Angela Rasmussen | |
|---|---|
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| Born | Angela Lynn Rasmussen |
| Nationality | American |
| Education |
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| Spouse | Alexei Krasnoselsky |
| Scientific career | |
| Fields | Virology |
| Institutions | |
| Thesis | Development of a Mouse Model of Rhinovirus Infection (2009) |
| Doctoral advisor | Vincent Racaniello |
| Website | angelarasmussen |
Angela Lynn Rasmussen is an American virologist at the Vaccine and Infectious Disease Organization at the University of Saskatchewan in Canada. [1]
During graduate school, Rasmussen worked in the laboratory of Vincent Racaniello where she developed a mouse model of rhinovirus infection in order to better understand the pathogenesis of illnesses caused by the virus, such as the common cold. [2]
Rasmussen joined the faculty at Columbia University Mailman School of Public Health, where she worked as an associate research scientist. There, she studied how hosts respond to infectious diseases like SARS and Ebola. [3]
During her tenure at University of Washington, she studied the response of mice to ebolavirus infection. The traditional mouse model, which is derived from a uniform genetic background, dies after being infected with the virus before the classical symptoms of the disease show up, making it difficult to study the pathogenesis of the virus. [4] Instead, Rasmussen and her team took advantage of a genetically diverse collection of mice, known as the Collaborative Cross; when infecting this collection of mice with ebolavirus, they observed a wide range of disease outcomes, ranging from complete resistance to the virus to severe hemorrhagic fever. [4] They concluded that the genetic background of the mice therefore plays a role in their susceptibility to the virus. [5] By understanding which genes in mice affect the course of infection, they can better determine which genes make humans more susceptible to the disease—and why some humans die, while others survive. [6] [7]
Rasmussen continued work on understanding genetic susceptibility with Ebola at Columbia University. There, she identified a gene expression signature that may predict the severity of Ebola infection. [8] Rasmussen and collaborators have also used human cell lines to investigate the course of infection. Upon infection, ebolavirus first targets macrophages, or white blood cells that engulf and clear away pathogens, which in turn release inflammatory cytokines that recruit more immune cells to the site of the infection to kill off infected tissue. If cytokine release goes unchecked it can lead to a profound inflammatory response—known as a cytokine storm—that can kill off healthy tissue, as is the case with an ebolavirus infection. [9] She and collaborators found that inhibiting the inflammatory response of virus-infected macrophages could be a potential therapeutic target, preventing a cytokine storm from occurring. [10]
Rasmussen's work investigating the heterogeneity in Ebola infections has translated into developing hypotheses around why some COVID-19 cases are worse than others. [11]
She has also been on the frontlines of communication around the novel coronavirus and COVID-19, applying her expertise in correspondence with the popular press to interpret preliminary results around how long immunity to the virus may last, how effective potential drugs may be in treating the disease, and whether biological sex plays a role in the severity of the disease. [12] [13] [14] Given the breakneck pace at which preliminary research results have been released—for example, through preprints—she has urged caution in reporting research findings too quickly and without the proper caveats to ensure the public is not misinformed. [15]
Rasmussen has served on a National Institutes of Health working group on "Changing the Culture to End Sexual Harassment" in biomedical research fields. [16] She formerly served on the leadership of the organization MeTooSTEM, before stepping down in February 2020 due to concerns with the organization's leadership and allegations of abuse. [17] [18]
The rhinovirus is a positive-sense, single-stranded RNA virus belonging to the genus Enterovirus in the family Picornaviridae. Rhinovirus is the most common viral infectious agent in humans and is the predominant cause of the common cold.
Poliovirus, the causative agent of polio, is a serotype of the species Enterovirus C, in the family of Picornaviridae. There are three poliovirus serotypes: types 1, 2, and 3.
An asymptomatic carrier is a person or other organism that has become infected with a pathogen, but shows no signs or symptoms.
The genus Ebolavirus is a virological taxon included in the family Filoviridae, order Mononegavirales. The members of this genus are called ebolaviruses, and encode their genome in the form of single-stranded negative-sense RNA. The six known virus species are named for the region where each was originally identified: Bundibugyo ebolavirus, Reston ebolavirus, Sudan ebolavirus, Taï Forest ebolavirus, Zaire ebolavirus, and Bombali ebolavirus. The last is the most recent species to be named and was isolated from Angolan free-tailed bats in Sierra Leone. Each species of the genus Ebolavirus has one member virus, and four of these cause Ebola virus disease (EVD) in humans, a type of hemorrhagic fever having a very high case fatality rate. The Reston virus has caused EVD in other primates. Zaire ebolavirus has the highest mortality rate of the ebolaviruses and is responsible for the largest number of outbreaks of the six known species of the genus, including the 1976 Zaire outbreak and the outbreak with the most deaths (2014).
Superantigens (SAgs) are a class of antigens that result in excessive activation of the immune system. Specifically they cause non-specific activation of T-cells resulting in polyclonal T cell activation and massive cytokine release. Superantigens act by binding to the MHC proteins on antigen-presenting cells (APCs) and to the TCRs on their adjacent helper T-cells, bringing the signaling molecules together, and thus leading to the activation of the T-cells, regardless of the peptide displayed on the MHC molecule. SAgs are produced by some pathogenic viruses and bacteria most likely as a defense mechanism against the immune system. Compared to a normal antigen-induced T-cell response where 0.0001-0.001% of the body's T-cells are activated, these SAgs are capable of activating up to 20% of the body's T-cells. Furthermore, Anti-CD3 and Anti-CD28 antibodies (CD28-SuperMAB) have also shown to be highly potent superantigens.
Viral pathogenesis is the study of the process and mechanisms by which viruses cause diseases in their target hosts, often at the cellular or molecular level. It is a specialized field of study in virology.
Itaconic acid (also termed methylidenesuccinic acid and 2-methylidenebutanedioic acid) is a fatty acid containing five carbons (carbon notated as C), two of which are in carboxyl groups (notated as -CO2H) and two others which are double bonded together (i.e., C=C). (itconic acid's chemical formula is C5H6O4, see adjacent figure and dicarboxylic acids). At the stronly acidic pH levels below 2, itaconic acid is electrically neutral because both of its carboxy residues are bound to hydrogen (notated as H); at the basic pH levels above 7, it is double negatively charged because both of its carboxy residues are not bound to H, i.e., CO2 (its chemical formula is C5H4O42-); and at the acidic pH's between 2 and 7, it exists as a mixture with none, one, or both of its carboxy residues being bound to hydrogen. In the cells and most tissue fluids of living animals, which generally have pH levels above 7, itaconic acid exists almost exclusively in its double negatively charged form; this form of itaconic acid is termed itaconate. Itaconic acid and itaconate exist as cis and trans isomers (see cis–trans isomerism). Cis-itaconic acid and cis-itaconate isomers have two H's bound to one carbon and two residues (noted as R) bound to the other carbon in the double bound (i.e., H2C=CR2) whereas trans-itaconaic acdi and trans-itaconate have one H and one R residue bound to each carbon of the double bound. The adjacent figure shows the cis form of itaconaic acid. Notably, cis-aconitic acid spontaneously converts to its thermodynamicall more stable (see chemical stability) isomer, trans-aconitic acid, at pH levels below pH 7. The medical literature commonly uses the terms itaconic acid and itaconate without identifying them as their cis isomers. This practice is used here, i.e., itaconic acid and itaconate refer to their cis isomers whereas the trans isomer of itaconate (which have been detected in fungi but not animal species) is specifically termed trans-itaconate (trans-itaconic acid is not mentioned here).
Interleukin-23 subunit alpha is a protein that in humans is encoded by the IL23A gene. The protein is also known as IL-23p19. It is one of the two subunits of the cytokine Interleukin-23.
Interleukin-29 (IL-29) is a cytokine and it belongs to type III interferons group, also termed interferons λ (IFN-λ). IL-29 plays an important role in the immune response against pathogenes and especially against viruses by mechanisms similar to type I interferons, but targeting primarily cells of epithelial origin and hepatocytes.
Interleukin 19 (IL-19) is an immunosuppressive protein that belongs to the IL-10 cytokine subfamily.
Toll-like receptor 7, also known as TLR7, is a protein that in humans is encoded by the TLR7 gene. Orthologs are found in mammals and birds. It is a member of the toll-like receptor (TLR) family and detects single stranded RNA.
Vincent R. Racaniello is a Higgins Professor in the Department of Microbiology and Immunology at Columbia University's College of Physicians and Surgeons. He is a co-author of a textbook on virology, Principles of Virology.
OX-2 membrane glycoprotein, also named CD200 is a human protein encoded by the CD200 gene. CD200 gene is in human located on chromosome 3 in proximity to genes encoding other B7 proteins CD80/CD86. In mice CD200 gene is on chromosome 16.
Toll-like receptor 11 (TLR11) is a protein that in mice and rats is encoded by the gene TLR11, whereas in humans it is represented by a pseudogene. TLR11 belongs to the toll-like receptor (TLR) family and the interleukin-1 receptor/toll-like receptor superfamily. In mice, TLR11 has been shown to recognise (bacterial) flagellin and (eukaryotic) profilin present on certain microbes, it helps propagate a host immune response. TLR11 plays a fundamental role in both the innate and adaptive immune responses, through the activation of Tumor necrosis factor-alpha, the Interleukin 12 (IL-12) response, and Interferon-gamma (IFN-gamma) secretion. TLR11 mounts an immune response to multiple microbes, including Toxoplasma gondii, Salmonella species, and uropathogenic E. coli, and likely many other species due to the highly conserved nature of flagellin and profilin.
C-type lectin domain family 5 member A (CLEC5A), also known as C-type lectin superfamily member 5 (CLECSF5) and myeloid DAP12-associating lectin 1 (MDL-1) is a C-type lectin that in humans is encoded by the CLEC5A gene.
Chronic Mycoplasma pneumonia and Chlamydia pneumonia infections are associated with the onset and exacerbation of asthma. These microbial infections result in chronic lower airway inflammation, impaired mucociliary clearance, an increase in mucous production and eventually asthma. Furthermore, children who experience severe viral respiratory infections early in life have a high possibility of having asthma later in their childhood. These viral respiratory infections are mostly caused by respiratory syncytial virus (RSV) and human rhinovirus (HRV). Although RSV infections increase the risk of asthma in early childhood, the association between asthma and RSV decreases with increasing age. HRV on the other hand is an important cause of bronchiolitis and is strongly associated with asthma development. In children and adults with established asthma, viral upper respiratory tract infections (URIs), especially HRVs infections, can produce acute exacerbations of asthma. Thus, Chlamydia pneumoniae, Mycoplasma pneumoniae and human rhinoviruses are microbes that play a major role in non-atopic asthma.
Ebola, also known as Ebola virus disease (EVD) and Ebola hemorrhagic fever (EHF), is a viral hemorrhagic fever in humans and other primates, caused by ebolaviruses. Symptoms typically start anywhere between two days and three weeks after infection. The first symptoms are usually fever, sore throat, muscle pain, and headaches. These are usually followed by vomiting, diarrhoea, rash and decreased liver and kidney function, at which point some people begin to bleed both internally and externally. It kills between 25% and 90% of those infected – about 50% on average. Death is often due to shock from fluid loss, and typically occurs between six and 16 days after the first symptoms appear. Early treatment of symptoms increases the survival rate considerably compared to late start. An Ebola vaccine was approved by the US FDA in December 2019.
Zaire ebolavirus, more commonly known as Ebola virus, is one of six known species within the genus Ebolavirus. Four of the six known ebolaviruses, including EBOV, cause a severe and often fatal hemorrhagic fever in humans and other mammals, known as Ebola virus disease (EVD). Ebola virus has caused the majority of human deaths from EVD, and was the cause of the 2013–2016 epidemic in western Africa, which resulted in at least 28,646 suspected cases and 11,323 confirmed deaths.
Sabra Klein is an American microbiologist who is a Professor of Molecular Microbiology and Immunology at the Johns Hopkins Bloomberg School of Public Health. Her research considers how sex and gender impact the immune system. During the COVID-19 pandemic, Klein investigated why men and women have different COVID-19 outcomes.
A viral vector vaccine is a vaccine that uses a viral vector to deliver genetic material (DNA) that can be transcribed by the recipient's host cells as mRNA coding for a desired protein, or antigen, to elicit an immune response. As of April 2021, six viral vector vaccines, four COVID-19 vaccines and two Ebola vaccines, have been authorized for use in humans.
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