ABSTRACT
Abundant evidence strongly suggests that the condition of pregnancy makes women and their fetuses highly vulnerable to severe Corona-virus 2019 (COVID-19) complications. Here, two novel hypoxia-related conditions are proposed to play a pivotal role in better understanding the relationship between COVID-19, pregnancy and poor health outcomes. The first condition, "misattributed dyspnea (shortness of breath)" refers to respiratory symptoms common to both advanced pregnancy and COVID-19, which are mistakenly perceived as related to the former rather than to the latter; as a result, pregnant women with this condition receive no medical attention until the disease is in an advanced stage. The second condition, "silent hypoxia", refers to abnormally low blood oxygen saturation levels in COVID-19 patients, which occur in the absence of typical respiratory distress symptoms, such as dyspnea, thereby also leading to delayed diagnosis and treatment. The delay in diagnosis and referral to treatment, due to either "misattributed dypsnea" or "silent hypoxia", may lead to rapid deterioration and poor health outcome to both the mothers and their fetuses. This is particularly valid among women during advanced stages of pregnancy as the altered respiratory features make the consequences of the disease more challenging to cope with. Studies have demonstrated the importance of monitoring blood oxygen saturation by pulse oximetry as a reliable predictor of disease severity and outcome among COVID-19 patients. We propose the use of home pulse oximetry during pregnancy as a diagnostic measure that, together with proper medical guidance, may allow early diagnosis of hypoxia and better health outcomes.
ABSTRACT
Diverse populations worldwide are differentially affected by coronavirus disease 2019 (COVID-19). While socioeconomic background has been studied extensively, little is known about the genetic variation underlying this phenomenon. This study is aimed at examining the genetic basis behind the great discrepancies among diverse ethnic groups in terms of COVID-19 susceptibility for viral infection, disease prognosis, and mortality. To this end, in silico analysis of single-nucleotide polymorphisms (SNPs) within regulatory sequences of the human angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS2)-the virus's gateway to host cells-and their plausible implications on expression levels was conducted. We provide indication that the variation in the human ACE2 and TMPRSS2 regulatory sequences is likely to be involved in and contribute to this phenomenon. SNPs that are abundant in the more susceptible populations introduce binding sites (BSs) for transcription factors or they may invalidate BSs for transcription repressor-both may enhance target gene (ACE2 or TMPRSS2) expression in the relevant target tissues. SNPs that are abundant in the more resistant populations may invalidate BSs for a transcriptional repressor or they may introduce BSs for a transcriptional repressor or initiator of mRNA degradation, which may reduce target gene expression levels. This aspect, when added to the socioeconomic factors, can be a cause for the divergent prevalence of the disease and the different mortality rates within diverse populations. This demonstration may call for a shift in the paradigm of searching for COVID-19 biomarkers, such that SNPs within regulatory sequences should be of high importance.