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Title : Dr.
First Name : UPDESH
Last Name : DIXIT
University/Institution : Albert Einstein College of Medicine
Email ID : updesh.dixit@einsteinmed.org
City : Bronx
Country : United States
State : New york
Zipcode : 10461
Department : Genetics
Company Name :
Area of Research
Area of Expertise
Brief Description of Research Interest :

Currently I am working on two major ongoingviral challenges which is HIV AIDS and CORONA VIRUS COVID-19. Worldwide,approximately 37.7 million individuals live with HIV, with approximately 1.1million such individuals in the United States alone. And with COVID-19 worldwide ~11.8 million infected and till date 544 thousand have lost their life. Specifically, In USA more the 3 million of confirm case with COVID-19 and133 K death.


I am working on potential treatments and vaccines for the new coronavirus disease known as COVID-19

With confirmed COVID-19 cases worldwide surpassing 9 million and In USA more the 3 million of confirm case with COVID-19 and 133 K death and continuing to grow, we are pushing forward with efforts to develop vaccines and treatments to slow the pandemic and lessen the disease’s damage.

Current research on COVID-19 has not yet elucidated the path to either “cure” approach, research remains highly prioritized and active, with promising novel drug mecha­nisms and emerging science. Evolving methods which can identified new therapeutics targets and inhibits virus replication. We are working on Virus and Host cell interaction and the mechanism which Hijacking cellular machinery for Viral replication.

Despite the widespread implementation of highly effective antiretroviral therapy (ART) and subsequent validation of the“undetectable equals untransmittable,” 1.7 million new cases occur annually alongside nearly 770,000 AIDS-related deaths. Although the cure for HIV has been a priority since the virus’ discovery, it remains elusive.


The FDA defines HIV cure research as “any investi­gation that evaluates (1) a therapeutic intervention or approach that controls or eliminates HIV infection to the point where no further medical interventions are needed to maintain health, and (2) preliminary scientific concepts that might ultimately lead to such a therapeutic intervention. Thus,we are pursuing 2 types of HIV cure research: eradicative and functional,also called HIV remission. Eradication, also known as steril­ization,implies that HIV has been removed completely from the human host.


Antiretroviral therapy (ART) targets only viral replication in activated cells. It cannot touch latent virus, meaning the vast amount of virus hidden in memory or inactive T cells or in Brain Microglial cells. This reservoir poses the biggest challenge to HIV elim­ination, as viral latency is a reversible process in the absence of effective ART (antiretroviral therapy). Complicating viral latency further, a latent reservoir may form in compartments of the human body that are spared from immune recognition and ART because of both physical and cellular barriers (also called viral escape). Some examples of these barriers include the blood-brain barrier, the Sertoli cell layer of the testes, and the B-cell follicles within the lymph nodes. Despite these challenges, eradica­tive cures exist.

No single approach has achieved long-term viral remis­sion. We are using several approaches that  are evaluating for a functional cure that maybe used in combination: early initiation, shock and kill (including severalpotential components), clustered regu­larly interspaced short palindromic repeats (CRISPR), and chimeric antigen receptor (CAR) T-cell technology.

The shock-and-kill method combines latency reversal agents such as histone deacetylase inhibitors and toll-like receptor (TLR) agonists to induce HIV-1 transcription followed by ART, therapeutic vaccines, and/or broadly neutralizing antibodies (bNAbs) to decrease the latent reservoir. This process of reac­tivation is then followed by immunomodulation with agents such as therapeutic vaccines and/or bNAbs. The aim of therapeutic vaccines (such as the modi­fied vaccinia Ankara B and the recombinant canarypox virus) is to elicit an antigenic immune response to suppress viral replication in the absence ofART. Broadly neutralizing antibodies (such as VRC01 and 3BNC117) induce hostimmunity by targeting specific epitopes of HIV.

I am are also working on emerging strategies and evolving science regarding genetic modification have unlocked new approaches for HIV cure research. These approaches include using CRISPR and CAR T-cell technology. CRISPR enables DNA cleavage to occur prior to proviral integration(resulting in proviral destruction) or after proviral integration (resulting in small insertions and deletions in the HIV genome). CAR T-cell technology uses cytotoxic T cells engineered with extracellular components to recognize both HIV epitopes and intracellular components with accompanying signal inductions.

Representative Publications :
Dixit U, Bhutoria S, Wu X., Spira M, Mathew S, Harris R, Adams L, Cahill S, Pathak R, Prakash R, Acharya S, Brenowitz M, Almo S, Steven A, Cowburn D, Girvin M and Kalpana G* "Structural mimicry of INI1/SMARCB1 Rpt1 domain to HIV-1 TAR RNA mediates its binding to HIV-1 integrase to facilitate viral replication" Nature communication. (Accepted)

1.Dixit U, Pandey AK, Mishra P, Sengupta A, Pandey VN. Staufen1 promotes HCV replication by inhibiting protein kinase R and transporting viral RNA to the site of translation and replication in the cells. Nucleic acids research. 2016;44(11):5271-87. (Impact factor 12)
2. Dixit U, Pandey AK, Liu Z, Kumar S, Neiditch MB, Klein KM, et al. FUSE binding protein 1 facilitates persistent hepatitis C virus replication in hepatoma cells by regulating tumor suppressor p53. Journal of virology. 2015;89(15):7905-21. (Impact factor 5)
3. Dixit U, Liu Z, Pandey AK, Kothari R, Pandey VN. Fuse binding protein antagonizes the transcription activity of tumor suppressor protein p53. BMC cancer.  2014;14(1):925. (Impact factor 4)
4. Dixit U, Pandey A, Mishra P. FUSE Binding Protein1 Facilitates Persistent Hepatitis C Virus Replication in Hepatoma Cells by Regulating Tumor Suppressor p53 and p53-Regulatory Factors. The FASEB Journal. (Impact factor 6)
5. Kumar S, Lu B, Dixit U, Hossain S, Liu Y, Li J, et al. Reciprocal regulation of Abl kinase by Crk Y251 and Abi1 controls invasive phenotypes in glioblastoma. Oncotarget. 2015;6(35):37792. (Impact factor 8)
6. Mishra P, Dixit U, Pandey AK, Upadhyay A, Pandey VN. Modulation of HCV replication and translation by ErbB3 binding protein1 isoforms. Virology. 2017;500:35-49. (Impact factor 4)
7. Pandey AK, Dixit U, Kholodovych V, Comollo TW, Pandey VN. he β1'-β2' Motif of the RNase H Domain of Human  Immunodeficiency Virus Type 1 Reverse Transcriptase Is Responsible for Conferring Open Conformation to the p66 Subunit
by Displacing the Connection Domain from the Polymerase Cleft. Biochemistry. 2017;56(27):3434-42. (Impact factor 4)
8. Upadhyay A, Dixit U, Manvar D, Chaturvedi N, Pandey VN. Affinity capture and identification of host cell factors associated with hepatitis C virus (+) strand subgenomic RNA. Molecular & Cellular Proteomics. 2013;12(6):1539-52. (Impact factor 8)
9. Mishra P, Dixit U, Pandey A, Pandey V. HCV-Host Cell Interactions: Role of Ebp-1 in Hepatitis C virus Replication. The FASEB Journal. 2015;29. (Impact factor 6)