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Benjamin Trinité
IrsiCaixa AIDS Research Institute, Germans Trias i Pujol Research Institute (IGTP)

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Article
Published: 13 August 2021
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Background Understanding the determinants of long-term immune responses to SARS-CoV-2 and the concurrent impact of vaccination and emerging variants of concern will guide optimal strategies to achieve global protection against the COVID-19 pandemic. Methods A prospective cohort of 332 COVID-19 patients was followed beyond one year. Plasma neutralizing activity was evaluated using HIV-based reporter pseudoviruses expressing different SARS-CoV-2 spikes and was longitudinally analyzed using mixed-effects models. Findings Long-term neutralizing activity was stable beyond one year after infection in mild/asymptomatic and hospitalized participants. However, longitudinal models suggest that hospitalized individuals generate both short- and long-lived memory B cells, while outpatient responses were dominated by long-lived B cells. In both groups, vaccination boosted responses to natural infection, although viral variants, mainly B.1.351, reduced the efficacy of neutralization. Importantly, despite showing higher neutralization titers, hospitalized patients showed lower cross-neutralization of B.1.351 variant compared to outpatients. Multivariate analysis identified severity of primary infection as the factor that independently determines both the magnitude and the inferior cross-neutralization activity of long-term neutralizing responses. Conclusions Neutralizing response induced by SARS-CoV-2 is heterogeneous in magnitude but stable beyond one year after infection. Vaccination boosts these long-lasting natural neutralizing responses, counteracting the significant resistance to neutralization of new viral variants. Severity of primary infection determines higher magnitude but poorer quality of long-term neutralizing responses.

ACS Style

Edwards Pradenas; Benjamin Trinité; Víctor Urrea; Silvia Marfil; Ferran Tarrés-Freixas; Raquel Ortiz; Carla Rovirosa; Jordi Rodon; Júlia Vergara-Alert; Joaquim Segalés; Victor Guallar; Alfonso Valencia; Nuria Izquierdo-Useros; Marc Noguera-Julian; Jorge Carrillo; Roger Paredes; Lourdes Mateu; Anna Chamorro; Ruth Toledo; Marta Massanella; Bonaventura Clotet; Julià Blanco. Clinical course impacts early kinetics and long-term magnitude and amplitude of SARS-CoV-2 neutralizing antibodies beyond one year after infection. 2021, 1 .

AMA Style

Edwards Pradenas, Benjamin Trinité, Víctor Urrea, Silvia Marfil, Ferran Tarrés-Freixas, Raquel Ortiz, Carla Rovirosa, Jordi Rodon, Júlia Vergara-Alert, Joaquim Segalés, Victor Guallar, Alfonso Valencia, Nuria Izquierdo-Useros, Marc Noguera-Julian, Jorge Carrillo, Roger Paredes, Lourdes Mateu, Anna Chamorro, Ruth Toledo, Marta Massanella, Bonaventura Clotet, Julià Blanco. Clinical course impacts early kinetics and long-term magnitude and amplitude of SARS-CoV-2 neutralizing antibodies beyond one year after infection. . 2021; ():1.

Chicago/Turabian Style

Edwards Pradenas; Benjamin Trinité; Víctor Urrea; Silvia Marfil; Ferran Tarrés-Freixas; Raquel Ortiz; Carla Rovirosa; Jordi Rodon; Júlia Vergara-Alert; Joaquim Segalés; Victor Guallar; Alfonso Valencia; Nuria Izquierdo-Useros; Marc Noguera-Julian; Jorge Carrillo; Roger Paredes; Lourdes Mateu; Anna Chamorro; Ruth Toledo; Marta Massanella; Bonaventura Clotet; Julià Blanco. 2021. "Clinical course impacts early kinetics and long-term magnitude and amplitude of SARS-CoV-2 neutralizing antibodies beyond one year after infection." , no. : 1.

Journal article
Published: 12 June 2021 in Viruses
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With the spread of new variants of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), there is a need to assess the protection conferred by both previous infections and current vaccination. Here we tested the neutralizing activity of infected and/or vaccinated individuals against pseudoviruses expressing the spike of the original SARS-CoV-2 isolate Wuhan-Hu-1 (WH1), the D614G mutant and the B.1.1.7 variant. Our data show that parameters of natural infection (time from infection and nature of the infecting variant) determined cross-neutralization. Uninfected vaccinees showed a small reduction in neutralization against the B.1.1.7 variant compared to both the WH1 strain and the D614G mutant. Interestingly, upon vaccination, previously infected individuals developed more robust neutralizing responses against B.1.1.7, suggesting that vaccines can boost the neutralization breadth conferred by natural infection.

ACS Style

Benjamin Trinité; Edwards Pradenas; Silvia Marfil; Carla Rovirosa; Víctor Urrea; Ferran Tarrés-Freixas; Raquel Ortiz; Jordi Rodon; Júlia Vergara-Alert; Joaquim Segalés; Victor Guallar; Rosalba Lepore; Nuria Izquierdo-Useros; Glòria Trujillo; Jaume Trapé; Carolina González-Fernández; Antonia Flor; Rafel Pérez-Vidal; Ruth Toledo; Anna Chamorro; Roger Paredes; Ignacio Blanco; Eulàlia Grau; Marta Massanella; Jorge Carrillo; Bonaventura Clotet; Julià Blanco. Previous SARS-CoV-2 Infection Increases B.1.1.7 Cross-Neutralization by Vaccinated Individuals. Viruses 2021, 13, 1135 .

AMA Style

Benjamin Trinité, Edwards Pradenas, Silvia Marfil, Carla Rovirosa, Víctor Urrea, Ferran Tarrés-Freixas, Raquel Ortiz, Jordi Rodon, Júlia Vergara-Alert, Joaquim Segalés, Victor Guallar, Rosalba Lepore, Nuria Izquierdo-Useros, Glòria Trujillo, Jaume Trapé, Carolina González-Fernández, Antonia Flor, Rafel Pérez-Vidal, Ruth Toledo, Anna Chamorro, Roger Paredes, Ignacio Blanco, Eulàlia Grau, Marta Massanella, Jorge Carrillo, Bonaventura Clotet, Julià Blanco. Previous SARS-CoV-2 Infection Increases B.1.1.7 Cross-Neutralization by Vaccinated Individuals. Viruses. 2021; 13 (6):1135.

Chicago/Turabian Style

Benjamin Trinité; Edwards Pradenas; Silvia Marfil; Carla Rovirosa; Víctor Urrea; Ferran Tarrés-Freixas; Raquel Ortiz; Jordi Rodon; Júlia Vergara-Alert; Joaquim Segalés; Victor Guallar; Rosalba Lepore; Nuria Izquierdo-Useros; Glòria Trujillo; Jaume Trapé; Carolina González-Fernández; Antonia Flor; Rafel Pérez-Vidal; Ruth Toledo; Anna Chamorro; Roger Paredes; Ignacio Blanco; Eulàlia Grau; Marta Massanella; Jorge Carrillo; Bonaventura Clotet; Julià Blanco. 2021. "Previous SARS-CoV-2 Infection Increases B.1.1.7 Cross-Neutralization by Vaccinated Individuals." Viruses 13, no. 6: 1135.

Article
Published: 23 February 2021
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Unraveling long-term kinetics of antibodies to SARS-CoV-2 and the factors influencing its course, like prior antibody levels to human coronaviruses causing common cold (HCoVs), is essential to understand protective immunity and effective surveillance strategies. Antibody levels against six SARS-CoV-2 and four HCoV antigens were quantified by Luminex, and antibody neutralization capacity was assessed by flow cytometry in a cohort of health care workers followed-up for 6 months. Seroprevalence increased over time from 13.5% (month 0) and 15.6% (month 1), to 16.4% (month 6). Levels of antibodies were stable over time, except IgG against nucleocapsid antigen and IgM levels that waned. After the peak response, anti-spike antibody levels increased from ~150 days post-symptom onset in all individuals (73% for IgG), in the absence of any evidence of re-exposure. The neutralizing capacity of antibodies was maintained. Pre-existing antibodies to alpha-HCoV were lower in individuals who subsequently seroconverted for SARS-CoV-2. IgG and IgA to HCoV were significantly higher in asymptomatic than symptomatic seropositive individuals. Thus, pre-existing cross-reactive HCoVs antibodies could have a protective effect against SARS-CoV-2 infection and COVID-19 disease.

ACS Style

Natalia Ortega; Marta Ribes; Marta Vidal; Rocio Rubio; Ruth Aguilar; Sarah Williams; Diana Barrios; Selena Alonso; Pablo Hernandez-Luis; Robert Andrew Mitchell; Chenjerai Jairoce; Angeline Marie Cruz; Alfons Jimenez; Rebeca Santano; Susana Mendez; Montserrat Lamoglia; Neus Rosell; Anna Llupia; Laura Puyol; Jordi Chi; Natalia Rodrigo; Daniel Parras; Pau Serra; Edwards Pradenas; Benjamin Trinite; Julia Blanco; Alfredo Mayor; Sonia Barroso; Pilar Varela; Anna Vilella; Antoni Trilla; Pere Santamaria; Carlo Carolis; Marta Tortajada; Luis Izquierdo; Ana Angulo; Pablo Engel; Alberto L. García-Basteiro; Gemma Moncunill; Carlota Dobano. Seven-month kinetics of SARS-CoV-2 antibodies and protective role of pre-existing antibodies to seasonal human coronaviruses on COVID-19. 2021, 1 .

AMA Style

Natalia Ortega, Marta Ribes, Marta Vidal, Rocio Rubio, Ruth Aguilar, Sarah Williams, Diana Barrios, Selena Alonso, Pablo Hernandez-Luis, Robert Andrew Mitchell, Chenjerai Jairoce, Angeline Marie Cruz, Alfons Jimenez, Rebeca Santano, Susana Mendez, Montserrat Lamoglia, Neus Rosell, Anna Llupia, Laura Puyol, Jordi Chi, Natalia Rodrigo, Daniel Parras, Pau Serra, Edwards Pradenas, Benjamin Trinite, Julia Blanco, Alfredo Mayor, Sonia Barroso, Pilar Varela, Anna Vilella, Antoni Trilla, Pere Santamaria, Carlo Carolis, Marta Tortajada, Luis Izquierdo, Ana Angulo, Pablo Engel, Alberto L. García-Basteiro, Gemma Moncunill, Carlota Dobano. Seven-month kinetics of SARS-CoV-2 antibodies and protective role of pre-existing antibodies to seasonal human coronaviruses on COVID-19. . 2021; ():1.

Chicago/Turabian Style

Natalia Ortega; Marta Ribes; Marta Vidal; Rocio Rubio; Ruth Aguilar; Sarah Williams; Diana Barrios; Selena Alonso; Pablo Hernandez-Luis; Robert Andrew Mitchell; Chenjerai Jairoce; Angeline Marie Cruz; Alfons Jimenez; Rebeca Santano; Susana Mendez; Montserrat Lamoglia; Neus Rosell; Anna Llupia; Laura Puyol; Jordi Chi; Natalia Rodrigo; Daniel Parras; Pau Serra; Edwards Pradenas; Benjamin Trinite; Julia Blanco; Alfredo Mayor; Sonia Barroso; Pilar Varela; Anna Vilella; Antoni Trilla; Pere Santamaria; Carlo Carolis; Marta Tortajada; Luis Izquierdo; Ana Angulo; Pablo Engel; Alberto L. García-Basteiro; Gemma Moncunill; Carlota Dobano. 2021. "Seven-month kinetics of SARS-CoV-2 antibodies and protective role of pre-existing antibodies to seasonal human coronaviruses on COVID-19." , no. : 1.

Abstract
Published: 01 January 2020 in Proceedings
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P-selectin glycoprotein ligand-1 (PSGL-1) is a dimeric, mucin-like, 120-kDa glycoprotein that binds to P-, E-, and L-selectins. PSGL-1 is primarily expressed on the surface of lymphoid and myeloid cells and is up-regulated during inflammation to mediate leukocyte tethering and rolling on the surface of endothelium for migration into inflamed tissues. Although it has been reported that PSGL-1 expression inhibits human immunodeficiency virus type 1 (HIV-1) replication, the mechanism of PSGL-1-mediated anti-HIV activity remains to be elucidated. Here, we report that PSGL-1 in virions blocks the infectivity of HIV-1 particles by preventing the binding of particles to target cells. This inhibitory activity is independent of the viral glycoprotein present on the virus particle; the binding of particles bearing the HIV-1 envelope glycoprotein, vesicular stomatitis virus G glycoprotein, or lacking a viral glycoprotein, is impaired by PSGL-1. Mapping studies show that the extracellular, N-terminal domain of PSGL-1 is necessary for its anti-HIV-1 activity, and the PSGL-1 cytoplasmic tail contributes to its inhibition. In addition, we demonstrate that the PSGL-1-related monomeric E-selectin-binding glycoprotein CD43 also effectively blocks HIV-1 infectivity. HIV-1 infection, or the expression of either Vpu or Nef, downregulates PSGL-1 from the cell surface; the expression of Vpu appears to be primarily responsible for enabling the virus to partially escape PSGL-1-mediated restriction. Finally, we show that PSGL-1 inhibits the infectivity of other viruses such as murine leukemia virus and influenza A virus. These findings demonstrate that PSGL-1 is a broad-spectrum antiviral host factor with a novel mechanism of action.

ACS Style

Yajing Fu; Sijia He; Abdul Waheed; Deemah Dabbagh; Zheng Zhou; Benjamin Trinité; Zhao Wang; Jieshi Yu; Dan Wang; Feng Li; David N Levy; Hong Shang; Eric O Freed; Yuntao Wu. PSGL-1 Restricts HIV-1 Infectivity by Blocking Virus Particle Attachment to Target Cells. Proceedings 2020, 50, 77 .

AMA Style

Yajing Fu, Sijia He, Abdul Waheed, Deemah Dabbagh, Zheng Zhou, Benjamin Trinité, Zhao Wang, Jieshi Yu, Dan Wang, Feng Li, David N Levy, Hong Shang, Eric O Freed, Yuntao Wu. PSGL-1 Restricts HIV-1 Infectivity by Blocking Virus Particle Attachment to Target Cells. Proceedings. 2020; 50 (1):77.

Chicago/Turabian Style

Yajing Fu; Sijia He; Abdul Waheed; Deemah Dabbagh; Zheng Zhou; Benjamin Trinité; Zhao Wang; Jieshi Yu; Dan Wang; Feng Li; David N Levy; Hong Shang; Eric O Freed; Yuntao Wu. 2020. "PSGL-1 Restricts HIV-1 Infectivity by Blocking Virus Particle Attachment to Target Cells." Proceedings 50, no. 1: 77.

Journal article
Published: 26 June 2019 in Retrovirology
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Current efforts towards HIV-1 eradication focus on the reactivation and elimination of the latent viral reservoir, so-called shock and kill therapy. However, work from several groups indicates that infected cell death following virus reactivation is not guaranteed. Thus, it is imperative to develop strategies to foster specific elimination of cells carrying integrated proviruses. It has been shown that some non-nucleoside reverse transcriptase inhibitors (NNRTIs) including efavirenz can induce premature HIV-1 GagPol dimerization in productively infected cells, resulting in intracellular HIV-1 Protease (PR) activation and a reduction in HIV-1 expressing cells. Here, we document that NNRTI-induced PR activation triggers apoptotic death of productively infected resting or activated T cells in as little as 2 h via caspase-dependent and independent pathways. Rilpivirine, efavirenz and etravirine were the most potent NNRTIs, whereas nevirapine had almost no effect. NNRTI-induced cell killing was prevented by inhibitors of HIV-1 Protease (PR) activity including indinavir and nelfinavir. HIV-1 transmitter founder viruses induced cell killing similarly to lab-adapted HIV-1 except when NNRTI resistance conferring mutations were present in reverse transcriptase. Mutations in PR that confer PR inhibitor (PI) resistance restore NNRTI-induced killing in the presence of PI. Finally, we show that NNRTIs can rapidly eliminate cells in which latent viruses are stimulated to active expression. This work supports the notion that select NNRTIs might help promote the elimination of HIV-1 producing cells as an adjuvant during shock and kill therapy.

ACS Style

Benjamin Trinité; Hongtao Zhang; David N. Levy. NNRTI-induced HIV-1 protease-mediated cytotoxicity induces rapid death of CD4 T cells during productive infection and latency reversal. Retrovirology 2019, 16, 1 -11.

AMA Style

Benjamin Trinité, Hongtao Zhang, David N. Levy. NNRTI-induced HIV-1 protease-mediated cytotoxicity induces rapid death of CD4 T cells during productive infection and latency reversal. Retrovirology. 2019; 16 (1):1-11.

Chicago/Turabian Style

Benjamin Trinité; Hongtao Zhang; David N. Levy. 2019. "NNRTI-induced HIV-1 protease-mediated cytotoxicity induces rapid death of CD4 T cells during productive infection and latency reversal." Retrovirology 16, no. 1: 1-11.

Clinical trial
Published: 09 January 2019 in Science Advances
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A functional HIV cure requires immune reconstitution for lasting viremia control. A major immune dysfunction persisting in HIV infection is the impairment of T helper cell migration and homing to lymphoid tissues such as GALTs (gut-associated lymphoid tissues). ART (antiretroviral therapy) does not fully restore T cell motility for tissue repopulation. The molecular mechanism dictating this persistent T cell dysfunction is not understood. Cofilin is an actin-depolymerizing factor that regulates actin dynamics for T cell migration. Here, we demonstrate that blood CD4 T cells from HIV-infected patients (n = 193), with or without ART, exhibit significantly lower levels of cofilin phosphorylation (hyperactivation) than those from healthy controls (n = 100; ratio, 1.1:2.3; P < 0.001); cofilin hyperactivation is also associated with poor CD4 T cell recovery following ART. These results suggest an HIV-mediated systemic dysregulation of T cell motility that cannot be repaired solely by ART. We further demonstrate that stimulating blood CD4 T cells with an anti–human α4β7 integrin antibody can trigger signal transduction and modulate the cofilin pathway, partially restoring T cell motility in vitro. However, we also observed that severe T cell motility defect caused by high degrees of cofilin hyperactivation was not repairable by the anti-integrin antibody, demonstrating a mechanistic hindrance to restore immune functions in vivo. Our study suggests that cofilin is a key molecule that may need to be therapeutically targeted early for T cell tissue repopulation, immune reconstitution, and immune control of viremia.

ACS Style

Sijia He; Yajing Fu; Jia Guo; Mark Spear; Jiuling Yang; Benjamin Trinité; Chaolong Qin; Shuai Fu; Yongjun Jiang; Zining Zhang; Junjie Xu; Haibo Ding; David N. Levy; Wanjun Chen; Emanuel Petricoin; Lance A. Liotta; Hong Shang; Yuntao Wu. Cofilin hyperactivation in HIV infection and targeting the cofilin pathway using an anti-α4β7 integrin antibody. Science Advances 2019, 5, eaat7911 .

AMA Style

Sijia He, Yajing Fu, Jia Guo, Mark Spear, Jiuling Yang, Benjamin Trinité, Chaolong Qin, Shuai Fu, Yongjun Jiang, Zining Zhang, Junjie Xu, Haibo Ding, David N. Levy, Wanjun Chen, Emanuel Petricoin, Lance A. Liotta, Hong Shang, Yuntao Wu. Cofilin hyperactivation in HIV infection and targeting the cofilin pathway using an anti-α4β7 integrin antibody. Science Advances. 2019; 5 (1):eaat7911.

Chicago/Turabian Style

Sijia He; Yajing Fu; Jia Guo; Mark Spear; Jiuling Yang; Benjamin Trinité; Chaolong Qin; Shuai Fu; Yongjun Jiang; Zining Zhang; Junjie Xu; Haibo Ding; David N. Levy; Wanjun Chen; Emanuel Petricoin; Lance A. Liotta; Hong Shang; Yuntao Wu. 2019. "Cofilin hyperactivation in HIV infection and targeting the cofilin pathway using an anti-α4β7 integrin antibody." Science Advances 5, no. 1: eaat7911.

Journal article
Published: 01 June 2018 in Journal of Clinical and Translational Science
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OBJECTIVES/SPECIFIC AIMS: Characterize the expression kinetics of HIV-1 Envelope and their relationship to virus production at the cellular level. METHODS/STUDY POPULATION: In vitro and ex vivo laboratory analyses. RESULTS/ANTICIPATED RESULTS: Initial studies addressing the kinetics of cell surface. Envelope (Env) expression reveal that Env expression to peaks on day 2 post infection. Next steps include a series of experiments to compare the kinetics of Env cell surface expression with broadly neutralizing antibody (bNAb)-mediated ADCC and the characterization of virus production kinetics in this same context. To be maximally effective, ADCC elimination of infected cells should occur before peak Env expression. DISCUSSION/SIGNIFICANCE OF IMPACT: Potent bNAbs to HIV-1 recognize vulnerable sites on the HIV-1 Envelope (Env) protein and are of great clinical interest due to their potential use in the prevention and treatment of HIV-1 infection. Their effectiveness depends not only on the neutralization of viral infectivity, but also on the elimination of productively infected cells via antibody-dependent cellular cytotoxicity (ADCC). On a cellular level, ADCC dynamics are determined by the timing and level of Env expression on the surface of HIV-infected cells. This study aims to delineate the expression kinetics of HIV-1 Envelope and their relationship to virus production. We expect that it will provide new insights into the utility of bNAb-mediated ADCC in treating and possibly curing HIV-1 infection; therefore results might have substantial impact on future HIV treatment strategies.

ACS Style

Djin-Ye Oh; Lihong Liu; Benjamin Trinité; En-Wei Hu-Van Wright; Vincent Sahi; Yaoxing Huang; David N. Levy; David D. Ho. 2549 Characterizing the expression kinetics of HIV-1 envelope protein. Journal of Clinical and Translational Science 2018, 2, 7 -7.

AMA Style

Djin-Ye Oh, Lihong Liu, Benjamin Trinité, En-Wei Hu-Van Wright, Vincent Sahi, Yaoxing Huang, David N. Levy, David D. Ho. 2549 Characterizing the expression kinetics of HIV-1 envelope protein. Journal of Clinical and Translational Science. 2018; 2 (S1):7-7.

Chicago/Turabian Style

Djin-Ye Oh; Lihong Liu; Benjamin Trinité; En-Wei Hu-Van Wright; Vincent Sahi; Yaoxing Huang; David N. Levy; David D. Ho. 2018. "2549 Characterizing the expression kinetics of HIV-1 envelope protein." Journal of Clinical and Translational Science 2, no. S1: 7-7.

Journal article
Published: 05 January 2016 in Retrovirology
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HIV-1 integration is prone to a high rate of failure, resulting in the accumulation of unintegrated viral genomes (uDNA) in vivo and in vitro. uDNA can be transcriptionally active, and circularized uDNA genomes are biochemically stable in non-proliferating cells. Resting, non-proliferating CD4 T cells are prime targets of HIV-1 infection and latently infected resting CD4 T cells are the major barrier to HIV cure. Our prior studies demonstrated that uDNA generates infectious virions when T cell activation follows rather than precedes infection. Here, we characterize in primary resting CD4 T cells the dynamics of integrated and unintegrated virus expression, genome persistence and sensitivity to latency reversing agents. Unintegrated HIV-1 was abundant in directly infected resting CD4 T cells. Maximal gene expression from uDNA was delayed compared with integrated HIV-1 and was less toxic, resulting in uDNA enrichment over time relative to integrated proviruses. Inhibiting integration with raltegravir shunted the generation of durable latency from integrated to unintegrated genomes. Latent uDNA was activated to de novo virus production by latency reversing agents that also activated latent integrated proviruses, including PKC activators, histone deacetylase inhibitors and P-TEFb agonists. However, uDNA responses displayed a wider dynamic range, indicating differential regulation of expression relative to integrated proviruses. Similar to what has recently been demonstrated for latent integrated proviruses, one or two applications of latency reversing agents failed to activate all latent unintegrated genomes. Unlike integrated proviruses, uDNA gene expression did not down modulate expression of HLA Class I on resting CD4 T cells. uDNA did, however, efficiently prime infected cells for killing by HIV-1-specific cytotoxic T cells. These studies demonstrate that contributions by unintegrated genomes to HIV-1 gene expression, virus production, latency and immune responses are inherent properties of the direct infection of resting CD4 T cells. Experimental models of HIV-1 latency employing directly infected resting CD4 T cells should calibrate the contribution of unintegrated HIV-1.

ACS Style

Chi N. Chan; Benjamin Trinité; Caroline S. Lee; Saurabh Mahajan; Akanksha Anand; Dominik Wodarz; Steffanie Sabbaj; Anju Bansal; Paul A. Goepfert; David N. Levy. HIV-1 latency and virus production from unintegrated genomes following direct infection of resting CD4 T cells. Retrovirology 2016, 13, 1 -22.

AMA Style

Chi N. Chan, Benjamin Trinité, Caroline S. Lee, Saurabh Mahajan, Akanksha Anand, Dominik Wodarz, Steffanie Sabbaj, Anju Bansal, Paul A. Goepfert, David N. Levy. HIV-1 latency and virus production from unintegrated genomes following direct infection of resting CD4 T cells. Retrovirology. 2016; 13 (1):1-22.

Chicago/Turabian Style

Chi N. Chan; Benjamin Trinité; Caroline S. Lee; Saurabh Mahajan; Akanksha Anand; Dominik Wodarz; Steffanie Sabbaj; Anju Bansal; Paul A. Goepfert; David N. Levy. 2016. "HIV-1 latency and virus production from unintegrated genomes following direct infection of resting CD4 T cells." Retrovirology 13, no. 1: 1-22.