OyaGen

Last updated
OyaGen, Inc.
Type Private
Industry
Founded Rochester, New York 2003
FounderHarold Smith
Headquarters,
US
Area served
Global
Key people
ProductsAntiviral therapeutic lead compounds
Services
Number of employees
6
Website oyageninc.com

OyaGen is a Rochester, New York-based startup company that is focused on developing treatments for HIV. The company was founded in 2003 by Harold Smith, a professor of biochemistry and biophysics at the University of Rochester. [1] [2] OyaGen was founded on research conducted by Smith and Hui Zang, an HIV researcher at Thomas Jefferson University. [1]

Contents

Research

OyaGen's research has focused on developing drug-based treatments for HIV and the company has three lead HIV drugs based upon editing enzymes in preclinical development. [3] The company is exploring ways to prevent HIV from disabling the production of APOBEC3G (A3G), a naturally occurring editing enzyme that stops HIV from replicating. [1] A3G combats HIV infection by interacting with and mutating the virus' RNA. [3] [4] The mutations genetically damage the virus protein and render HIV unable to replicate which halts the spread of the virus. [3] [4] In laboratory testing, OyaGen was able to use drug therapy to shield A3G from HIV, which allowed A3G to function normally and halt the spread of the virus. [5]

The company is also researching drugs that protect A3G from viral infectivity factor (ViF). [4] [6] ViF is a protein created by HIV that "tricks" the body into destroying A3G by binding to it. [4] [6] Interfering with ViF's ability to bind to A3G can effectively block HIV replication. [7] OyaGen is researching several compounds that prevent ViF from disabling A3G, including A3G agonists, ViF destabilizers and ViF dimerization antagonists. [7] [8]

Funding

The company received seed funding from Trillium Group's University Technology Fund and the University of Rochester Medical Center. [1] [5] It has also received funding from the New York State Retirement Common Fund's Private Equity Program. [9] [10] The New York State Retirement Common Fund has invested approximately $1.4 million in the company since 2006. [10] OyaGen's research has also been underwritten in part by the National Institutes of Health, which awarded grants to the company in 2011, [11] 2012, [12] and 2013. [13]

See also

Related Research Articles

<span class="mw-page-title-main">HIV</span> Human retrovirus, cause of AIDS

The human immunodeficiency viruses (HIV) are two species of Lentivirus that infect humans. Over time, they cause acquired immunodeficiency syndrome (AIDS), a condition in which progressive failure of the immune system allows life-threatening opportunistic infections and cancers to thrive. Without treatment, average survival time after infection with HIV is estimated to be 9 to 11 years, depending on the HIV subtype.

<span class="mw-page-title-main">Retrovirus</span> Family of viruses

A retrovirus is a type of virus that inserts a DNA copy of its RNA genome into the DNA of a host cell that it invades, thus changing the genome of that cell. After invading a host cell's cytoplasm, the virus uses its own reverse transcriptase enzyme to produce DNA from its RNA genome, the reverse of the usual pattern, thus retro (backwards). The new DNA is then incorporated into the host cell genome by an integrase enzyme, at which point the retroviral DNA is referred to as a provirus. The host cell then treats the viral DNA as part of its own genome, transcribing and translating the viral genes along with the cell's own genes, producing the proteins required to assemble new copies of the virus. Many retroviruses cause serious diseases in humans, other mammals, and birds.

<span class="mw-page-title-main">HIV vaccine development</span> In-progress vaccinations that may prevent or treat HIV infections

An HIV vaccine is a potential vaccine that could be either a preventive vaccine or a therapeutic vaccine, which means it would either protect individuals from being infected with HIV or treat HIV-infected individuals.

Lentivirus is a genus of retroviruses that cause chronic and deadly diseases characterized by long incubation periods, in humans and other mammalian species. The genus includes the human immunodeficiency virus (HIV), which causes AIDS. Lentiviruses are distributed worldwide, and are known to be hosted in apes, cows, goats, horses, cats, and sheep as well as several other mammals.

The genome and proteins of HIV (human immunodeficiency virus) have been the subject of extensive research since the discovery of the virus in 1983. "In the search for the causative agent, it was initially believed that the virus was a form of the Human T-cell leukemia virus (HTLV), which was known at the time to affect the human immune system and cause certain leukemias. However, researchers at the Pasteur Institute in Paris isolated a previously unknown and genetically distinct retrovirus in patients with AIDS which was later named HIV." Each virion comprises a viral envelope and associated matrix enclosing a capsid, which itself encloses two copies of the single-stranded RNA genome and several enzymes. The discovery of the virus itself occurred two years following the report of the first major cases of AIDS-associated illnesses.

<span class="mw-page-title-main">Viral infectivity factor</span> Protein found in lentiviruses

Viral infectivity factor, or Vif, is an accessory protein found in HIV and other lentiviruses. Its role is to disrupt the antiviral activity of the human enzyme APOBEC by targeting it for ubiquitination and cellular degradation. APOBEC is a cytidine deaminase enzyme that mutates viral nucleic acids.

Human foamy virus (HFV) is a retrovirus and specifically belongs to the genus Spumavirus. The spumaviruses are complex and significantly different from the other six genera of retroviruses in several ways. The foamy viruses derive their name from the characteristic ‘foamy’ appearance of the cytopathic effect (CPE) induced in the cells. Foamy virus in humans occurs only as a result of zoonotic infection.

<span class="mw-page-title-main">APOBEC3G</span> Protein and coding gene in humans

APOBEC3G is a human enzyme encoded by the APOBEC3G gene that belongs to the APOBEC superfamily of proteins. This family of proteins has been suggested to play an important role in innate anti-viral immunity. APOBEC3G belongs to the family of cytidine deaminases that catalyze the deamination of cytidine to uridine in the single stranded DNA substrate. The C-terminal domain of A3G renders catalytic activity, several NMR and crystal structures explain the substrate specificity and catalytic activity.

HIV superinfection is a condition in which a person with an established human immunodeficiency virus infection acquires a second strain of HIV, often of a different subtype. These can form a recombinant strain that co-exists with the strain from the initial infection, as well from reinfection with a new virus strain, and may cause more rapid disease progression or carry multiple resistances to certain HIV medications.

Visna-maedi virus from the genus Lentivirus and subfamily Orthoretrovirinae, is a retrovirus that causes encephalitis and chronic pneumonitis in sheep. It is known as visna when found in the brain, and maedi when infecting the lungs. Lifelong, persistent infections in sheep occur in the lungs, lymph nodes, spleen, joints, central nervous system, and mammary glands; The condition is sometimes known as ovine progressive pneumonia (OPP), particularly in the United States, or Montana sheep disease. White blood cells of the monocyte/macrophage lineage are the main target of the virus.

<span class="mw-page-title-main">HIV-1 protease</span> Enzyme involved with peptide bond hydrolysis in retroviruses

HIV-1 protease (PR) is a retroviral aspartyl protease (retropepsin), an enzyme involved with peptide bond hydrolysis in retroviruses, that is essential for the life-cycle of HIV, the retrovirus that causes AIDS. HIV protease cleaves newly synthesized polyproteins at nine cleavage sites to create the mature protein components of an HIV virion, the infectious form of a virus outside of the host cell. Without effective HIV protease, HIV virions remain uninfectious.

<span class="mw-page-title-main">APOBEC3C</span> Protein-coding gene in humans

DNA dC->dU-editing enzyme APOBEC-3C is a protein that in humans is encoded by the APOBEC3C gene.

Intrinsic immunity refers to a set of cellular-based anti-viral defense mechanisms, notably genetically encoded proteins which specifically target eukaryotic retroviruses. Unlike adaptive and innate immunity effectors, intrinsic immune proteins are usually expressed at a constant level, allowing a viral infection to be halted quickly. Intrinsic antiviral immunity refers to a form of innate immunity that directly restricts viral replication and assembly, thereby rendering a cell non-permissive to a specific class or species of viruses. Intrinsic immunity is conferred by restriction factors preexisting in certain cell types, although these factors can be further induced by virus infection. Intrinsic viral restriction factors recognize specific viral components, but unlike other pattern recognition receptors that inhibit viral infection indirectly by inducing interferons and other antiviral molecules, intrinsic antiviral factors block viral replication immediately and directly.

<span class="mw-page-title-main">Virus</span> Infectious agent that replicates in cells

A virus is a submicroscopic infectious agent that replicates only inside the living cells of an organism. Viruses infect all life forms, from animals and plants to microorganisms, including bacteria and archaea. Since Dmitri Ivanovsky's 1892 article describing a non-bacterial pathogen infecting tobacco plants and the discovery of the tobacco mosaic virus by Martinus Beijerinck in 1898, more than 11,000 of the millions of virus species have been described in detail. Viruses are found in almost every ecosystem on Earth and are the most numerous type of biological entity. The study of viruses is known as virology, a subspeciality of microbiology.

<span class="mw-page-title-main">APOBEC3H</span> Protein-coding gene in the species Homo sapiens

DNA dC->dU-editing enzyme APOBEC-3H, also known as Apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like 3H or APOBEC-related protein 10, is a protein that in humans is encoded by the APOBEC3H gene.

Vpx is a virion-associated protein encoded by human immunodeficiency virus type 2 HIV-2 and most simian immunodeficiency virus (SIV) strains, but that is absent from HIV-1. It is similar in structure to the protein Vpr that is carried by SIV and HIV-2 as well as HIV-1. Vpx is one of five accessory proteins carried by lentiviruses that enhances viral replication by inhibiting host antiviral factors.

<span class="mw-page-title-main">HIV/AIDS research</span> Field of immunology research

HIV/AIDS research includes all medical research that attempts to prevent, treat, or cure HIV/AIDS, as well as fundamental research about the nature of HIV as an infectious agent and AIDS as the disease caused by HIV.

<span class="mw-page-title-main">Harold Smith (scientist)</span>

Harold C. Smith Jr. is an American scientist, researcher, professor, founder and CEO of OyaGen. Smith has written over 100 publications on his research in RNA editing, AIDS, oncology, and immunodeficiency, among others.

Paul Darren Bieniasz is a British-American virologist whose main area of research is HIV/AIDS. He is currently a professor of retrovirology at the Rockefeller University. He received the 2015 KT Jeang Retrovirology Prize and the 2010 Eli Lilly and Company Research Award. Bieniasz has been a Howard Hughes Medical Institute investigator since 2008.

Viviana Simon is a Professor of Microbiology at the Icahn School of Medicine at Mount Sinai (ISMMS). She is a member of the ISMMS Global Health and Emerging Pathogens Institute. Her research considers viral-host interactions and the mode of action of retroviral restriction factors. During the COVID-19 pandemic, Simon developed an antibody test that can determine immunity to Coronavirus disease 2019.

References

  1. 1 2 3 4 Michael Wentzel (12 January 2004). "UR Invests in Anti-HIV Startup". Rochester Chronicle.
  2. Thomas Adams (16 September 2013). "Henrietta firm OyaGen receives $150,000 investment". Rochester Business Journal. Retrieved 1 June 2014.
  3. 1 2 3 Gail Dutton (1 October 2013). "HIV Researchers Seek a Potential Cure". Genetic Engineering & Biotechnology News. Retrieved 1 June 2014.
  4. 1 2 3 4 James H Miller; Vlad Presnyak; Harold C Smith (27 July 2007). "The dimerization domain of HIV-1 viral infectivity factor Vif is required to block virion incorporation of APOBEC3G". Department of Biochemistry and Biophysics, 601 Elmwood Ave, Rochester, NY 14642, USA. Retrovirology (published 24 November 2007). 4 (1): 81. doi:10.1186/1742-4690-4-81. PMC   2222665 . PMID   18036235.
  5. 1 2 Tom Tobin (2 April 2010). "Will health reform be shot in arm for biotech firms?". Rochester Democrat & Chronicle. Retrieved 1 June 2014.
  6. 1 2 Nishad Majmudar (1 September 2005). "OyaGen blazing path toward anti-AIDS drug". Rochester Democrat & Chronicle. Retrieved 28 May 2014.
  7. 1 2 Mariel Selbovitz; David Miller (5 March 2014). "The Deeper End of the Ocean: Host restrictive factors create research excitement". A&U: America's Aids Magazine. p. 52. Retrieved 28 May 2014.
  8. Salter, Jason D.; Morales, Guillermo A.; Smith, Harold C. (11 August 2014). "Structural insights for HIV-1 therapeutic strategies targeting Vif". Trends in Biochemical Sciences. CellPress. 39 (9): 373–380. doi:10.1016/j.tibs.2014.07.001. PMC   4511815 . PMID   25124760.
  9. "State pension fund invests in Rochester venture". The Daily Record. 24 September 2010. Retrieved 1 June 2014.
  10. 1 2 "DiNapoli Tours OyaGen, Touts State Pension Fund". Rochester Homepage. 16 September 2013. Retrieved 1 June 2014.
  11. "Awards summary for Fiscal Year". Research Portfolio Online Reporting Tools. 2011. Retrieved 1 June 2014.
  12. "Awards summary for Fiscal Year". Research Portfolio Online Reporting Tools. 2012. Retrieved 1 June 2014.
  13. "Awards summary for Fiscal Year". Research Portfolio Online Reporting Tools. 2013. Retrieved 1 June 2014.

Further reading