Viviana Simon

Last updated
Viviana A. Simon
Alma mater University of Rostock
Humboldt University
Auguste Viktoria Hospital
Scientific career
Institutions Icahn School of Medicine at Mount Sinai
Thesis Methodische Untersuchung zum Nachweis humanpathogener Herpesviren aus klinischen Materialien mittels Polymerase-Ketten-Reaktion  (1997)

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.

Contents

Early life and education

Simon completed her medical training at the Vivantes Auguste Viktoria Hospital in Berlin. She earned her doctoral degree at the University of Rostock, where she researched herpesviridae using a polymerase chain reaction. [1] Simon started her career at Rockefeller University.

Research and career

Simon studies the biology of HIV and which aspects of the infection make it difficult to treat or cure. [2] She has studied the modes of action of HIV restriction factors as well as the escape of lentiviral vectors. Simon investigates a group of genes that can restrict the replication of exo- and endogenous viruses. [3] APOBEC is a family of cytidine deaminases (enzymes) that are expressed in cells that are susceptible to HIV-1. [4] She has shown that APOBEC Complex 3G (C3G) is active against HIV-1 and HIV-2, as well as LTR retrotransposon and Hepatitis B. Simon has demonstrated that the HIV Viral infectivity factor protein counters the antiretroviral activity of APOBEC3G by inducing its degradation by proteasome. [4] [5] She has also generated a HIV/SIV Viral infectivity factor (Vif)-APOlipoprotein B mRNA-Editing Catalytic polypeptide (APOBEC) interface model. [2] She believes that restriction mediated by APOBEC cytidine deaminase causes the diversification of HIV-1. [3]

Working with Florian Krammer, a colleague in the Department of Microbiology at the Icahn School of Medicine at Mount Sinai, Simon created an antibody test that can determine immunity to Coronavirus disease 2019. [6] The test makes use of an serological enzyme-linked-immuno-sorbent-assays (ELISA), which measure the presence of coronavirus antibodies in the blood. [6] The test can tell whether someone has ever had coronavirus disease, which allows researchers to better understand which members of the population do or do not have the disease. Coronavirus disease patients who have recently recovered have high levels of antibodies in the blood, and this convalescent plasma can be used to treat critically ill patients. [7] Antibody testing can also support medical professionals in deciding which staff take on the riskiest tasks (for example, intubating infected patients) as they can identify healthcare workers who have been exposed and are immune. [6]

Selected publications

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">Seroconversion</span> Development of specific antibodies in the blood serum as a result of infection or immunization

In immunology, seroconversion is the development of specific antibodies in the blood serum as a result of infection or immunization, including vaccination. During infection or immunization, antigens enter the blood, and the immune system begins to produce antibodies in response. Before seroconversion, the antigen itself may or may not be detectable, but the antibody is absent. During seroconversion, the antibody is present but not yet detectable. After seroconversion, the antibody is detectable by standard techniques and remains detectable unless the individual seroreverts. Seroreversion, or loss of antibody detectability, can occur due to weakening of the immune system or waning antibody concentration over time. Seroconversion refers the production of specific antibodies against specific antigens, meaning that a single infection could cause multiple waves of seroconversion against different antigens. Similarly, a single antigen could cause multiple waves of seroconversion with different classes of antibodies. For example, most antigens prompt seroconversion for the IgM class of antibodies first, and subsequently the IgG class.

<i>Feline immunodeficiency virus</i> Species of virus

Feline immunodeficiency virus (FIV) is a Lentivirus that affects cats worldwide, with 2.5% to 4.4% of felines being infected.

<span class="mw-page-title-main">Activation-induced cytidine deaminase</span> Enzyme that creates mutations in DNA

Activation-induced cytidine deaminase, also known as AICDA, AID and single-stranded DNA cytosine deaminase, is a 24 kDa enzyme which in humans is encoded by the AICDA gene. It creates mutations in DNA by deamination of cytosine base, which turns it into uracil. In other words, it changes a C:G base pair into a U:G mismatch. The cell's DNA replication machinery recognizes the U as a T, and hence C:G is converted to a T:A base pair. During germinal center development of B lymphocytes, AID also generates other types of mutations, such as C:G to A:T. The mechanism by which these other mutations are created is not well understood. It is a member of the APOBEC family.

<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.

<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.

Human Immunodeficiency Virus (HIV) and Hepatitis C Virus (HCV) co-infection is a multi-faceted, chronic condition that significantly impacts public health. According to the World Health Organization (WHO), 2 to 15% of those infected with HIV are also affected by HCV, increasing their risk of morbidity and mortality due to accelerated liver disease. The burden of co-infection is especially high in certain high-risk groups, such as intravenous drug users and men who have sex with men. These individuals who are HIV-positive are commonly co-infected with HCV due to shared routes of transmission including, but not limited to, exposure to HIV-positive blood, sexual intercourse, and passage of the Hepatitis C virus from mother to infant during childbirth.

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.

Long-term nonprogressors (LTNPs), sometimes also called elite controllers, are individuals infected with HIV, who maintain a CD4 count greater than 500 without antiretroviral therapy with a detectable viral load. Many of these patients have been HIV positive for 30 years without progressing to the point of needing to take medication in order not to develop AIDS. They have been the subject of a great deal of research, since an understanding of their ability to control HIV infection may lead to the development of immune therapies or a therapeutic vaccine. The classification "Long-term non-progressor" is not permanent, because some patients in this category have gone on to develop AIDS.

<span class="mw-page-title-main">PSME4</span> Protein found in humans

Proteasome activator complex subunit 4 is a protein that in humans is encoded by the PSME4 gene.

<span class="mw-page-title-main">APOBEC3F</span> Protein-coding gene in the species Homo sapiens

DNA dC->dU-editing enzyme APOBEC-3F is a protein that in humans is encoded by the APOBEC3F gene.

<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.

<span class="mw-page-title-main">APOBEC3A</span> Protein-coding gene in the species Homo sapiens

Apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like 3A, also known as APOBEC3A, or A3A is a gene of the APOBEC3 family found in humans, non-human primates, and some other mammals. It is a single-domain DNA cytidine deaminase with antiviral effects. While other members of the family such as APOBEC3G are believed to act by editing ssDNA by removing an amino group from cytosine in DNA, introducing a cytosine to uracil change which can ultimately lead to a cytosine to thymine mutation, one study suggests that APOBEC3A can inhibit parvoviruses by another mechanism. The cellular function of APOBEC3A is likely to be the destruction of foreign DNA through extensive deamination of cytosine.Stenglein MD, Burns MB, Li M, Lengyel J, Harris RS. "APOBEC3 proteins mediate the clearance of foreign DNA from human cells". Nature Structural & Molecular Biology. 17 (2): 222–9. doi:10.1038/nsmb.1744. PMC 2921484. PMID 20062055.

<span class="mw-page-title-main">APOBEC3B</span> Protein-coding gene in the species Homo sapiens

Probable DNA dC->dU-editing enzyme APOBEC-3B is a protein that in humans is encoded by the APOBEC3B gene.

<span class="mw-page-title-main">APOBEC3D</span> Protein-coding gene in the species Homo sapiens

Probable DNA dC->dU-editing enzyme APOBEC-3D is a protein that in humans is encoded by the APOBEC3D 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.

A neutralizing antibody (NAb) is an antibody that defends a cell from a pathogen or infectious particle by neutralizing any effect it has biologically. Neutralization renders the particle no longer infectious or pathogenic. Neutralizing antibodies are part of the humoral response of the adaptive immune system against viruses, intracellular bacteria and microbial toxin. By binding specifically to surface structures (antigen) on an infectious particle, neutralizing antibodies prevent the particle from interacting with its host cells it might infect and destroy.

<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.

<span class="mw-page-title-main">Kataegis</span>

In molecular biology, kataegis describes a pattern of localized hypermutations identified in some cancer genomes, in which a large number of highly patterned basepair mutations occur in a small region of DNA. The mutational clusters are usually several hundred basepairs long, alternating between a long range of C→T substitutional pattern and a long range of G→A substitutional pattern. This suggests that kataegis is carried out on only one of the two template strands of DNA during replication. Compared to other cancer-related mutations, such as chromothripsis, kataegis is more commonly seen; it is not an accumulative process but likely happens during one cycle of replication.

Nicole M. Bouvier is an American physician who is Professor of Medicine at Icahn School of Medicine at Mount Sinai. Her research considers the environmental and viral factors that impact respiratory transmission of influenza viruses.

References

  1. Simon, Viviana (1998). Methodische Untersuchung zum Nachweis humanpathogener Herpesviren aus klinischen Materialien mittels Polymerase-Ketten-Reaktion (Thesis) (in German). Aachen: Shaker. OCLC   1072722256.
  2. 1 2 "Dr. Viviana Simon | OyaGen". www.oyageninc.com. Retrieved 2020-03-28.
  3. 1 2 "Simon Lab | exploring virus host interactions". labs.icahn.mssm.edu. Retrieved 2020-03-28.
  4. 1 2 Binka, M.; Ooms, M.; Steward, M.; Simon, V. (2012-01-01). "The Activity Spectrum of Vif from Multiple HIV-1 Subtypes against APOBEC3G, APOBEC3F, and APOBEC3H". Journal of Virology. 86 (1): 49–59. doi:10.1128/JVI.06082-11. ISSN   0022-538X. PMC   3255910 . PMID   22013041.
  5. Mulder, L. C. F.; Harari, A.; Simon, V. (2008-04-07). "Cytidine deamination induced HIV-1 drug resistance". Proceedings of the National Academy of Sciences. 105 (14): 5501–5506. Bibcode:2008PNAS..105.5501M. doi: 10.1073/pnas.0710190105 . ISSN   0027-8424. PMC   2291111 . PMID   18391217.
  6. 1 2 3 "Mount Sinai Developing an "End-to-End" Diagnostics Solution for COVID-19 That Incorporates Diagnosis, Treatment Selection, and Monitoring of Disease Course | Mount Sinai - New York". Mount Sinai Health System. Retrieved 2020-03-28.
  7. Tanne, Janice Hopkins (2020-03-26). "Covid-19: FDA approves use of convalescent plasma to treat critically ill patients". BMJ. 368: m1256. doi: 10.1136/bmj.m1256 . ISSN   1756-1833. PMID   32217555.