
Choosen immunoglobulin Risk factors for severe COVID-19 include a deficit.
When IgA levels are below 0.07 g/L, the most prevalent primary immunodeficiency condition (PID) is selective IgA deficiency (sIgAD). The vast majority of its sufferers are asymptomatic because it is a minor illness. Because severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) attacks the upper respiratory tract (URT) mucosa, where IgA plays a vital protective function, recent studies suggest that patients with sIgAD may be at increased risk of severe COVID-19.

The three clinical phases of SARS-CoV-2 infection overlap. The nasopharynx is where SARS-CoV-2 enters, but this phase is asymptomatic. But when it gets into the lungs, patients get fever, myalgia, and worsening dyspnea. A chest computed tomography (CT) scan during this time has a ground-glass look because inflammatory markers including interleukin 6 (IL6) and tumor necrosis factor are high (TNF).
A few individuals advance to the severe systemic phase, where hypoxia can sometimes result in mortality and their many organs are at risk of malfunction. The outcome of COVID-19 is significantly influenced by the immune response at each stage of the SARS-CoV-2 infection. Studies have revealed that individuals who succumb to infection frequently experience an adverse immune response and antibody-dependent enhancement (ADE).
Chronic COVID-19 is appropriately described as a standoff between SARS-CoV-2 and a poor immune response. It extends the time that viruses are shed and emphasizes how unpredictable humoral immunity is when it comes to pathogenic infections. Only 30% of people with sIgAD experience PID-like symptoms. IgAD, however, only makes up a small portion of other PIDs including comorbid variable immunodeficiency diseases (CVID). Studies have clarified the genetic pathways driving IgAD in CVID, where clinical manifestations are predominated by deficits of particular immune components (not IgA).
When IgA is absent, mucosal immunity is typically made up for by IgG or IgM. Future research should, however, look into whether SARS-CoV-2 specific IgG or IgM in a patient's saliva after COVID-19 vaccination would be useful for predicting prognosis in sIgAD patients. Prospective investigations may also reveal whether in vitro T-cell responses to SARS-CoV-2 can act as a stand-in marker for COVID-19 protection in sIgAD patients. When combined, the information from these research may aid in the creation of COVID-19 customized therapy for sIgAD patients.






