COVID-19's Deadly Impact on the Immune System Unveiled
COVID-19 fatalities primarily stem from severe complications in affected individuals, especially those with underlying health conditions or weakened immune systems, according to scientific research.
The gruesome reality of COVID-19 has been laid bare by scientists at Rockefeller University (USA) who've linked life-threatening and fatal cases of the virus to the malfunctioning of the immune system. According to research published in the journal Science and reported by Almaty.tv, citing Lenta.ru, this immune system havoc is a major factor behind severe COVID-19 complications.
Researchers found that about 3.5% of patients with severe COVID-19 have mutations in genes essential for antiviral defense. To make matters worse, a whopping 10% of patients (that's 101 out of 987) with severe symptoms produce "auto-antibodies" that attack the immune system itself. Interestingly, the vast majority of these victims are men, accounting for 94% of the cases.
Scientists have pinpointed errors in genes responsible for producing antiviral interferons. Without a proper set of these defense molecules, the body struggles to fight off the virus. In many cases, these interferons are damaged by antibodies, creating an autoimmune disease-like scenario, similar to rheumatoid arthritis or type 1 diabetes. These "auto-antibodies" are notably absent in patients with mild COVID-19.
Putting the Brakes on the Body's Defense System
Specific autoantibodies in severe COVID-19 cases work by targeting various immune components and self-antigens. For instance, Interferon-I (IFN-I) neutralizing autoantibodies knock out antiviral defenses by hindering their signaling, making people susceptible to severe pneumonia and viral replication [1][3].
Other autoantibodies, such as those against angiotensin type-1 receptor (AT1R) and MAS1 receptor, mess with the renin-angiotensin system (RAS), aggravate inflammation, damage endothelial cells, and complicate the lung and nervous systems [4].
ACE2 autoantibodies work against the ACE2 enzyme, disrupting the balance in the RAS system and causing vascular injury [4].
Antiphospholipid antibodies and rheumatoid factors contribute to the formation of blood clots and systemic inflammation [3].
When Politics Meet Pathology
While the studies don't provide a detailed explanation for the gender disparity in severe COVID-19 cases, pre-pandemic data suggests that autoantibodies are more common in autoimmune conditions among females. Yet, men are disproportionately affected by severe COVID-19. Possible factors could include androgen-mediated pathways affecting ACE2 expression and differences in immune response between the sexes, such as stronger innate immunity in females, which may help mitigate autoantibody-driven damage. Autoantibody production seems to correlate with age and pre-existing immune dysregulation, which may intersect with sex-specific immune aging patterns [3][4].
Persistent autoantibodies in LongCOVID and post-acute syndromes continue promoting inflammation and organ dysfunction, emphasizing their role in long-term complications [2][5].
- The research on COVID-19 has uncovered a link between severe cases and malfunctions in the immune system, specifically the production of auto-antibodies that attack the immune system itself.
- In severe COVID-19 cases, Interferon-I (IFN-I) neutralizing autoantibodies impair the signaling of antiviral defenses, making individuals vulnerable to severe pneumonia and viral replication.
- ACE2 autoantibodies, discovered in severe COVID-19 cases, disrupt the balance in the renin-angiotensin system (RAS) and cause vascular injury.
- Autoantibody production, which can lead to long-term complications, appears to correlate with age and pre-existing immune dysregulation in both genders, but men are disproportionately affected by severe COVID-19, possibly due to androgen-mediated pathways and differences in immune response.
