When the Coronavirus disease (COVID-19)—caused by novel coronavirus SARS-CoV-2—emerged in Wuhan, Hubei province, China in December 2019, it quickly spread across the world. As it merged into an ongoing pandemic with numerous medical, societal, and financial challenges, one of the biggest public health concerns continues to be the urgent need for an effective therapeutic measure, pathogenesis, and a stronger understanding of its epidemiology.
In a study published on PubMed.gov on May 20, 2020, scientists, researchers, and medical professionals analyzed the clinical molecular immunological data from 326 confirmed cases of COVID-19 in Shanghai.
In this study, it’s reported that genomic sequences of SARS-CoV-2 assembled from 112 quality samples together (with the sequences in the Global Initiative on Sharing All Influenza Data) showed a stable evolution that might suggest two notable lineages with different exposure histories during the earliest phase of the beginning of the outbreak in Wuhan.
Regardless, they experienced similar virulence and clinical outcomes.
The clinical and epidemiological information for the cohort included 326 patients in Shanghai between Jan 20 and Feb 25, 2020.
This study divided the infected cases into four unique categories—five individual were considered asymptomatic (as having no obvious fever, radiological manifestations, or respiratory symptoms; a majority (239) had a mild disease with fever and radiological manifestations of pneumonia; 12 had symptoms of dyspnea and signs of ground-glass opacity in their lungs within 24-48 hours, and another 16 deteriorated into acute respiratory distress syndrome (ARDs) and required mechanical ventilation or extracorporeal membrane oxygenation (categorized as critical).
The analysis based on this study suggests evidence that the viral genome is largely stable and, in consistence with a recent study, that small sequence variations divided the viral genomes into two major clades.
This study suggests that lymphocytopenia—especially the reduced CD4+ and CD8+ T Cell counts upon admission—was a predictive factor of how the disease would progress. Higher levels of IL-6 and IL-8 during the treatment process were observed within patients who had a severe or a critical disease and correlated with the decrease lymphocyte count.
As the study suggests, the determinants of how severe the disease was and how it affected each patient diagnosed with it was based on and stemmed mostly from host factors like age, lymphocytopenia, and its associated cytokine storm.
Alternatively, viral genetic variation did not affect the outcomes of this significant enough to take note.