Here’s why COVID-19 is so much worse than the flu

Medicine seems to have largely adhered to the analogy of the seasonal influenza SARS-CoV-2. Everything seems to be focused on lung disease. Fringe coronavirus deniers started the story that COVID-19 was like the flu. This misinformation narrative has taken hold and has even affected the decision-making of leading scientific committees, where the severity of the disease is increasingly defined as hospitalization (most often due to pulmonary distress), rather as potential long-term chronic and disabling sequelae. This unfortunately seemed to be the focus of some of the members of the Center for Disease Control and Prevention’s Advisory Committee on Immunization Practices (ACIP), which did not approve recalls for people at high risk of occupational exposure, a decision that the director of the CDC quickly reversed.

COVID-19 has a number of presentations and pulmonary is just one. More than anything else, the receptor used for attachment determines the behavior of any virus, as well as the organs and even the species it can infect.

Human rhinoviruses, the most common cause of a cold, use the ICAM-1 receptor (intercellular adhesion molecule-1) to enter cells. This receptor allows the virus to replicate in sinus tissue but not in various other tissues. The influenza virus attaches to cells via sialic acid receptors, which are sugar-protein and sugar-fat complexes. There are a number of modifications of this receptor across species which require different viral mutations to allow cell attachment and entry. The influenza virus primarily targets a patient’s lungs, but the patient’s immune response can also produce a myriad of systemic symptoms due to loss of appetite and myalgia. HIV uses the CD4 receptor residing on lymphocytes. HIV is initially asymptomatic and the initial stages of the disease can easily be classified as “mild,” a disease which, if left untreated, becomes almost uniformly aggressive and fatal over the course of 8-10 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 totally different from that used by rhinovirus and seasonal influenza. It is made up of amino acids and a zinc ligand. This receptor is present throughout the body, not just in the lungs.

Clinically, SARS-CoV-2 combines some of the properties of seasonal influenza and HIV. Similar to the seasonal flu, SARS-CoV-2 can primarily attack the lungs. But ACE2 receivers are everywhere. Similar to HIV, the virus can also go into a stealth mode, spreading silently throughout the host’s body and attacking almost all organs, especially those with a high concentration of ACE2 receptors. And like HIV, SARS-CoV-2 also frequently causes asymptomatic spread. In full stealth mode, SARS-CoV-2 can asymptomatically attack the vascular system and the heart. Myocarditis can occur and the patient is completely unaware of the damage, until symptomatic arrhythmia or myocarditis develops. In young asymptomatic patients, this is not a rare sequel.

SARS-CoV-2 targeting the body’s cardiovascular system should be obvious. It has long been known that ACE receptors are involved in cardiovascular regulation. ACE inhibitors and ACE II blockers have long been used to treat high blood pressure. This is the same route that the virus infects.

Thus, there are several presentations of SARS-CoV-2, including pulmonary, cardiac, gastrointestinal (GI) and central nervous system (CNS).

Recently, there has been growing evidence regarding the effects of SARS-CoV-2 on the CNS. As early as July 2020, scientists were sounding the alarm bells regarding brain damage caused by COVID-19: including temporary brain dysfunction, stroke, nerve damage and brain inflammation. At that time, these conditions were still considered relatively rare. An article published in Lancet Psychology found that one in three COVID-19 survivors had been diagnosed with brain or mental health disorders, but separating what is due to the stressors of the disease versus the direct effects of the virus was problematic.

Sandra Lopez-Léon, et al. conducted a system review and meta-analysis of long COVID-19 and found that the 3 most common symptoms of long COVID-19 were “fatigue (58%), headaches (44%) and disturbance in attention (27%) ”, all of which can affect concentration.

Ritchie, et al, noted that cognitive dysfunction has been commonly reported with COVID-19, but the true incidence is unknown, and notes that: “The hippocampus appears to be particularly vulnerable to coronavirus infections, thus increasing the likelihood of memory. post-infection. attack… ”and that the virus can enter the CNS through the olfactory bulb. Finally, in August 2021, research by Gwenaëlle Douaud, et al. documented with brain imaging “abnormalities in limbal cortical areas with direct neuronal connectivity to the primary olfactory system”. In addition, there was “a marked reduction in the thickness of gray matter in the fronto-parietal and temporal regions”. “The 401 participants infected with SARS-CoV-2 also showed a greater cognitive decline between the two time points of the trail creation test (visual attention and task change) compared to the controls…”

Again, none of this should come as a surprise, as anosmia or lack of smell is one of the most common symptoms of COVID-19. The olfactory nerve is not really 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 sequelae. Just because COVID-19 is asymptomatic or does not produce “severe” lung disease does not mean the patient does not have a serious infection. It is of the utmost importance for public health officials to implement strategies to prevent the onset of long-term disabilities related to COVID-19 and not to focus solely on acute pulmonary symptoms.