Dangerous Shifts in Coronavirus Infection
Medical professionals issue alert on escalated harmful strategies
Troubling changes are appearing in the coronavirus infection, warns Dr. Svetlana Malinovskaya, as reported by FAN.
This new, aggressive form of the virus is displaying erratic behavior, according to Malinovskaya, who pointed out that blood tests suggest rapid changes could be happening within hours. A notable difference observed is an exponential increase in platelets, leading to blood clots and heart attacks for infected individuals.
Malinovskaya stressed that it's crucial to readjust treatment strategies for new patients, tailoring the approach to address each individual's unique needs, as prior treatment methods often fail to deliver desirable results.
In previous reports, it's been noted that COVID-19 has been battling back against human efforts with new mutations. India has acknowledged the emergence of the "delta plus" strain, which weakens the effectiveness of antibodies in those who recovered and those who have been vaccinated. The first five cases of this new strain were detected in Ratnagiri, and now, there are numerous cases throughout the country.
New studies consistently demonstrate that in severe cases, SARS-CoV-2 triggers a heightened risk of blood clots. This is due to the virus's ability to initiate a hypercoagulable state through several mechanisms:
- The virus's spike protein, fundamental for viral entry into host cells, also plays a role in coagulation abnormalities and clot formation. It activates platelets and interacts with fibrinogen, potentially causing clots. Free spike protein fragments have been detected in COVID-19 patients' plasma and are suggested to trigger independent clot formation without the presence of viral RNA[1][2].
- The infection induces inflammation, which stimulates the coagulation system. In severe cases, an excessive immune response, or a "cytokine storm," amplifies clotting signals. This environment promotes clot formation[3].
Furthermore, the infection causes platelets to become hyperactive and prone to aggregation due to both viral proteins and inflammatory mediators. Certain strains of the virus, like Omicron (BA.1.1) with the N501Y mutation, have been connected to decreased platelet counts and increased levels of plasminogen activator inhibitor-1 (PAI-1), contributing further to a hypercoagulable state[1][2].
Research on Long COVID underscores the necessity for continuous monitoring of coagulation disorders, as the condition can lead to cardiovascular complications. Repeated haemostatic tests may be essential in assessing treatment effects for coagulopathy in Long COVID patients[5].
As our understanding of the virus expands, long-term cohort studies will be essential in determining the persistence of coagulation risks and potential long-term cardiovascular consequences after infection[3]. Additionally, integrating findings from viral coagulopathy with cancer-related thrombosis research will advance patient-centered approaches to clot prevention and treatment[3].
- Dr. Svetlana Malinovskaya warns that the new, aggressive form of the coronavirus is displaying erratic behavior and causing exponential increases in platelets, leading to blood clots and heart attacks for infected individuals.
- Malinovskaya stresses the importance of tailoring treatment strategies for new patients, as prior methods often fail to deliver desirable results due to the virus's mutations.
- India has acknowledged the emergence of the "delta plus" strain, which weakens the effectiveness of antibodies in those who recovered and those who have been vaccinated.
- New studies consistently demonstrate that SARS-CoV-2 triggers a heightened risk of blood clots due to the virus's ability to initiate a hypercoagulable state, caused by the virus's spike protein, inflammation, and hyperactive platelets.
