Eleanor (Pitt) Wilson, a native of Louisville, Kentucky, attended medical school at the Johns Hopkins Medical Institute, in Baltimore, Maryland. She completed residency training in Internal Medicine at Vanderbilt University Medical Center in Nashville, Tennessee, and subspecialty fellowship training in Infectious Disease at the National Institute of Allergy and Infectious Diseases in Bethesda, Maryland. She obtained her Masters in Clinical Research as part of a collaborative program between Duke University and the National Institutes of Health. Despite dramatic improvements in the life expectancy of persons with human immunodeficiency virus (HIV) infection, non-AIDS events such as liver disease and cancer are now the predominant causes of morbidity and mortality in treated populations. Markers of immune activation have been associated with HIV disease progression, predict mortality, and persist despite effective antiretroviral therapy; patients co-infected with hepatitis C virus (HCV) and HIV have higher levels of immune activation than those infected with HIV or HCV alone and are at increased risk for mortality due to liver and cardiovascular disease. Understanding the role of immune activation in the rapid progression of hepatic fibrosis in patients with HIV and HCV co-infection will help us to address this burgeoning public health problem, and at the same time, understand how the clearance of a chronic viral infection affects global immune activation and what can be done to augment treatment responses and improve rates of viral clearance and resolution of hepatic fibrosis. My scientific interests and investigations have focused on the alterations to innate and adaptive immunity in chronic viral infections, including HIV and viral hepatitis. Beginning with my work with Dr. Robert Siliciano during medical school investigating HIV persistence in latently infected T cell subsets, extending through my fellowship research with Dr. Irini Sereti regarding the mechanisms connecting soluble and cellular immune activation with clinical outcomes in HIV, and now working with Dr. Shyam Kottilil on the reconstitution of innate and adaptive immunology following clearance of HCV, I have developed expertise in the translational research techniques required to address these questions. As a Principal Investigator and Lead Associate Investigator on multiple clinical trials in the beginning of my career at the National Institute of Allergy and Infectious Diseases and now at the Institute of Human Virology, I am eager to continue working on ways to improve the health of patients with chronic viral infections and advanced liver disease.
"[On the Delta variant] we do know that the amount of time required for face to face, within six feet contact to infect somebody is really probably less than a minute with the Delta variant, which does mean that it can be extremely quick and transmitted."
"Right now we know that vaccines are really the best way to protect yourself, but it's part of an entire strategy of masking, of social distancing, of being careful, of limiting interactions. And so I think the best approach to this virus is still the multipronged one, but vaccination is absolutely a central component of that."
"The Delta variant has much higher viral loads, which probably reflects a higher amount of virus in the mucosal surfaces, in the nose and then later, as the disease progresses, there can be higher viral levels within the lungs or in other places within the CNS, although the question is still out on that exactly what levels make it into the CNS, the central nervous system. But we don't know exactly what the levels are of Delta variant in any of these specific places but we know that they are much, as you said, much more likely to be higher than the Beta variant or the Alpha variants because they are so much higher in the blood already. And there's no indication that they would be different for this virus. So, those studies are still ongoing. They're still in review. There's definitely the suggestion that that is what is driving the increased transmissibility of this variant."