Basic Science Award

Note:  Beginning with Fall 2016, The Basic Science program has been combined into the Mentored Scientist Award mechanism - which now has three scientific priority areas for funding: Basic Science, Clinical/ Translational/ Epidemiological/ Behavioral, and Implementation Science.

Below are the awards made under the Basic Science program from 1994 to 2016.

58 Awards

Award Recipient Award date Award Type
Transcriptome analysis of HIV latently infected cells Koh Fujinaga , PhD Spring Basic Science Award
The Role of LEDGF in establishing HIV latency in primary CD4 T cells Judd Hultquist, PhD Spring Basic Science Award
Rapid Genetic Interaction Mapping of HIV-1 Host Factors in Cultured T-Cells David Gordon, PhD Fall Basic Science Award
Quantifying the Role of Stochastic Gene Expression in HIV-1 Latency Establishment and Reactivation Anand Pai, PhD Spring Basic Science Award
Genetic Interaction Analysis of HIV-1 Rev Host Regulatory Networks Jason Wojcechowskyj, PhD Spring Basic Science Award
A Novel Dual Florescent HIV-1 to Study Latency Emily Battivelli, PhD Fall Basic Science Award
Exploring the Role of Caspase-1-Mediated-Pyroptosis in Promoting Chronic Inflammation in HIV Patients Gilad Doitsh, PhD Spring Basic Science Award
Mechanistic and Phenotypic Characterization of Semen Amyloid Disassembler as Novel Approach to HIV Microbicide Development Nadia Roan, PhD Spring Basic Science Award
Mucosal Natural Killer T (NKT) cells and the Gut Microbiome in HIV-1 Infection Devi SenGupta, MD Spring Basic Science Award
Intrapatient Coevolution Between the Antibody Repertoire and HIV Populations Ryan Hernandez, PhD Fall Basic Science Award
Investigating the interface between HIV-1 proteins and the host cellular ubiquitin machinery Ruth Huettenhain, PhD Fall Basic Science Award
Mechanisms Underlying CD4 T-Cell Depletion and Inflammation During Aids Progression Xin Geng, PhD Fall Basic Science Award
The Anti-HIV mechanism of human Piwil2 Pingyang Liu, PhD Fall Basic Science Award
Cytokine Responses in Elite Controllers of HIV Evan Jacobs, PhD Spring Basic Science Award
Identifying the Killing Pathway that Mediates CD4 T-cell Depletion in HIV-Infected Lymphoid Tissues Zhiyuan Yang, PhD Spring Basic Science Award
Structure-Function Study of Semen-Derived HIV Enhancing Amyloids and Their Interactors Haichuan Liu, PhD Spring Basic Science Award
Human Macrophage Heterogeneity in HIV-1 Infection Wes Yonemoto, PhD Spring Basic Science Award
Detection of HIV Transcription in Individual Cells by Flow Cytometry Elizabeth Sinclair, PhD Spring Basic Science Award
Hyperthermia and HSP90AB1 Facilitate HIV Infection Pheroze Joshi, PhD Fall Basic Science Award
Identification of Anti-HIV Factor(s) from CD8+ Cell Antiviral Factor Gene Candidates Lianxing Liu, PhD Fall Basic Science Award
Study of Tat Lysine 41 Post-translational Modification in HIV Transcription Gregory Camus, PhD Fall Basic Science Award
Understanding the Role of Inflamasome Activation in AIDS Progression Kathryn Monroe, PhD Fall Basic Science Award
HIV Transcription Inhibition by Newly Identified p300 Inhibitors Kotaro Shirakawa, MD, PhD Fall Basic Science Award
Role of Telomere maintenance in HIV-Associated Cardiovascular Disease Jue Lin, PhD Spring Basic Science Award
pDC Activation and Chronic Immune Activation in AIDS Richard Dunham, PhD Spring Basic Science Award
Do HIV Neutralizing Antibodies Recognize Inflammatory-mimetic Modifications of the HIV gp41 MPR? Vincent Venditto, PhD Spring Basic Science Award
SAHA Induced Mechanism of HIV Reactivation from Latency Koen Bartholomeeusen, PhD Fall Basic Science Award
HPV-associated Disruption of Anal Epithelium may Facilitate HIV Mucosal Transmission Sharof Tugizov, PhD Fall Basic Science Award
Investigation of the Effects of IL-2 on the Frequency of FcRL3+ Tregs and T cell Activation in HIV-infected Patients Louise Swainson, PhD Fall Basic Science Award
Differential Regulation of Basal and Tat-mediated HIV Transcription by Acetylation of P-TEFb Sungyoo Cho, PhD Fall Basic Science Award
Do Human Natural Killer Cells Acquire Immune Memory to Viral Infections? Lewis Lanier, PhD Spring Basic Science Award
The Role of P Bodies and Stress Granules in the HIV-1 Replicative Cycles Chunye Lu, PhD Fall Basic Science Award
Role of Double Modified Tat Protein in HIV-1 Transcription Sara Pagans, PhD Fall Basic Science Award
Activation of the SIRT1 Deacetylase as a Therapeutic Concept in HIV-induced T Cell Hyperactivation Xavier Contreras, PhD Spring Basic Science Award
Role of Chromatin Remodeling in HIV Transcriptional Regulation Shweta Hakre, PhD Spring Basic Science Award
The Role of Autophagy in HIV Infection Michael Killian, PhD, MPH Spring Basic Science Award
Activation of transcriptional elongation in HIV latently infected cells by SAHA Xavier Contreras, PhD Spring Basic Science Award
Defining the role of lysine methylation in HIV-1 Tat transactivation Melanie Ott, PhD Spring Basic Science Award
The role of transcriptional interference and inhibition of transcriptional elongation in HIV latency Valentina Lenasi, PhD Spring Basic Science Award
BRD4 Overexpression Increases the Propensity for Proviral Latency and Determine how this Relates to HIV Latency in vivo. Dwayne Bisgrove, PhD Spring Basic Science Award
High CD8+ T cell Activation Associates with HIV Disease Outcome Jason Barbour, PhD, MHS Spring Basic Science Award
Genetic Diversity of HIV-1 in vivo During Very Early Primary Infection Eric Delwart, PhD Spring Basic Science Award
Optimization of Cytokine Flow Cytometry (CFC) for Trans-Shipped Specimens Mike McCune, MD, PhD Fall Basic Science Award
Development and Validation of a Cytokine Flow Cytometry Assay to Detect T Cell Immune Responses Against Pneumocystis Carinii Laurence Huang, MD Fall Basic Science Award
Evaluation of Thymic Mass in HIV-1 Infected Patients Mike McCune, MD, PhD Fall Basic Science Award
Expanded Cellular Tropism of Human Immunodeficiency Virus 1 by a Trans-Receptor Mechanism Roberto Speck, MD Spring Basic Science Award
Identification of Novel HIV Co-Receptors and Characterization of Their Role in Viral Transmission Laura Digilio, MD Spring Basic Science Award
The Biology of Coreceptors for HIV and Chemokine Receptors in vivo as a Factor in Regulating HIV Disease Progression Mark Goldsmith, MD, PhD Fall Basic Science Award
Characterization of the Epstein Barr Virus BMRF-2 Gene and its Role in the Pathogenesis of Hairy Leukoplakia Laurel Lagenaur, PhD Spring Basic Science Award
Characterization and Inhibition of Kaposi's Sarcoma Herpesvirus Protease Charles Craik Spring Basic Science Award
Transgenic Rabbits and HIV Infection Mark Goldsmith, MD, PhD Spring Basic Science Award
Molecular Interactions Between HIV and HPV Joel Palefsky, MD Spring Basic Science Award
Biochemical and Clinical Consequences of Antiviral Resistance Mutations in HIV-1 Protease Charles Craik Spring Basic Science Award
Pilot Study of HIV-1-Specific Immunity Following Antiretroviral Treatment Interruption Mike McCune, MD, PhD Spring Basic Science Award
The Kinetics of Primary Viremia in Macaques and Sooty Mangabeys Infected with Simian Immunodeficiency Virus Mark Feinberg, MD, PhD Spring Basic Science Award
Molecular Biology of HIV Macrophage Infection Kathleen Page, PhD Spring Basic Science Award
Lymphocyte Apoptosis and Disease Progression Following HIV Infection Teri Liegler, PhD Fall Basic Science Award
Direct Measurement of Rate of Synthesis and Removal of Circulating HIV in Infected Humans Marc Hellerstein, MD, PhD Fall Basic Science Award
Contacts
  • The Role of LEDGF in establishing HIV latency in primary CD4 T cells

    The Role of LEDGF in establishing HIV latency in primary CD4 T cells

    Abstract

    One of the most promising strategies for curing HIV infection is referred to as “shock and kill,” whereby latently infected cells are induced to express the virus and subsequently cleared from the body. Understanding how certain cells become latently infected, however, has been a major hurdle towards realizing this strategy. It is known that certain host factors, such as the chromatin bound protein LEDGF, can influence latency by dictating the site of HIV integration and recruiting epigenetic factors.

  • Transcriptome analysis of HIV latently infected cells

    Transcriptome analysis of HIV latently infected cells

    Abstract

    HIV latency is a major hurdle to overcome in the efforts to cure AIDS. Latently infected cells produce infectious viruses upon cessation of the treatment and immune activation. A challenge to achieving an effective HIV anti-latency therapy (HALT) is that these latently infected cells are very difficult to detect. Although latently infected cells do not express productive viral mRNAs, defective or non-productive viral RNA are expressed and can be detected, which could serve as an excellent biomarker to detect latently infected cells.

  • Rapid Genetic Interaction Mapping of HIV-1 Host Factors in Cultured T-Cells

    Rapid Genetic Interaction Mapping of HIV-1 Host Factors in Cultured T-Cells

    Abstract

    Mapping genetic interactions (GIs) by simultaneously perturbing pairs of genes is a powerful tool for understanding complex biological phenomena. While the bulk of genetic interaction data has previously been generated in simpler model organisms such as yeast and bacteria, we recently developed an experimental platform for generating GI maps in mammalian cells using a combinatorial RNAi strategy, and applied this towards the construction of a genetic interaction map of HIV-1 host factors in cultured HeLa (cervical carcinoma) cells.

  • Genetic Interaction Analysis of HIV-1 Rev Host Regulatory Networks

    Genetic Interaction Analysis of HIV-1 Rev Host Regulatory Networks

    Abstract

    Human immunodeficiency virus-1 (HIV-1), the causative agent of AIDS, remains a global health crisis with millions of new infections each year. HIV-1 hijacks diverse host factor regulatory networks in order to replicate, yet the precise components of these networks and the relationships among these host factors remain poorly characterized. HIV-1 Rev is an essential HIV-1 gene that regulates the export of HIV-1 transcripts. While putative Rev host factors have been described in the literature, few have been definitively linked to Rev function during HIV-1 infection.

  • Quantifying the Role of Stochastic Gene Expression in HIV-1 Latency Establishment and Reactivation

    Quantifying the Role of Stochastic Gene Expression in HIV-1 Latency Establishment and Reactivation

    Abstract

    The primary barrier to eliminating HIV with antiretroviral therapy (ART) is its persistence as a long-lived transcriptionally silent “latent” population. Several host and epigenetic factors affect viral latency and its long-term stability. Underlying these, however, is HIV’s genetic circuitry that drives viral decision-making: large stochastic gene-expression fluctuations driven by HIV’s LTR promoter, together with Tat-mediated positive feedback, execute the latent-or-active decision.

  • A Novel Dual Florescent HIV-1 to Study Latency

    A Novel Dual Florescent HIV-1 to Study Latency

    Abstract

    HIV-1 latency is a state of reversible, non-productive infection that occurs primarily in long-lived memory CD4+ T cells. Latency allows infected cells to evade both the host immune response and antiretroviral drugs, thereby making it one of the most significant barriers to viral eradication. HIV-1 latency is a product of proviral transcriptional silencing and can occur both directly upon infection (primary latency), as well as by progressive silencing of productive infections (secondary latency).

  • HPV-associated Disruption of Anal Epithelium may Facilitate HIV Mucosal Transmission

    HPV-associated Disruption of Anal Epithelium may Facilitate HIV Mucosal Transmission

    Abstract

    Mucosal epithelia are the first tissue sites of contact of HIV with the human body during the course of infection, and these play a critical role in determining its success in establishing systemic infection. We have shown that experimental disruption of tight junctions of mucosal epithelium may facilitate HIV transmission across mucosal epithelia by paracellular penetration, which requires no viral replication and, therefore, antiretroviral therapy would not be expected to block such transmission.

  • Differential Regulation of Basal and Tat-mediated HIV Transcription by Acetylation of P-TEFb

    Differential Regulation of Basal and Tat-mediated HIV Transcription by Acetylation of P-TEFb

    Abstract

    We try to understand the mechanisms of HIV transcriptional regulation as target for therapy. The viral transactivator Tat and its interacting cofactors play an important role in HIV transcription. Tat binds to an RNA structure called TAR and recruits the positive elongation factor b (P-TEFb) to HIV-1 transcripts. P-TEFb is composed of the cyclin T1 and cyclin-dependent kinase 9 (CDK9). We identified four acetylation sites in cyclin T1.