Immunological Aspects Related to Viral Infections in Severe Asthma and the Role of Omalizumab

Abstract

Viral respiratory infections are recognized risk factors for the loss of control of allergic asthma and the induction of exacerbations, both in adults and children. Severe asthma is more susceptible to virus-induced asthma exacerbations, especially in the presence of high IgE levels. In the course of immune responses to viruses, an initial activation of innate immunity typically occurs and the production of type I and III interferons is essential in the control of viral spread. However, the Th2 inflammatory environment still appears to be protective against viral infections in general and in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections as well. As for now, literature data, although extremely limited and preliminary, show that severe asthma patients treated with biologics don't have an increased risk of SARS-CoV-2 infection or progression to severe forms compared to the non-asthmatic population. Omalizumab, an anti-IgE monoclonal antibody, exerts a profound cellular effect, which can stabilize the effector cells, and is becoming much more efficient from the point of view of innate immunity in contrasting respiratory viral infections. In addition to the antiviral effect, clinical efficacy and safety of this biological allow a great improvement in the management of asthma.

Keywords: biologicals; immune response; omalizumab; severe asthma; viral respiratory infections.

Figure 1

Protective action of omalizumab towards viral infections.Omalizumab acts directly forming IgE / anti-IgE immune complexes that prevent the interaction of IgE with high affinity (FcϵRI) and low affinity (FcϵRII / CD23) membrane receptors of PD cells, indirectly, PD cells binds viruses by TLCR7 that release INFα and activate innate immune response. X is the blockade of binding on the receptor.