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People infected with SARS-Cov-2(the cornavirus that causes covid-19) can show an array of different symptoms and comlications. One complication occurs in the same patients is the development of blood clots throughout the body. Thevirus can infect endothelial cells.
How are endothelia involved with blood clotting?
If you were to design a pharmaceutical (medication) taht reduced blood clotting, how might it work?
There are many ways to approach this question. Please mention at least one SPECIFIC REACTION in your explanation.
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- When an antibody binds to the spike protein of SARS-CoV-2, it may block access of the spike protein to the ACE2 protein on human cells. This is one way an antibody can prevent the virus from attaching to and getting inside of human cells. But antibodies can do more than just block virus entry. Due to the symmetrical structure of the immunoglobulin molecule, it can bind to two antigen molecules simultaneously, like this: As a result, antibodies can cross-link multiple viruses in a three-dimensional network. Using this diagram as a starting point, draw several additional viruses and antibodies to illustrate what a cross-linked antigen-antibody complex might look like.“The SARS Coronavirus Type 2 (SARS-CoV-2) is known to cause respiratory tract infections and has been isolated from several bodily fluids. Although there is still no concrete evidence of an animal reservoir, the World Health Organization has prematurely classified the Coronavirus disease (COVID-19), caused by SARS-CoV-2, as a zoonotic disease”.2.1 In your own view, discuss the possible route of transmission of SARS-CoV-2 from an animalsource to humansIf antibody responses are not elicited by a Covid-19 vaccine, are there other types of immune response that could provide protection from the SARS-Co-V2 virus following vaccination? Explain why or why not.
- We now have at least three SARS-CoV-2/COVID-19 vaccines approved by the FDA for use in the United States. These vaccines cause cells in the body to make the spike protein that is on the surface of the virus, and subsequently, stimulate an antibody response to this antigen. A. What do these antibodies do to prevent infection by SARS-CoV-2? How do they interact with the virus particles? B. Which kind of cells in the immune system are responsible for synthesizing these antibodies?When vesicular stomatitis virus (VSV) is used to infect mice via footpad injection, viral particles are trapped in the draining lymph node (the popliteal lymph node) within 5 minutes of injection. These viral particles are then retained in the lymph node for many hours, where they can be visualized on cells that are interacting with B cells. The cells retaining the viral particles in the lymph node are not tissue-resident dendritic cells that have migrated to the lymph node with the virus, as this process takes much longer than 5 minutes. In which region of the lymph node would you expect to find the trapped viral particles and on which cells?Given your current understanding of what we have learned about the SARS-CoV-2 virus and the disease it causes, CoVID-19, which of the following recommended practices make sense, based on the scientific knowledge you now have? Explain your answer for each: Remaining 6 feet away from other people, wearing non-medical masks, screening people for fevers before they can board planes or enter schools, not gathering in large groups.
- Let’s say there are two closely related viruses, let’s call them Guernsey virus and Micro virus. These two viruses only infect epithelial cells. Their surface antigens are sufficiently similar that there are a number of shared epitopes between the two viruses. Choose one of the following: A) If you get infected and successfully recover from one virus, it’s quite possible that you’ll have neutralizing antibodies against the other. B) If you get infected and successfully recover from one virus, you’ll still be susceptible to the other one because the antigens aren’t exactly the same. C) If you get infected and successfully recover from one virus, it’s likely that getting infected with the other virus will be worse because of the common phenomena of antibody-dependent enhancement. D) Not enough information has been given.Over the past year we have endured the Covid-19 pandemic. Accumulating evidence suggests that the host immunity response is contributing in severe forms COVID-19 caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). COVID-19 causes mild to severe illness with high morbidity and mortality, especially in preexisting risk groups. These immunologic reactions in severe COVID-19 may characterize the cytokine storm that is associated with untoward clinicopathological consequences. The cytokine storm is an out-of-control cytokine release that has been observed in some infectious and noninfectious diseases, leading to a hyperinflammation condition in the host. This immune response has been associated with a higher intensive care unit (ICU) admissions and mortality in COVID-19. In fact, higher concentrations of granulocyte-colony stimulating factor (G-CSF), interferon gamma-induced protein 10 (IP10), monocyte chemo-attractant protein 1 (MCP1), macrophage inflammatory protein…Typical symptoms of COVID-19 include: (1) fever (83-98%), (2) cough (46-82%), (3) muscle pain or fatigue (11-44%), (4) shortness of breath (31%), and in some severe cases, (5) acute respiratory failure, (6) secondary infection and (7) interferon gamma-related cytokine storm. Pick 3 of the above symptoms, and explain why the patients may have these symptoms.
- Antibodies play a critical role in the prevention of infection by the specific viruses the antibody is designed to detect. Which immune system cell produces antibodies? Indicate four ways that antibodies can disrupt the ability of a virus to infect a cell. PLEASE ANSWER ALL PARTS TO THIS QUESTIONThe vaccine Gardasil that targets human papilloma virus (HPV), the etiological agent of genital warts, was developed after the anti-HPV medication podofilox. Why would doctors still want a vaccine created after anti-viral medications were available?If you looked at H&E staining of a fungal-infected mouse tongue vs a non-infected mouse tongue, would you expect to see more neutrophils? Why or why not?
