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High-probability grants
According to our matching algorithm, Koh Fujinaga is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2004 — 2005 |
Fujinaga, Koh |
R21Activity Code Description: To encourage the development of new research activities in categorical program areas. (Support generally is restricted in level of support and in time.) |
Roles of Nelf On Hiv Replication and Viral Latency @ Case Western Reserve University
[unreadable] DESCRIPTION (provided by applicant): Highly active antiretroviral therapy (HAART) has been shown to significantly lower morbidity and mortality rates from HIV-l infection by reducing levels of plasma virus to below detectable limits in many instances. However, recent studies indicate that there remains a small population of resting CD4+ T cells containing inducible, replication competent provirus in patients receiving HAART for extended periods of time. This latent HIV-1 reservoir creates an obstacle for the successful eradication of the virus. Previous observations suggest that in latently infected cells HIV transcription is blocked mainly at the elongation step, which is regulated positively and negatively by host cellular transcription factors and the viral protein Tat. We have demonstrated that a cellular protein complex, negative elongation factor (NELF) is recruited to the HIV-1 promoter in a virus specific manner. The RD subunit of this complex binds directly to HIV-l TAR in the presence and absence of Tat and the positive elongation factor 13(P-TEF[3), and phosphorylation of RD by the kinase activity of P-TEFI 3 abolishes this interaction with TAR. The block to productive HIV-1 transcription caused by the binding of NELF to TAR may indicate a reason for the detection of predominantly short, promoter proximal transcripts by various assays observed in the latently infected PBMCs derived from HAART responders. Therefore NELF may be one of the key players involved in the transition from nonproductive to productive HIV-1 transcription. We hypothesize that NELF is a factor contributing to the low level of HIV transcription in latently infected cells. In this proposed study, we will define the precise roles of NELF in Tat-dependent and Tat-independent transcription using a newly developed siRNA technology and a highly sensitive assay in a model cell line, as wells as PBMCs collected from HIV-1 infected patients. Moreover, we will attempt to activate viral transcription in latently infected cells by regulating NELF activity in hopes of developing potential treatments to reduce or abolish this latent reservoir. The results obtained from this study will increase our understanding of HW-1 pathogenesis and may suggest new therapeutic directions. [unreadable] [unreadable]
|
1 |
2016 — 2017 |
Fujinaga, Koh |
R21Activity Code Description: To encourage the development of new research activities in categorical program areas. (Support generally is restricted in level of support and in time.) |
Hiv Transcriptome Analysis During Viral Latency @ University of California, San Francisco
PROJECT SUMMARY HIV latency is a major hurdle to overcome in the efforts to cure AIDS. Latently infected cells do not express viral proteins and escape immune surveillance during HAART treatment. These 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. To this end, it is critical to develop a sensitive method to detect latently infected cells in HIV-infected individuals. 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. Highly sensitive next-generation sequencing techniques have revealed that HIV-infected cells express less characterized HIV RNAs including short RNAs, antisense RNAs, host-viral hybrid RNAs and splice variants from cryptic splicing sites, although the role(s) of these RNA species in the viral latency and pathogenesis are largely unknown. However, RT-qPCR analyses of patient cells would often underestimate these aberrant RNAs because of their instability. It is therefore critical to obtain comprehensive catalogues of viral RNA species expressed in latently infected cells using methods that can also detect unstable and short-lived RNA species. My preliminary results of RNA-seq analysis using well-established Jurkat latent models indicate that these cells exclusively express host-viral hybrid RNAs in unstimulated states. Also, reduction of the RNA exosome components by siRNA increased the level of these hybrid RNAs as well as antisense viral RNA. In the proposed study, exact patterns of viral RNA expression (transcriptome) during the establishment of viral latency and its reactivation will be revealed using ex vivo latency models of primary CD4+ cells as well as HIV-infected cells derived from HAART-suppressed patients. In addition, these analyses will determine the proportion of latently infected cells that express these aberrant RNAs, and whether there is a bias in the correlation between HIV RNA expression and provirus integration sites (orientation, genetic environment). Finally, a highly sensitive assay to detect and quantify HIV RNAs expressed specifically in latently infected cells will be developed. These studies will provide important information for developing an efficient therapeutic approach to improve our current HALT regimen.
|
0.933 |
2018 |
Fujinaga, Koh |
R56Activity Code Description: To provide limited interim research support based on the merit of a pending R01 application while applicant gathers additional data to revise a new or competing renewal application. This grant will underwrite highly meritorious applications that if given the opportunity to revise their application could meet IC recommended standards and would be missed opportunities if not funded. Interim funded ends when the applicant succeeds in obtaining an R01 or other competing award built on the R56 grant. These awards are not renewable. |
Anti-Hiv Effects by Human Piwi Proteins @ University of California, San Francisco
ABSTRACT Besides eliciting adaptive immune responses, there are many anti-viral factors expressed in host cells to combat viral infection. The recent discovery of numerous such factors indicates that most viral replication steps are kept in check by host defense mechanisms. Of course, viruses evolve to escape from these mechanisms. Therefore, the history of viral evolution is a constant cat-and-mouse game between human anti-viral defense mechanisms and viral escape mutants. Nevertheless, studying these cellular anti-viral mechanisms is extremely important for developing potent and specific anti-HIV therapies. We recently observed that the human piwi-like RNA-mediated gene silencing 2 (Hili) protein strongly inhibits HIV replication. Hili's anti-HIV effect occurs at the step of viral protein synthesis (translation) by binding and depleting several tRNAs corresponding to amino acid codons rarely used in the human genome but frequently found in HIV. In addition, levels of Hili mRNA expression are increased upon stimulation via the T-cell receptor, indicating that Hili is a cellular anti-viral factor responding to T-cell activation. Based on these results, we hypothesize that human Piwi-family proteins are new potent anti-HIV factors expressed in CD4+ T cells. The goal of the proposed study is to understand the anti-HIV mechanism of Piwi-family proteins and evaluate their roles in the maintenance of HIV cellular resistance to new HIV infection and replication. Also, the mechanism whereby Piwi expression is regulated in CD4+ T cells will be further explored. Finally, several new approaches for effectively inhibiting HIV replication by depleting these tRNAs will be developed and validated. The proposed study will lead to a development of new anti-HIV strategies by manipulating viral protein expression.
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0.933 |