Several proteins encoded by viral RNA can also interact with various human cellular proteins to disrupt their function. Once the viral RNA has access to the cytoplasm, translation of viral proteins and replication of viral RNA can occur, ultimately leading to the assembly of virions that are released from infected cells by exocytosis 10. Following receptor binding, proteolytic cleavage of the viral S protein by TMPRRS2 exposes a fusion peptide signal that permits mixing of viral and human membranes and release of viral RNA into the cytoplasm 10. Both SARS-CoV-1 and SARS-CoV-2 enter cells via the angiotensin-converting enzyme 2 (ACE2) receptor using the serine protease TMPRSS2 (transmembrane protease, serine 2) 9. There is a high degree of homology between the genetic sequences of SARS-CoV-1 and SARS-CoV-2 and extensive similarity in the predicted viral:human interactome between the 2 strains 7, 8. In addition to SARS-CoV-2, there are 6 other strains of coronavirus that are known to infect humans, including 4 less severe strains that cause mild symptoms, as well as the more pathogenic viruses SARS-CoV-1, which causes severe acute respiratory syndrome (SARS), and MERS-CoV, which is responsible for Middle East respiratory syndrome (MERS) 6. SARS-CoV-2 belongs to the coronavirus family of positive-sense, single-stranded RNA viruses 6. However, as many countries prioritize testing only for hospitalized patients, determining the exact percentages of patients in the general population is challenging 4, 5. The percentages of patients vary, but mild cases are reported to be approximately 80%, severe cases are 14%, and critical cases are 6% 2, 3. Severely ill patients require hospitalization for treatment of the infection because of respiratory issues, and critical patients are a subset of the severely ill patients who experience respiratory failure that requires mechanical ventilation support. Patients with mild COVID-19 may or may not seek medical treatment and can sometimes present with mild pneumonia. Mild COVID-19, which, along with asymptomatic COVID-19, comprises the majority of cases, is characterized by symptoms such as fever, shortness of breath, gastrointestinal distress, malaise, headaches, and a loss of taste and smell. The severity of COVID-19 can be roughly categorized into 3 groups based on the severity of the initial infection 2, 3. By April 27, 2020, the virus had spread to at least 185 countries or regions and infected >3 million people, causing at least 210,000 deaths 1. The purpose of this article was to summarize the known musculoskeletal pathologies in patients with SARS or COVID-19 and to combine this with computational modeling and biochemical signaling studies to predict musculoskeletal cellular targets and long-term consequences of the SARS-CoV-2 infection.Ĭoronavirus disease 2019 (COVID-19) is an emerging, worldwide infectious disease pandemic that is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).
Early studies have indicated that there is also considerable musculoskeletal dysfunction in some patients with COVID-19, although long-term follow-up studies have not yet been conducted. Epidemiological data from the SARS pandemic of 2002 to 2004 identified myalgias, muscle dysfunction, osteoporosis, and osteonecrosis as common sequelae in patients with moderate and severe forms of this disease. Both viruses infect the respiratory system, and there are direct and indirect effects of this infection on multiple organ systems, including the musculoskeletal system.
SARS-CoV-2 is closely related to SARS-CoV-1, which causes severe acute respiratory syndrome (SARS). Although the majority of patients who become infected with SARS-CoV-2 are asymptomatic or have mild symptoms, some patients develop severe symptoms that can permanently detract from their quality of life. Coronavirus disease 2019 (COVID-19) is an emerging pandemic disease caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).
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