The past year, the scientific community has scrambled to better understand the mechanics of COVID-19 in the hopes of translating their findings into the development of treatment options.

As an organization committed to our vision of a world free of lung disease, the American Lung Association has invested in this effort since the very beginning of the pandemic. In fact, this dedication led to the rollout of our COVID-19 Action Initiative, a $25 million investment to help end COVID-19 and defend against future respiratory virus pandemics. It includes our COVID-19 and Respiratory Virus Research Award helping to advance research for emerging respiratory pathogens.

Research is in progress for 12 projects funded through this worthy initiative, and our second round of awardees will be announced this summer. Dr. Marcia Goldberg, M.D., infectious disease expert at Massachusetts General Hospital (MGH), is one such recipient for her project, “High Resolution Definition of the Pathogenic Immune Response in ARDS during COVID-19 Infection.” It aims to detail the response of multiple types of inflammatory cells to COVID-19 infection in humans through the in-depth proteomic [study of proteins and their functions] and expression analysis of nearly 400 patients and over 800 blood samples. “My interest primarily lies in identifying different immunological profiles to ascertain why some people develop severe COVID-19 disease – even go on to die from it, while others don’t. It’s my belief the answer can be found in the bloodstream,” said Dr. Goldberg, who serves as the study’s senior author.

The resulting data, published in Cell Reports Medicine, interestingly revealed that the patients who had COVID-19 showed a distinctive pattern of proteins, regardless of their disease severity. When the data of the patients with severe disease was compared to the data of those with less severe disease, Dr. Goldberg and her team of investigators were able to identify more than 250 proteins associated with severity. Among them are several inflammatory and some non-inflammatory proteins, a few of which had not been described in earlier studies.

Added Michael Filbin, M.D., M.S., director of clinical research at MGH and study co-investigator, “While we’re still in the understanding phase of interpreting the proteomics, we observed a small subset of patients who did not mount a significant pro-inflammatory response to COVID, yet they had equally severe disease. These patients tended to be older and have more chronic medical conditions, and we think their protein signature might reflect impaired immune response to disease. We’re further investigating antibody responses to disease and viral load data of these blood samples – the degree to which there was virus in the bloodstream – that we think may be underlying drivers to some of the signatures we’re seeing.”

“One of our next steps is to take a closer look at the association of these identified proteins with ARDS (acute respiratory distress syndrome) and how they may contribute to lung injury. ARDS, after all, is a major clinical feature of severe COVID. Virtually every patient who died from COVID suffered from ARDS,” Dr. Goldberg concluded. “There remains a lot we can learn from our unique cohort.”

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