R., additional, Thoryk, Elizabeth A., additional, Pfaff, Jennifer M., additional, Wang, Qihui, additional, Salazar, Georgina T., additional, Barnes, Trevor, additional, Doranz, Benjamin J., additional, Bett, Andrew J., additional, Casimiro, Danilo R., additional, Vora, Kalpit A., additional, An, Zhiqiang, additional, and Zhang, Ningyan, additional

Published
2019
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4. SELfies and CELLfies: Whole Genome Sequencing and Annotation of Five Antibiotic Resistant Bacteria Isolated from the Surfaces of Smartphones, An Inquiry Based Laboratory Exercise in a Genomics Undergraduate Course at the Rochester Institute of Technology

Author

Parthasarathy, Anutthaman, primary, Wong, Narayan H., additional, Weiss, Amanda N., additional, Tian, Susan, additional, Ali, Sara E., additional, Cavanaugh, Nicole T., additional, Chinsky, Tyler M., additional, Cramer, Chelsea E., additional, Gupta, Aditya, additional, Jha, Rakshanda, additional, Johnson, Loryn K., additional, Tuason, Elizabeth D., additional, Klafehn, Lauren M., additional, Krishnadas, Varada, additional, Musich, Ryan J., additional, Pfaff, Jennifer M., additional, Richman, Spencer C., additional, Shumway, Alexandria J., additional, and Hudson, André O., additional

Published
2019
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5. Probing the antigenicity of hepatitis C virus envelope glycoprotein complex by high-throughput mutagenesis

Author

Gopal, Radhika, primary, Jackson, Kelli, additional, Tzarum, Netanel, additional, Kong, Leopold, additional, Ettenger, Andrew, additional, Guest, Johnathan, additional, Pfaff, Jennifer M., additional, Barnes, Trevor, additional, Honda, Andrew, additional, Giang, Erick, additional, Davidson, Edgar, additional, Wilson, Ian A., additional, Doranz, Benjamin J., additional, and Law, Mansun, additional

Published
2017
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6. Broadly neutralizing antibodies with few somatic mutations and hepatitis C virus clearance

Author

Bailey, Justin R., primary, Flyak, Andrew I., additional, Cohen, Valerie J., additional, Li, Hui, additional, Wasilewski, Lisa N., additional, Snider, Anna E., additional, Wang, Shuyi, additional, Learn, Gerald H., additional, Kose, Nurgun, additional, Loerinc, Leah, additional, Lampley, Rebecca, additional, Cox, Andrea L., additional, Pfaff, Jennifer M., additional, Doranz, Benjamin J., additional, Shaw, George M., additional, Ray, Stuart C., additional, and Crowe, James E., additional

Published
2017
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7. Mapping the Human Memory B Cell and Serum Neutralizing Antibody Responses to Dengue Virus Serotype 4 Infection and Vaccination

Author

Nivarthi, Usha K., primary, Kose, Nurgun, additional, Sapparapu, Gopal, additional, Widman, Douglas, additional, Gallichotte, Emily, additional, Pfaff, Jennifer M., additional, Doranz, Benjamin J., additional, Weiskopf, Daniela, additional, Sette, Alessandro, additional, Durbin, Anna P., additional, Whitehead, Steve S., additional, Baric, Ralph, additional, Crowe, James E., additional, and de Silva, Aravinda M., additional

Published
2017
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9. Functional Transplant of a Dengue Virus Serotype 3 (DENV3)-Specific Human Monoclonal Antibody Epitope into DENV1

Author

Messer, William B., primary, Yount, Boyd L., additional, Royal, Scott R., additional, de Alwis, Ruklanthi, additional, Widman, Douglas G., additional, Smith, Scott A., additional, Crowe, James E., additional, Pfaff, Jennifer M., additional, Kahle, Kristen M., additional, Doranz, Benjamin J., additional, Ibarra, Kristie D., additional, Harris, Eva, additional, de Silva, Aravinda M., additional, and Baric, Ralph S., additional

Published
2016
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10. Lower IgG somatic hypermutation rates during acute dengue virus infection is compatible with a germinal center-independent B cell response

Author

Godoy-Lozano, Elizabeth Ernestina, primary, Téllez-Sosa, Juan, additional, Sánchez-González, Gilberto, additional, Sámano-Sánchez, Hugo, additional, Aguilar-Salgado, Andrés, additional, Salinas-Rodríguez, Aarón, additional, Cortina-Ceballos, Bernardo, additional, Vivanco-Cid, Héctor, additional, Hernández-Flores, Karina, additional, Pfaff, Jennifer M., additional, Kahle, Kristen M., additional, Doranz, Benjamin J., additional, Gómez-Barreto, Rosa Elena, additional, Valdovinos-Torres, Humberto, additional, López-Martínez, Irma, additional, Rodriguez, Mario H., additional, and Martínez-Barnetche, Jesús, additional

Published
2016
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11. Dengue Virus prM-Specific Human Monoclonal Antibodies with Virus Replication-Enhancing Properties Recognize a Single Immunodominant Antigenic Site

Author

Smith, Scott A., primary, Nivarthi, Usha K., additional, de Alwis, Ruklanthi, additional, Kose, Nurgun, additional, Sapparapu, Gopal, additional, Bombardi, Robin, additional, Kahle, Kristen M., additional, Pfaff, Jennifer M., additional, Lieberman, Sherri, additional, Doranz, Benjamin J., additional, de Silva, Aravinda M., additional, and Crowe, James E., additional

Published
2016
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13. Dengue virus envelope protein domain I/II hinge determines long-lived serotype-specific dengue immunity

Author

Messer, William B., primary, de Alwis, Ruklanthi, additional, Yount, Boyd L., additional, Royal, Scott R., additional, Huynh, Jeremy P., additional, Smith, Scott A., additional, Crowe, James E., additional, Doranz, Benjamin J., additional, Kahle, Kristen M., additional, Pfaff, Jennifer M., additional, White, Laura J., additional, Sariol, Carlos A., additional, de Silva, Aravinda M., additional, and Baric, Ralph S., additional

Published
2014
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14. The Potent and Broadly Neutralizing Human Dengue Virus-Specific Monoclonal Antibody 1C19 Reveals a Unique Cross-Reactive Epitope on the bc Loop of Domain II of the Envelope Protein

Author

Smith, Scott A., primary, de Alwis, A. Ruklanthi, additional, Kose, Nurgun, additional, Harris, Eva, additional, Ibarra, Kristie D., additional, Kahle, Kristen M., additional, Pfaff, Jennifer M., additional, Xiang, Xiaoxiao, additional, Doranz, Benjamin J., additional, de Silva, Aravinda M., additional, Austin, S. Kyle, additional, Sukupolvi-Petty, Soila, additional, Diamond, Michael S., additional, and Crowe, James E., additional

Published
2013
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15. Transmitted/Founder and Chronic Subtype C HIV-1 Use CD4 and CCR5 Receptors with Equal Efficiency and Are Not Inhibited by Blocking the Integrin α4β7

Author

Parrish, Nicholas F., primary, Wilen, Craig B., additional, Banks, Lauren B., additional, Iyer, Shilpa S., additional, Pfaff, Jennifer M., additional, Salazar-Gonzalez, Jesus F., additional, Salazar, Maria G., additional, Decker, Julie M., additional, Parrish, Erica H., additional, Berg, Anna, additional, Hopper, Jennifer, additional, Hora, Bhavna, additional, Kumar, Amit, additional, Mahlokozera, Tatenda, additional, Yuan, Sally, additional, Coleman, Charl, additional, Vermeulen, Marion, additional, Ding, Haitao, additional, Ochsenbauer, Christina, additional, Tilton, John C., additional, Permar, Sallie R., additional, Kappes, John C., additional, Betts, Michael R., additional, Busch, Michael P., additional, Gao, Feng, additional, Montefiori, David, additional, Haynes, Barton F., additional, Shaw, George M., additional, Hahn, Beatrice H., additional, and Doms, Robert W., additional

Published
2012
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16. Primary Infection by a Human Immunodeficiency Virus with Atypical Coreceptor Tropism

Author

Jiang, Chunlai, primary, Parrish, Nicholas F., additional, Wilen, Craig B., additional, Li, Hui, additional, Chen, Yue, additional, Pavlicek, Jeffrey W., additional, Berg, Anna, additional, Lu, Xiaozhi, additional, Song, Hongshuo, additional, Tilton, John C., additional, Pfaff, Jennifer M., additional, Henning, Elizabeth A., additional, Decker, Julie M., additional, Moody, M. Anthony, additional, Drinker, Mark S., additional, Schutte, Robert, additional, Freel, Stephanie, additional, Tomaras, Georgia D., additional, Nedellec, Rebecca, additional, Mosier, Donald E., additional, Haynes, Barton F., additional, Shaw, George M., additional, Hahn, Beatrice H., additional, Doms, Robert W., additional, and Gao, Feng, additional

Published
2011
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17. Phenotypic and Immunologic Comparison of Clade B Transmitted/Founder and Chronic HIV-1 Envelope Glycoproteins

Author

Wilen, Craig B., primary, Parrish, Nicholas F., additional, Pfaff, Jennifer M., additional, Decker, Julie M., additional, Henning, Elizabeth A., additional, Haim, Hillel, additional, Petersen, Josiah E., additional, Wojcechowskyj, Jason A., additional, Sodroski, Joseph, additional, Haynes, Barton F., additional, Montefiori, David C., additional, Tilton, John C., additional, Shaw, George M., additional, Hahn, Beatrice H., additional, and Doms, Robert W., additional

Published
2011
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19. HIV-1 Resistance to CCR5 Antagonists Associated with Highly Efficient Use of CCR5 and Altered Tropism on Primary CD4+ T Cells.

Author

Pfaff, Jennifer M., Wilen, Craig B., Harrison, Jessamina E., Demarest, James F., Lee, Benhur, Doms, Robert W., and Tilton, John C.

Subjects
*HIV, *PROTEIN conformation, *CD4 antigen, *T cells, *HOMEOSTASIS
Abstract

We previously reported on a panel of HIV-1 clade B envelope (Env) proteins isolated from a patient treated with the CCR5 antagonist aplaviroc (APL) that were drug resistant. These Envs used the APL-bound conformation of CCR5, were cross resistant to other small-molecule CCR5 antagonists, and were isolated from the patient's pretreatment viral quasispecies as well as after therapy. We analyzed viral and host determinants of resistance and their effects on viral tropism on primary CD4+ T cells. The V3 loop contained residues essential for viral resistance to APL, while additional mutations in gp120 and gp41 modulated the magnitude of drug resistance. However, these mutations were context dependent, being unable to confer resistance when introduced into a heterologous virus. The resistant virus displayed altered binding between gp120 and CCR5 such that the virus became critically dependent on the N' terminus of CCR5 in the presence of APL. In addition, the drug-resistant Envs studied here utilized CCR5 very efficiently: robust virus infection occurred even when very low levels of CCR5 were expressed. However, recognition of drug-bound CCR5 was less efficient, resulting in a tropism shift toward effector memory cells upon infection of primary CD4+ T cells in the presence of APL, with relative sparing of the central memory CD4+ T cell subset. If such a tropism shift proves to be a common feature of CCR5-antagonist-resistant viruses, then continued use of CCR5 antagonists even in the face of virologic failure could provide a relative degree of protection to the TCM subset of CD4+ T cells and result in improved T cell homeostasis and immune function. [ABSTRACT FROM AUTHOR]

Published
2010
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20. Protective Capacity of the Human Anamnestic Antibody Response during Acute Dengue Virus Infection.

Author

Meihui Xu, Züst, Roland, Ying Xiu Toh, Pfaff, Jennifer M., Kahle, Kristen M., Davidson, Edgar, Doranz, Benjamin J., Velumani, Sumathy, Tukijan, Farhana, Cheng-I Wang, and Fink, Katja

Subjects
*DENGUE, *IMMUNE response, *MONOCLONAL antibodies, *GLYCOPROTEINS, *STATISTICAL correlation, *VACCINATION
Abstract

Half of the world's population is exposed to the risk of dengue virus infection. Although a vaccine for dengue virus is now available in a few countries, its reported overall efficacy of about 60% is not ideal. Protective immune correlates following natural dengue virus infection remain undefined, which makes it difficult to predict the efficacy of new vaccines. In this study, we address the protective capacity of dengue virus-specific antibodies that are produced by plasmablasts a few days after natural secondary infection. Among a panel of 18 dengue virus-reactive human monoclonal antibodies, four groups of antibodies were identified based on their binding properties. While antibodies targeting the fusion loop of the glycoprotein of dengue virus dominated the antibody response, two smaller groups of antibodies bound to previously undescribed epitopes in domain II of the E protein. The latter, largely serotype-cross-reactive antibodies, demonstrated increased stability of binding at pH 5. These antibodies possessed weak to moderate neutralization capacity in vitro but were the most efficacious in promoting the survival of infected mice. Our data suggest that the cross-reactive anamnestic antibody response has a protective capacity despite moderate neutralization in vitro and a moderate decrease of viremia in vivo. [ABSTRACT FROM AUTHOR]

Published
2016
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21. Dengue Virus prM-Specific Human Monoclonal Antibodies with Virus Replication-Enhancing Properties Recognize a Single Immunodominant Antigenic Site.

Author

Smith SA, Nivarthi UK, de Alwis R, Kose N, Sapparapu G, Bombardi R, Kahle KM, Pfaff JM, Lieberman S, Doranz BJ, de Silva AM, and Crowe JE Jr

Subjects
Dengue Virus physiology, Epitope Mapping, Humans, Protein Binding, Antibodies, Monoclonal metabolism, Antibodies, Viral metabolism, Antibody-Dependent Enhancement, Dengue Virus drug effects, Epitopes metabolism, Viral Envelope Proteins metabolism, Virus Replication drug effects
Abstract

Unlabelled: The proposed antibody-dependent enhancement (ADE) mechanism for severe dengue virus (DENV) disease suggests that non-neutralizing serotype cross-reactive antibodies generated during a primary infection facilitate entry into Fc receptor bearing cells during secondary infection, resulting in enhanced viral replication and severe disease. One group of cross-reactive antibodies that contributes considerably to this serum profile target the premembrane (prM) protein. We report here the isolation of a large panel of naturally occurring human monoclonal antibodies (MAbs) obtained from subjects following primary DENV serotype 1, 2, or 3 or secondary natural DENV infections or following primary DENV serotype 1 live attenuated virus vaccination to determine the antigenic landscape on the prM protein that is recognized by human antibodies. We isolated 25 prM-reactive human MAbs, encoded by diverse antibody-variable genes. Competition-binding studies revealed that all of the antibodies bound to a single major antigenic site on prM. Alanine scanning-based shotgun mutagenesis epitope mapping studies revealed diverse patterns of fine specificity of various clones, suggesting that different antibodies use varied binding poses to recognize several overlapping epitopes within the immunodominant site. Several of the antibodies interacted with epitopes on both prM and E protein residues. Despite the diverse genetic origins of the antibodies and differences in the fine specificity of their epitopes, each of these prM-reactive antibodies was capable of enhancing the DENV infection of Fc receptor-bearing cells., Importance: Antibodies may play a critical role in the pathogenesis of enhanced DENV infection and disease during secondary infections. A substantial proportion of enhancing antibodies generated in response to natural dengue infection are directed toward the prM protein. The fine specificity of human prM antibodies is not understood. Here, we isolated a panel of dengue prM-specific human monoclonal antibodies from individuals after infection in order to define the mode of molecular recognition by enhancing antibodies. We found that only a single antibody molecule can be bound to each prM protein at any given time. Distinct overlapping epitopes were mapped, but all of the epitopes lie within a single major antigenic site, suggesting that this antigenic domain forms an immunodominant region of the protein. Neutralization and antibody-dependent enhanced replication experiments showed that recognition of any of the epitopes within the major antigenic site on prM was sufficient to cause enhanced infection of target cells., (Copyright © 2015, American Society for Microbiology. All Rights Reserved.)

Published
2015
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22. HIV-1 resistance to CCR5 antagonists associated with highly efficient use of CCR5 and altered tropism on primary CD4+ T cells.

Author

Pfaff JM, Wilen CB, Harrison JE, Demarest JF, Lee B, Doms RW, and Tilton JC

Subjects
Benzoates pharmacology, CCR5 Receptor Antagonists, Diketopiperazines, HIV Envelope Protein gp120 genetics, HIV Envelope Protein gp41 genetics, HIV-1 physiology, Humans, Mutation, Missense, Piperazines pharmacology, Receptors, HIV antagonists & inhibitors, Spiro Compounds pharmacology, Virus Attachment, Anti-HIV Agents pharmacology, CD4-Positive T-Lymphocytes virology, Drug Resistance, Viral, HIV-1 drug effects, Receptors, CCR5 physiology, Receptors, HIV physiology, Viral Tropism
Abstract

We previously reported on a panel of HIV-1 clade B envelope (Env) proteins isolated from a patient treated with the CCR5 antagonist aplaviroc (APL) that were drug resistant. These Envs used the APL-bound conformation of CCR5, were cross resistant to other small-molecule CCR5 antagonists, and were isolated from the patient's pretreatment viral quasispecies as well as after therapy. We analyzed viral and host determinants of resistance and their effects on viral tropism on primary CD4(+) T cells. The V3 loop contained residues essential for viral resistance to APL, while additional mutations in gp120 and gp41 modulated the magnitude of drug resistance. However, these mutations were context dependent, being unable to confer resistance when introduced into a heterologous virus. The resistant virus displayed altered binding between gp120 and CCR5 such that the virus became critically dependent on the N' terminus of CCR5 in the presence of APL. In addition, the drug-resistant Envs studied here utilized CCR5 very efficiently: robust virus infection occurred even when very low levels of CCR5 were expressed. However, recognition of drug-bound CCR5 was less efficient, resulting in a tropism shift toward effector memory cells upon infection of primary CD4(+) T cells in the presence of APL, with relative sparing of the central memory CD4(+) T cell subset. If such a tropism shift proves to be a common feature of CCR5-antagonist-resistant viruses, then continued use of CCR5 antagonists even in the face of virologic failure could provide a relative degree of protection to the T(CM) subset of CD4(+) T cells and result in improved T cell homeostasis and immune function.

Published
2010
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