The World Health Organization (WHO) recognized the coronavirus disease (COVID-19) as a worldwide pandemic caused by a newly discovered coronavirus responsible for Severe Acute Respiratory Syndrome (SARS-Cov2). The virus appeared in Wuhan, China in December 2019 and spread throughout the world, causing several mortality cases particularly in older people and those with chronic diseases. A body of evidence suggests a multi-target of SARS-Cov2, which may act beyond the respiratory system being responsible for other pathological complications, including the gastrointestinal tract, nervous, and the renal functions. The chapter will provide a literature review of the recent data on COVID-19 physiopathology involving in addition to the respiratory dysfunction all the potential physiological functions which could be independently and directly impaired by the SARS-Cov2.
TopIntroduction
Since December 2019, cases of pneumonia related to a new coronavirus have been reported in China (Ren et al., 2020). This coronavirus, called SARS-CoV-2, causes a disease called COVID-19 (Corona-Virus Disease of 2019). It is an emerging infectious disease of viral zoonosis type. On March 11, 2020, the World Health Organization (WHO) declared COVID-19 a pandemic (WHO, 2020). SARS-CoV-2 infection is characterized by its high contagiousness and unusual potential lethality. Understanding the mechanisms underlying the worsening of COVID-19 is important for the prompt and proactive management of these patients to reduce mortality and morbidity.
A report from the Chinese CDC (Centre of Disease Control), based on data from 72,314 cases, identified several risk factors associated with increased disease severity and mortality, including age over 70 years, cardiovascular disease, diabetes, hypertension, cancer, and chronic respiratory or renal failure (Wu et al., 2020). In Italy, among 355 patients who died, the predictive risk factors for death were high age, high Sequential Organ Failure Assessment (SOFA) index and the presence of co-morbidities. The mean number of co-morbidities in deceased patients was 2.7 (Onder et al., 2020). Some biological abnormalities are associated with a poorer prognosis and/or imminent worsening, such as the depth of lymphopenia and a major increase in inflammation markers (CRP, ferritin, etc.). Other abnormalities are observed in severe forms such as increased transaminases, LDH, troponin and acute renal failure. Several data show that coagulopathy is also central to the process of deterioration of the clinical condition of patients (Onder et al., 2020; Huang et al., 2020).
SARS-CoV-2, like SARS-CoV-1, uses angiotensin converting enzyme 2 (ACE2) as the primary cellular receptor to enter the host cell (Zhou et al., 2020). After an incubation of approximately five days, 70% of infected patients develop cough, fever, or dyspnea (Guan et al., 2020). This phase of viral invasion is followed, in some patients, by an inappropriate immune response marked by worsening of the respiratory symptomatology and inflammatory syndrome, usually eight to ten days after the first symptoms (Huang et al., 2020). This dysimmune phase, sometimes called cytokine storm, may be associated with coagulopathy, the whole corresponding, for some authors, to a viral sepsis (Li et al., 2020a). In bacterial sepsis, the inflammatory reaction, which is deleterious and responsible for organ damage, is particularly difficult to explore (Remy et al., 2020), which may explain the large number of works concerning the cytokine storm in COVID-19. The current pandemic context, accompanied by a multitude of scientific publications, leads to a large and rapidly evolving literature. We propose in this chapter to synthesize the pathogenesis and physiopathology of the SARS-CoV-2 infection as it is known at the date of publication, knowing that it is still subject to evolution.