Here’s why COVID-19 is so much worse than the flu
Unlike influenza, SARS-CoV-2 uses ACE2 receptors to penetrate cells. Similar to HIV, SARS-CoV-2 can spread silently throughout the host’s body and attack nearly every organ.
Medicine seems to have largely bought into the SARS-CoV-2 seasonal flu analogy. Everything seems to focus on lung disease. Fringe coronavirus deniers began telling that COVID-19 was like the flu. This misinformation narrative has taken hold and even influenced the decision-making process of eminent scientific committees, where disease severity is increasingly defined as hospitalization (mostly due to pulmonary distress), rather than potential disabling chronic and long-term consequences. Unfortunately, this appears to have been the focus of some members of the CDC’s Advisory Committee on Immunization Practices (ACIP) that failed to approve boosters for those at high risk of occupational exposure, a decision made by the CDC director Immediately reverse.
COVID-19 has multiple presentations and only one lung. More than anything else, the receptors used for attachment determine the behavior of any virus, along with the organs and even species it can infect.
Human rhinoviruses, the most common cause of the common cold, use the ICAM-1 (intercellular adhesion molecule-1) receptor. Enter cells. This receptor allows the virus to replicate in sinus tissues but not in a variety of other tissues. The influenza virus binds to cells via sialic acid receptors, which are sugar proteins and Sugar and fat complexes. There are a number of modifications to this receptor across species, which require different viral mutations to enable cellular binding and enter. The influenza virus primarily targets the patient’s lungs, but then the patient’s immune response can also trigger a myriad of systemic symptoms from loss of appetite and muscular. HIV uses CD4 receptors found in lymphocytes. HIV has no symptoms at first, and the initial stages of the disease can easily be categorized as “mild,” a disease that, if left untreated, turns almost uniformly into aggressive and fatal over a period of time. 8 to 10 years.
In the case of SARS-CoV-2, the virus that causes COVID-19, the ACE2 receptor is used for viral entry into cells. The ACE2 receptor is completely different from that used in rhinovirus and seasonal influenza. Consists of amino acids with a zinc ligand. This receptor is found throughout the body, not just the lungs.
Clinically, SARS-CoV-2 combines some characteristics of seasonal influenza as well as HIV. Similar to seasonal influenza, SARS-CoV-2 can primarily attack the lungs. But ACE2 receptors are ubiquitous. Similar to HIV, the virus can also go into stealth mode, silently spreading throughout the host’s body and attacking almost every organ, especially those with a high concentration of ACE2 receptors. Similar to HIV, it causes The SARS-CoV-2 virus is also in asymptomatic spread. In complete stealth mode, SARS-CoV-2 can attack blood vessels and heart. Myocarditis can occur with the patient completely unaware of the damage, until arrhythmia or symptomatic myocarditis develops. In young asymptomatic patients, these sequelae are not uncommon.
SARS-CoV-2 that targets the body’s cardiovascular system must be given. It has long been known that ACE receptors are involved in cardiovascular regulation. ACE inhibitors and ACE-B blockers have long been used to treat high blood pressure. This is the same path that the virus infects.
Thus, there are multiple presentations of SARS-CoV-2 including lung, heart, gastrointestinal (GI) and central nervous system (CNS).
Recently, there has been increasing evidence regarding the central nervous system effects of SARS-CoV-2. As early as July 2020, scientists were sounding the alarm about COVID-19 brain damage: including temporary brain dysfunction, strokes, nerve damage, and Brain inflammation. At the time, these cases were still considered relatively uncommon. Article published in Lancet psychology He found that 1 in 3 coronavirus survivors have been diagnosed with brain disorders or mental health disorders, but separating what is due to stressors of the disease versus the direct effects of the virus has been problematic.
Sandra Lopez Leon et al. conducted a system review and long-term COVID-19 meta-analysis and found that the three most common symptoms of coronavirus were “fatigue (58%), headache (44%) and attention disturbance (27%), all of which can affect focus.
Ricci et al note that cognitive dysfunction has been commonly reported in the case of COVID-19, but the true incidence is unknown, and note that: “The hippocampus appears to be particularly susceptible to infection with COVID-19, increasing the likelihood of post-infection memory Weakness…”and that the virus may enter the central nervous system through olfactory bulb. Finally, in August 2021, research by Gwenaëlle Douaud et al. Documented by brain imaging “abnormalities in areas of the limbic cortex with direct neural connection to the primary system” olfactory system. In addition, there was a “significant decrease in gray matter thickness in the frontal, parietal, and temporal regions.” “Participants with 401 SARS-CoV-2 also showed greater cognitive decline between the two time points on the pathway making test (visual attention and task switching) compared to With the controls…”
Again, none of this should be surprising, given that loss of smell, or lack of smell, is one of the most common symptoms of COVID-19. The olfactory nerve is not actually a nerve but a projection of the brain itself.
Thus, COVID-19 has a myriad of different presentations, all of which can lead to serious and long-term consequences. Just because COVID-19 is asymptomatic or does not result in “severe” lung disease does not mean that the patient does not have lung disease. Serious infection: It is critical for public health officials to implement strategies to prevent long-term disabilities associated with COVID-19 and not focus solely on acute pulmonary symptoms.