Weill Cornell Medicine researchers recently discovered that SARS-CoV-2 — the virus that causes COVID-19 — can infect not only the lungs but also the brain.
The study, published in Cell Stem Cell on Jan. 17, was conducted in collaboration with researchers from the Sloan-Kettering Institute for Cancer Research and the Columbia University Vagelos College of Physicians and Surgeons.
Researchers specifically studied the effects of COVID-19 on the brain’s dopaminergic neurons, which are midbrain cells dedicated to dopamine secretion. Their loss or degeneration often indicates neurological disorders, such as Parkinson’s disease.
According to one of the authors of the study Prof. Shuibing Chen, cell and developmental biology, unlike lung cells, which may ultimately die after SARS-CoV-2 infection, dopamine neurons begin aging faster. Finding this aging, or senescence, in brain cells was an unexpected result, Chen explained.
“We put the same type of [dopamine] cells in 300 wells, and after several days, we can see markers,” Chen said. “We found a senescence pathway come up. They don’t die. They just become older.”
A senescence pathway is a formal term for the aging noted here in infected brain cells.
With this study, researchers delved beyond the impacts of COVID-19 on previously investigated regions, including the lung, pancreatic beta and placenta.
“Traditionally, if you talk about COVID-19, the first target is always the cells in the lung, then the cells in the gut, and also liver cells. We know they can be affected,” Chen said.
However, studying the impact of SARS-CoV-2 on the brain’s dopaminergic neurons did not come without its challenges, according to Chen.
Laboratories have different biosafety levels for viruses, and SARS-CoV-2 is a Biosafety Level 3 virus for clinical specimens. This means that only specially equipped laboratories can work with it.
Despite Cornell not having a BSL-3 facility, the researchers were still able to carry out their research by working in Columbia’s BSL-3 facility.
“You have to be fully protected when you’re working [with this kind of virus] in a BSL-3 lab. It’s a special type of lab, and unfortunately, we don’t have that.” Chen said. “That [access to other resources] is a part of what I really appreciate about this [kind of] large collaborative work.”
Chen affirmed that working in Columbia’s BSL-3 facility and maintaining open communication with collaborators enabled the discovery. The researchers from different institutions were united under the shared goal of furthering scientific comprehension of COVID-19’s impact on the human body.
While this work reveals new insight into the relationships between COVID-19 and the brain’s dopamine system, Chen noted that there is much more to understand about the subject. Specifically, there is a lack of knowledge on the long-term impacts of COVID-19 on neural senescence, Chen said.
“We learned that different cells may respond differently to viral infection,” Chen said. “If we want to study the right organ, we need to use the right type of cells.”
Ultimately, this research is a starting point for future investigations on viruses, including SARS-CoV-2, and their physical effects on different parts of the human body.
Ava Malkin can be reached at [email protected].