Department


Basic & Clinical Sciences

Assistant Professor
Focus: Antiviral Restriction Factors

Contact Information
(518) 694-7299
Hamayun.Sharifi@acphs.edu


Speaker Request
H. John Sharifi, Ph.D.

EDUCATION

  • Ph.D. in Biomedical Research, Department of Immunology and Microbial Disease, Albany Medical College
  • B.S. in Biology, Siena College

COURSES TAUGHT AT ACPHS

  • Microbiology Laboratory
  • Cell Biology
  • Microbial Genetics
  • Medical Mycology and Parasitology
  • Journal Club

RESEARCH INTERESTS

All viruses absolutely require a host cell to facilitate viral replication and propagation. Infected cells, however, do not go down without a fight. Several factors (typically cellular proteins) antagonize the virus in an effort to defeat viral replication. This is termed “intrinsic immunity”. For the vast majority of virus-types found on Earth, human cells are successful at defending themselves from invasion. However, many viruses that are significant human pathogens have evolved mechanisms to counter cellular defenses and thus enable viral replication and spread.

The majority of my research has focused on this evolutionary arms race between viruses and host-cells. My thesis and post-doctoral work revolved around the human immunodeficiency virus (HIV) and the virus’s ability to usurp the cellular protein-recycling machinery to target cellular anti-viral proteins for destruction, thus paving the way for viral replication. As is the case with many studies involving virus replication, this work also provided novel insight into the biology of cells outside of the context of an infection thereby leading to a better understanding of normal cell biology. Like most research projects, this work also generated several questions that are perfect catalysts for student-centered research.

PEER-REVIEWED PUBLICATIONS

  • Shi B, Sharif HJ, DiGrigoli S, Kinnetz M, Mellon K, Hu W, de Noronha CM. Inhibition of HIV early replication by the p53 and its downstream gene p21. Virology Journal. 2018.
  • Furuya AK, Sharifi HJ, Jellinger RM, Cristofano P, Shi Binshan, de Noronha CM. Sulforaphane inhibits HIV infection of macrophages through Nrf2. PLoS Pathogens. 2016.
  • Sharifi HJ, Furuya AK, Jellinger RM, Nekorchuk MD, de Noronha CM. Cullin4A and Cullin4B are Interchangeable for HIV Vpr and Vpx Action Through the CRL4 Ubiquitin Ligase Complex. J Virol. 2014.
  • Furuya AKM, Sharifi HJ, de Noronha CM. The curious case of type I IFN and MxA: Tipping the immune balance in AIDS. Frontiers in Immunology. 2014.
  • Porter KA, Duffy EB, Nyland P, Atianand MK, Sharifi HJ, Harton JA. The CLRX.1/NOD24 (NLRP2P) pseudogene codes a functional negative regulator of NF-kappaB, pyrin-only protein 4. Genes Immun. 2014.
  • Nekorchuk MD, Sharifi HJ, Furuya AK, Jellinger R, de Noronha CM. HIV relies on neddylation for ubiquitin ligase-mediated functions. Retrovirology, 2013.
  • Casey Klockow L, Sharifi HJ, Wen X, Flagg M, Furuya AK, Nekorchuk M, de Noronha CM. The HIV-1 protein Vpr targets the endoribonuclease Dicer for proteasomal degradation to boost macrophage infection. Virology. 2013.
  • Sharifi HJ, Furuya AM, de Noronha CM. The role of HIV-1 Vpr in promoting the infection of nondividing cells and in cell cycle arrest. Curr Opin HIV AIDS. 2012.
  • Wen X, Casey Klockow L, Nekorchuk M, Sharifi HJ, de Noronha CM. The HIV1 protein Vpr acts to enhance constitutive DCAF1-dependent UNG2 turnover. PLoS One. 2012.

PUBLICATIONS

Shi B, Sharifi HJ, DiGrigoli SKinnetz MMellon K, Hu W, de Noronha CMC. Inhibition of HIV early replication by the p53 and its downstream gene p21. Virology Journal. 2018 Mar 27;15(1):53. PubMed PMID: 29587790; PubMed Central PMCID: PMC5870690.

CONFERENCES AND PRESENTATIONS

Petersen JC, Goyette MT, Lucey ES, Sharifi HJ, Porter KA. Characterization of Macrophage Growth, Maturation and Polarization: Best-Practices for the THP-1 Cell Line. Upstate New York Immunology Conference, Cooperstown NY, October 2018.

EXTRAMURAL GRANTS

Investigator: John Sharifi
Project Title: Understanding NRF2 Mediated Restriction of HIV Infection
Grantor: National Institutes of Health - National Institute of Allergy and Infectious Diseases
Amount: $50,000 (sub-award)
Project Number: 1R21AI140993-01
Term: May 14, 2018 - April 30, 2020