SARS virus and SARS-CoV-2 belong to the genus coronavirus, with a genome length of about 29,000 bp, and invade cells by recognizing and binding to the angiotensin-converting enzyme 2 (ACE2) receptor via the S protein. The genome sequences of the two viruses share 79% homology. The intermediate hosts of the SARS virus are bats and palm civets, whereas those of the SARS-CoV-2 are species of bats, pangolins, and humans[4]. Because of limitations in technology, the duration of the epidemic, and the number of infected people, we have less research on the SARS virus. SARS-CoV-2 has a much longer range and duration of the epidemic, and with the development of molecular detection technology and mRNA technology, SARS-CoV-2 has been studied more intensively. The receptor distribution of SARS-CoV-2 is much broader, and they are also distributed in animals such as pigs, ferrets, and rhesus monkeys, which show different susceptibility due to the different abundance of ACE2. Therefore, SARS-CoV-2 is more widely spread than SARS. Nevertheless, the primary cause of death is the rapid replication of the virus in the lungs, triggering a robust immune response and cytokine storm, which induces acute respiratory distress syndrome and respiratory failure.
In this study, we found that SARS pneumonia infections were more common in young and middle-aged patients, new crown infections were more common in middle-aged and old-aged patients, and there was a population susceptibility difference between the two viruses. There were more males than females in both groups. Megan O'Driscoll et al[5] evaluated the relationship between age and mortality in patients infected with SARS-COV-2 in 13 countries. Although SARS-COV-2 infection was highly heterogeneous, age and mortality were positively correlated in young adults < 65 and older adults ≥ 65. Zunyou Wu et al [6] found a generalized susceptibility to SARS-COV-2 in the population; however, older men over 60 years of age with comorbidities were more likely to develop severe and critical infections and even had a higher mortality rate.[4] Initial studies found that pregnant women were not at high risk.[7] Follow-up studies have also found that the prevalence of infection in pregnant women ranges from 3 to 20%, which is lower than that in the general population, and this finding may be related to the special immunity status of pregnant women[8]. The higher rates of severe illness and mortality in elderly patients are also related to decreased immunity[9]. However, there are few studies related to SARS, and the amount of data is insufficient to make comparisons; improving the body's immunity is a way to treat SARS-CoV-2 infections.
The number of perfect humoral immunity indexes of SARS and SARS-CoV-2 pneumonia patients in this study did not exceed 50%. There was no significant difference between IgG and IgA in the antibody indexes, and the IgM indexes were higher in patients with SARS pneumonia than those with SARS-CoV-2 pneumonia; this finding suggests that the immune system responses to the viruses differ, possibly because of the differing mechanisms of interaction between the viruses and the human host.
Previous studies found that the most common symptoms of SARS-CoV-2 pneumonia are fever, malaise, and dry cough[2, 7, 10]. The most common symptoms of SARS pneumonia were fever, cough, and malaise[11]. This result is in general agreement with the results of our study. Bo Shen et al. [12] found that SARS-CoV-2 infection led to downregulation of platelet expression of chemokines such as platelet pro-alkaline protein and platelet factor 4, which led to thrombocytopenia; however, the average values of platelet indexes in the SARS and coronavirus pneumonia groups were within the normal range and did not show any statistically significant difference. Lymphocytes are an essential immune system element, and the abundance of naïve T cells decreases significantly with age. Divij Mathew et al. [13] found a negative correlation between the severity of SARS-CoV-2 pneumonia and the number of T-lymphocytes; in this study, we found that the percentage of lymphocytes in patients with SARS-CoV-2 pneumonia was significantly lower than in the SARS pneumonia group, suggesting that the viruses cause different degrees of bone marrow suppression.
On account of ACE2 receptors are widely distributed in cardiomyocytes, SARS-CoV-2 invades cardiomyocytes through ACE2 receptors. Oudit et al. [14, 15] found coronavirus RNA in autopsied heart samples from patients with SARS-CoV-2 infection. The primary markers of myocardial injury in SARS-CoV-2 patients were creatine kinase, troponin T, and NT-pro BNP. Only lactate dehydrogenase and creatine kinase were available during the SARS pneumonia epidemic due to limitations in detection technology. In this study, creatine kinase was higher in patients with SARS pneumonia than in patients with coronavirus infections. The fact that SARS patients had more symptoms of chest tightness and fewer symptoms of myalgia suggests that SARS may cause more myocardial damage; due to limitations of the testing technology, definitive results are not yet available.
As the coronaviruses iterate, their pathogenicity may decrease, their infectivity may increase, and they will probably coexist with humans for a long time. SARS-CoV-2 infecting humans will cause long-term effects on the on the cardiovascular system, respiratory system and nervous system, among other systems[16], such as myocardial damage, decreased lung function, pulmonary fibrosis, loss of smell, headache, vertigo, etc. Rare sequelae include decreased vision and cognitive deficits. The sequelae of SARS pneumonia are unclear; telephone follow-up revealed osteoporosis, visual impairment, and even mobility problems after high-dose hormone treatment. The problem of how the human body defends itself against the virus and how we address the effects of long SARS-CoV-2 must be faced now and in the future. Defending against the virus includes improving immunity and regular vaccination. Improving the functional deficits caused by SARS-CoV-2 requires rehabilitation interventions. Research on the disease's mechanisms and medical technology exploration is needed to prevent and develop strategies for emerging pathogens.