BBC News - Dr Jeremy Kamil, a virologist at LSU Health Shreveport, says if enough mutations happen in a viral family tree or a lineage, the virus can begin to function differently and the lineage can become a so-called 'variant of concern'.
Jeremy Kamil, PhD
Associate Professor of Microbiology and Immunology
Bachelor of Arts, General Biology - Cornell University
PhD, Microbiology - University of California at Davis
Post-Doctoral Fellowships - Cornell University and Harvard Medical School
Congrats to recent Kamil Lab graduate Dr. Christopher Nguyen, who finished his PhD requirements in September 2019 and recently started a job at Voyager Therapeutics in Cambridge, MA.
Kudos to Postdoc Fellow Dr. Hongbo Zhang whose first author manuscript was recently accepted at mBio (November 2019).
KCBS Radio - We're taking a closer look at variants and how the current vaccines are performing against them. To answer your questions KCBS Radio's Stan Bunger spoke with Dr. Jeremy Kamil, an associate professor of microbiology and immunology at Louisiana State University Health Shreveport.
Nature.com - Ramped-up sequencing efforts are helping to identify mutations that might boost transmission or help a virus evade immune responses. For the scientists who have spent the past year poring over hundreds of thousands of coronavirus genomes, the United States has been an enigma.
NBC CT - LSU Health Shreveport Virologist Jeremy Kamil told NBC Connecticut Investigates that halting their spread will require other measures. Kamil was among a team of researchers that discovered seven new COVID-19 strains, known as "variants," aside from the variants first identified in the UK, South Africa, and Brazil.
NBC News - "There are certain variants that are more transmissible, and we have strong data on that, but the thing people should take away from the variant story is just: Don't let your guard down," said Dr. Jeremy Kamil, an associate professor of microbiology and immunology at Louisiana State University Health Shreveport.
The World - Lots of new coronavirus variants that have emerged in recent weeks. Beyond worries over how some of them may impact the pandemic, it’s also prompted concerns over what to name them, and the unintended harms of using shortcuts that link the variant to a specific country.
NPR - A virus that spreads a lot has many chances to mutate, and COVID-19 is doing both in this country. Researchers in the U.S. now say they've found at least seven new variants here.
The New York Times - “There’s clearly something going on with this mutation,” said Jeremy Kamil, a virologist at Louisiana State University Health Shreveport. "It’s unclear whether it makes the variants more contagious. But because the mutation appears in a gene that influences how the virus enters human cells, the scientists are highly suspicious."
Major Research Interest
Human Cytomegalovirus (HCMV)
The Kamil laboratory is focused on human cytomegalovirus (HCMV), a beta-herpesvirus that is a leading cause of birth defects and of life-threatening infections in the immunocompromised. Dr. Kamil’s group employs molecular genetic and pharmacological approaches to tackle basic research questions concerning virus biology. NIH-sponsored projects in the Kamil laboratory concern HCMV cell tropism and the regulation of viral gene expression during myeloid cell differentiation. Our work on viral cell tropism stems from an interest in the viral endoplasmic reticulum (ER)-resident protein UL148, which influences the expression of a viral glycoprotein complex required for cell entry. Intriguingly, UL148 is also an immuneëvasin that impedes cell surface presentation of CD58. Recent findings from the lab indicate that UL148 activates an ancient ER stress response pathway called the unfolded protein response (UPR). The data suggest that UL148 stabilizes a viral glycoprotein called “gO” by interfering with ER-associated degradation (ERAD), a cellular pathway that removes misfolded proteins from the ER. Moreover, the observation that UL148 activates the UPR may prove relevant for understanding immune evasion mechanisms. Dr. Kamil’s areas of expertise include viral replication, viral protein kinases, protein-protein interactions, antiviral drug targets, ERAD, UPR, and proteostasis, cell stress responses, cell-cycle regulation, tumor suppressors, viral glycoproteins, and HCMV cell entry.
Human cytomegalovirus replication, regulation of viral cell tropism Human cytomegalovirus (CMV) is a widespread herpesvirus that infects a majority of the human population. Although CMV does not usually cause disease in healthy people, the virus often crosses the placenta to infect the developing fetus, which can result in serious birth defects. In addition, CMV causes life threatening infections in immunocompromised patients. A major goal of our laboratory is to help develop a better understanding of this complex viral pathogen. In 2015, we identified a virally-encoded glycoprotein, UL148, that impacts the virus’ ability to infect different types of human cells. UL148 modulates the expression of alternative viral glycoprotein complexes that play key roles in cell entry, which likely explains its effects on cell tropism. UL148 resides in the endoplasmic reticulum (ER), an organelle at which proteins destined for secretion are first synthesized, folded, and processed before they can be transported further along the secretory pathway. During infection, UL148 stabilizes a subset of newly synthesized viral glycoproteins before they mature beyond the ER to become incorporated into virions. In particular, UL148 regulates the abundance of multi-subunit glycoprotein complexes that are built upon a viral glycoprotein called glycoprotein H (gH), which is a central component of the cell entry machinery shared by all herpesviruses and an important target for the vaccines. Another set of projects in the lab are focused on trying to understand how the virus regulates its genes during infection. In certain cell types, CMV rapidly undergoes lytic replication, during which huge amounts of viral macromolecules are produced to drive the assembly and release of progeny virions, and the host cell is ultimately destroyed as a result. In other cell types, however, the virus persists in a largely silent state called “latency.” We are currently investigating how viral and cellular protein kinases work together to control whether or not the virus actively replicates.
- Oguntuyo KY, Stevens CS, Hung CT, Ikegame S, Acklin JA, Kowdle SS, Carmichael JC, Chiu HP, Azarm KD, Haas GD, Amanat F, Klingler J, Baine I, Arinsburg S, Bandres JC, Siddiquey MNA, Schilke RM, Woolard MD, Zhang H, Duty AJ, Kraus TA, Moran TM, Tortorella D, Lim JK, Gamarnik AV, Hioe CE, Zolla-Pazner S, Ivanov SS, Kamil JP, Krammer F, Lee B. Quantifying Absolute Neutralization Titers against SARS-CoV-2 by a Standardized Virus Neutralization Assay Allows for Cross-Cohort Comparisons of COVID-19 Sera. mBio. 2021 Feb 16;12(1) PubMed PMID: 33593976. https://mbio.asm.org/content/12/1/e02492-20.long
- Hodcroft EB, Domman DB, Snyder DJ, Oguntuyo K, Van Diest M, Densmore KH, Schwalm KC, Femling J, Carroll JL, Scott RS, Whyte MM, Edwards MD, Hull NC, Kevil CG, Vanchiere JA, Lee B, Dinwiddie DL, Cooper VS, Kamil JP. Emergence in late 2020 of multiple lineages of SARS-CoV-2 Spike protein variants affecting amino acid position 677. medRxiv. 2021 Feb 14; PubMed Central PMCID: PMC7885944. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7885944/
- Zeller M, Gangavarapu K, Anderson C, Smither AR, Vanchiere JA, Rose R, Dudas G, Snyder DJ, Watts A, Matteson NL, Robles-Sikisaka R, Marshall M, Feehan AK, Sabino-Santos G, Bell-Kareem A, Hughes LD, Alkuzweny M, Snarski P, Garcia-Diaz J, Scott RS, Melnik LI, Klitting R, McGraw M, Belda-Ferre P, DeHoff P, Sathe S, Marotz C, Grubaugh N, Nolan DJ, Drouin AC, Genemaras KJ, Chao K, Topol S, Spencer E, Nicholson L, Aigner S, Yeo GW, Farnaes L, Hobbs CA, Laurent LC, Knight R, Hodcroft EB, Khan K, Fusco DN, Cooper VS, Lemey P, Gardner L, Lamers SL, Kamil JP, Garry RF, Suchard MA, Andersen KG. Emergence of an early SARS-CoV-2 epidemic in the United States. medRxiv. 2021 Feb 8; PubMed Central PMCID: PMC7872376. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7872376/
- Oguntuyo KY, Stevens CS, Siddiquey MN, Schilke RM, Woolard MD, Zhang H, Acklin JA, Ikegame S, Hung CT, Lim JK, Cross RW, Geisbert TW, Ivanov SS, Kamil JP, Lee B. In plain sight: the role of alpha-1-antitrypsin in COVID-19 pathogenesis and therapeutics. bioRxiv. 2020 Aug 15; PubMed Central PMCID: PMC7430570. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7430570/
- Zhang H, Read C, Nguyen CC, Siddiquey M, Shang C, Hall CM, von Einem J, and JP Kamil. In Press. 2019. The human cytomegalovirus nonstructural glycoprotein UL148 reorganizes the endoplasmic reticulum. mBio. Preprint: bioRxiv 641068; doi: https://doi.org/10.1101/641068
- Collins-McMillen D, Rak M, Kamil JP, Moorman NJ, and Goodrum FD. 2019. Alternative Promoters Drive Human Cytomegalovirus Reactivation from Latency. 2019. Proc. Natl. Acad. Sci., U.S.A. https://www.pnas.org/content/116/35/17492
- Siddiquey M, Zhang, H, Nguyen CC, Domma A, and JP Kamil. 2018. The human cytomegalovirus ER resident glycoprotein UL148 activates the unfolded protein response. J. Virol. 92 (20): e00896-18. https://jvi.asm.org/content/92/20/e00896-18
- Li G, Nguyen CC, Ryckman BJ, Britt WJ, and JP Kamil. 2015. A viral regulator of glycoprotein complexes contributes to human cytomegalovirus cell tropism. Proc. Natl. Acad. Sci., U.S.A. 112:4471-6. https://www.pnas.org/content/112/14/4471
See more publications at https://pubmed.ncbi.nlm.nih.gov/?term=jeremy+kamil&sort=date