The direct access to the brain enables a sort of double attack, with a direct hit by the virus to an organ, like the lungs, and to the organ's control centers in the brain. There are reports, Rutkowski notes, of patients seeming to do better but then they just stop breathing. While she and Hess agree that it's most often the lung failure that causes death with COVID-19, they suspect it's both this direct lung invasion and infection of breathing centers in the brain responsible.

While investigators are working in real time to determine what treatments are best for the still emerging array of problems caused by COVID-19, the MCG neurologists say the limited data out there on stroke indicate the standard therapies should work in this scenario as well.

"We think the pathogenesis behind the clots that form during this infection are a little different, but those clots people are describing with COVID-19 are very fresh and tPA seems to be really effective for those," says Rutkowski. "You see this in people with sepsis and with other viruses," Hess says of the clotting that can result in stroke and as well as damage to other organs. The neurologists suspect it is this propensity to clot coupled with the virus' attachment to ACE2 receptors, found throughout the body and considered protective, that leaves patients vulnerable to stroke.

Many viruses, including influenza and shingles, as well as other overwhelming infections such as sepsis, which is often driven by bacteria, result in excessive inflammation which can lead to increased coagulation that causes blood clots, including producing microscopic clots in the tiny air sacs of the lung, that can contribute to adult respiratory distress syndrome -- a major cause of severe illness and death in COVID-19 -- as well as the dysfunction and failure of other organs.

Patients' blood will have telltale high levels of D-dimer, a protein fragment produced when a clot is degraded, and their blood clots much faster than usual.

The now familiar spiky virus latches onto the angiotensin converting enzyme 2, or ACE2, an enzyme found on cells -- in the lungs, heart, kidneys, intestines and brain as well as the nasal mucosa - which explains its pervasive impact in the body. ACE2 is a part of the renin angiotensin system, which helps regulate blood pressure and is essentially a balance for angiotensin II, a powerful blood vessel constrictor and inflammation promoter. "It probably depletes ACE2 so you get this imbalance, you get too much angiotensin II, which is generally very bad," Hess says.

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