Section 6: Host-Specific Variations in COVID-19 Immune Response (from DOI: 10.1007/s11886-020-01292-3)
From publication: "Cardiovascular Complications in Patients with COVID-19: Consequences of Viral Toxicities and Host Immune Response" published as Curr Cardiol Rep; 2020 04 21 ; 22 (5) 32. DOI: https://doi.org/10.1007/s11886-020-01292-3
Section 6: Host-Specific Variations in COVID-19 Immune Response
Age and gender differences in COVID-19 infection rates have raised interest in possible differences in age- and gender-dependent immune responses to viral exposure. Children account for the minority of laboratory-confirmed cases of COVID-19 in China and appear less susceptible to severe disease. Although the functions of both innate and adaptive immune immunity declines with aging, this does not typically start until late adulthood, and thus would not fully explain the decreased severity of disease in children compared with even young adults.. The effect of age on the immune system can be demonstrated by the low protective titers among 50% of adults older than 65 who receive the influenza vaccine. Additional information about the differential response of SARS-CoV and SARS-CoV-2 with aging comes from animal models; in comparison with SARS-CoV-MA15-infected young C57BL/6 mice, infection of aged mice (12 months) is associated with severe reduction in the number of virus-specific CD8+ T cells in the lungs.
In addition to the effect of aging, gender is also thought to play a role in outcomes in SARS-CoV-2 infection. One study demonstrated a higher incidence of SARS-CoV-2 infection in older adult males compared with females. Sex differences in immune response have been noted in literature, although the reasons are not clear. Males experience greater severity and prevalence of bacterial, viral, fungal and parasitic infections than females, who also mount a more robust response to antigenic challenges including infection and vaccination. We (Davis et al) have used machine learning approaches to identify a cluster of genes involved in lipid biosynthesis, previously shown to be upregulated by testosterone, which correlates with poor virus-neutralizing activity in men. Interestingly, the stronger immune response in females is thought to explain why females are more prone to immune-mediated pathologies including autoimmune disease and cytokine storm. However, in the case of COVID-19, there is no data to currently support a female-predominance toward cytokine storm; if anything, males are prone to more severe disease and mortality. Thus, it would be important to gather more data and larger number cohort studies on the current SARS-CoV-2 pandemic to study further delineate whether there is a gender-dependent risk for cytokine storm and subsequent cardiac injury in COVID-19 infection.
