Scientists and Economists Alert! Global Emergency  Compounded by the AIDS-like Features of SARS-CoV-2 Infection Over a million people in the US are being infected with severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) every day.  Originally named after the acute respiratory syndrome it can cause as a consequence of blood vessel damage in the lungs, … Continued

Life-threatening thrombotic events and neurological symptoms are prevalent in COVID-19 and are persistent in patients with long COVID experiencing post-acute sequelae of SARS-CoV-2 infection1,2,3,4. Despite the clinical evidence1,5,6,7, the underlying mechanisms of coagulopathy in COVID-19 and its consequences in inflammation and neuropathology remain poorly understood and treatment options are insufficient. Fibrinogen, the central structural component of blood clots, is abundantly deposited in the lungs and brains of patients with COVID-19, correlates with disease severity and is a predictive biomarker for post-COVID-19 cognitive deficits1,5,8,9,10. Here we show that fibrin binds to the SARS-CoV-2 spike protein, forming proinflammatory blood clots that drive systemic thromboinflammation and neuropathology in COVID-19. Fibrin, acting through its inflammatory domain, is required for oxidative stress and macrophage activation in the lungs, whereas it suppresses natural killer cells, after SARS-CoV-2 infection. Fibrin promotes neuroinflammation and neuronal loss after infection, as well as innate immune activation in the brain and lungs independently of active infection. A monoclonal antibody targeting the inflammatory fibrin domain provides protection from microglial activation and neuronal injury, as well as from thromboinflammation in the lung after infection. Thus, fibrin drives inflammation and neuropathology in SARS-CoV-2 infection, and fibrin-targeting immunotherapy may represent a therapeutic intervention for patients with acute COVID-19 and long COVID.

The pandemic isn’t over. Why is it so hard to find accurate information about it?

Albany Medical Center-led research shows that long Covid patients have the same blood biomarkers, regardless of their symptoms.

A new study finds the risks of developing long COVID declined over the first two years of the pandemic. But unvaccinated adults were more than twice as likely to get long COVID compared with those who were vaccinated.

Budget and other project documents obtained through the Freedom of Information Act show how the National Institutes of Health set up its flagship long Covid research initiative, including the scientific expertise that government reviewers prioritized in selecting research teams to lead the RECOVER program and the early goals and timelines. Experts who reviewed the contracts and project documents say the agency set itself up for failure.

“Unless you’re an unborn fetus, they don’t give a shit about you.”

CDC data shows nearly 18m people could be living with long Covid even as health agency relaxes isolation recommendations