Approximately one-third of infected pregnant women died from severe acute respiratory syndrome coronavirus (SARS-CoV) and the Middle East respiratory syndrome coronavirus (MERS-CoV) epidemics of the past two decades. It is logical to predict that pregnant women infected with the novel coronavirus (SARS-CoV-2) might be at higher risk for severe illness, morbidity, or mortality compared with non-pregnant women. However, a review of the literature indicates that pregnant women are not more likely to be seriously ill than other healthy non-pregnant women if they develop coronavirus disease (COVID-19). This observation begs the question: "Why does pregnancy not increase the risk for acquiring SARS-CoV-2 infection, nor does it worsen the clinical course of COVID-19 compared with nonpregnant individuals?" Herein, we try to explain our observations when considering whether the immunologic changes of pregnancy and other physiologic adaptations of pregnancy affect the virulence and course of SARS-CoV-2 infection.

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CD4 is a candidate gene in autoimmune diseases, including rheumatoid arthritis (RA). Because the CD4 receptor is crucial for appropriate antigen responses of CD4+ T cells, changes in CD4 expression and CD4+ T-cell activity may influence tolerance or tissue destruction in autoimmune diseases and contribute to their risk. We analyzed two polymorphisms of the CD4 in 172 female Egyptian patients with RA and in 112 matched healthy control. Genotyping of CD4-11743 and CD4-10845 was determined by restriction fragment length polymorphism-polymerase chain reaction (PCR-RFLP). Subjects with the CC genotype of CD4-11743 were significantly more likely to develop RA (OR = 2.7, P = 0.03) and more likely to have sever RA (OR = 2.7, P = 0.024). Carrier of A allele of CD4-10845 was significantly more likely to develop sever RA (OR = 3.7, P = 0.000). CD4-11743 genetic polymorphisms are associated with the susceptibility and severity of RA, and CD4-10845 genetic polymorphisms are associated with the severity of RA.