No abstract
Since SARS-CoV-2 first appeared in humans, the scientific community has tried to gather as much information as possible in order to find effective strategies for the containment and treatment this pandemic coronavirus. We reviewed the current published literature on SARS-CoV-2 with an emphasis on the distribution of SARS-CoV-2 in tissues and body fluids, as well as data on the expression of its input receptors on the cell surface. COVID-19 affects many organ systems in many ways. These varied manifestations are associated with viral tropism and immune responses of the infected person, but the exact mechanisms are not yet fully understood. We emphasize the broad organotropism of SARS-CoV-2, as many studies have identified viral components (RNA, proteins) in many organs, including immune cells, pharynx, trachea, lungs, blood, heart, blood vessels, intestines, brain, kidneys, and male reproductive organs. Viral components are present in various body fluids, such as mucus, saliva, urine, cerebrospinal fluid, semen and breast milk. The main SARS-CoV-2 receptor, ACE2, is expressed at different levels in many tissues throughout the human body, but its expression levels do not always correspond to the detection of SARS-CoV-2, indicating a complex interaction between the virus and humans. We also highlight the role of the renin-angiotensin aldosterone system and its inhibitors in the context of COVID-19. In addition, SARS-CoV-2 has various strategies that are widely used in various tissues to evade innate antiviral immunity. Targeting immune evasion mediators of the virus can block its replication in COVID-19 patients. Together, these data shed light on the current understanding of the pathogenesis of SARS-CoV-2 and lay the groundwork for better diagnosis and treatment of patients with COVID-19.
Since its first detection, coronavirus disease 2019 (COVID-19) caused by coronavirus SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) infection has spread rapidly around the world. Although coronavirus SARS-CoV-2 primarily targets the respiratory system, complications in other organ systems (cardiovascular, neurological, and renal) can also contribute to death from the disease. Clinical experience thus far has shown substantial heterogeneity in the trajectory of SARS-CoV-2 infection, spanning from asymptomatic to mild, moderate, and severe disease forms with low survival rates. Accurate prediction of COVID-19 mortality and the identification of contributing factors would allow for targeted strategies in patients with the high risk of death. We aimed to identify clinical and laboratory features that contributed the most to this prediction. An improved understanding of predictive factors for COVID-19 is crucial for identify those with higher risk of mortality and for clinical decision making to reduce the risk of death. The main risk factors for the severe course of COVID-19, the development of complications and death include old age, concomitant diseases (cardiovascular diseases, chronic lung diseases, diabetes mellitus and hypertension), body temperature 37.8C, oxygen saturation 92%, quantitative and functional depletion of innate immunity, bilateral pulmonary infiltrates, increased levels of laboratory parameters of systemic inflammation, respiratory, cardiac, renal and/or hepatic failure. Proper assessment of prognostic factors and careful monitoring to ensure the necessary interventions at the appropriate time in high-risk patients can reduce the fatality rate from COVID-19.
Not all the patients who are diagnosed with COVID-19 can completely recover; some of them experience miscellaneous persistent symptoms that subsequently wax or wane. As the COVID-19 pandemic continues, the number of people with long-term symptoms is rapidly increasing, adding to the burden on healthcare and society. The prevalence of the consequences of COVID-19 varies between studies, with some reporting that more than half of hospitalized patients have prolonged symptoms for at least 6 months after acute SARS-CoV-2 infection, and others for more than 12 months. The overall prevalence of residual symptoms in patients infected with SARS-CoV-2 is currently estimated to be 1030%. This clinical syndrome is commonly referred to as post-acute COVID syndrome (PACS) or long COVID. This multifactorial syndrome is characterised by a variety of debilitating symptoms, including fatigue, brain fog, postural hypotension with tachycardia, and post-exertional malaise. Many of the observations of post COVID-19 condition, including changes in immune, cardiovascular, gastrointestinal, nervous and autonomic systems, are shared with the symptoms described in myalgic encephalitis/chronic fatigue syndrome (ME/CFS) patients. Comprehensive longitudinal symptom monitoring is required to confirm of diagnosis, uncover the mechanisms of post-COVID-19-associated ME/CFS, and develop prevention and treatment measures. Current absence of the effective treatment reflects the unclear causes of the post COVID-19 conditions which cannot be targeted properly until the mechanism is established and confirmed. The multisystem aspects of long COVID remain poorly understood. The COVID-19 pandemic has exposed a significant gap in knowledge about the post-acute consequences of infectious diseases and the need for a unified nomenclature and classification of post-COVID conditions, diagnostic criteria, and reliable assessments of these disorders. Unraveling the complex biology of PACS relies on the identification of biomarkers in plasma and tissue samples taken from individuals infected with SARS-CoV-2 that will allow classification of the phenotypes of patients who develop PACS. For the full treatment of patients with post-COVID syndrome, multidisciplinary therapy and rehabilitation are required. Understanding the physiological mechanisms underlying the long-term clinical manifestations of COVID-19 and the post-COVID-19 state is vital to the development of appropriate effective therapies.
COVID-19 is characterized by a wide range of clinical manifestations, from asymptomatic to extremely severe. At the onset of the pandemic, it became clear that old age and chronic illness were the major risk factors. However, they do not fully explain the variety of symptoms and complications of the SARS-COV-2 coronavirus infection. The research on genetic risk factors for COVID-19 is still at its early stages. A number of mutations and polymorphisms have been identified that affect the structure and stability of proteins factors of susceptibility to SARS-COV-2 infection, as well as a predisposition to the development of respiratory failure and the need for intensive care. Most of the identified genetic factors are related to the function of the immune system. On the other hand, the genetic polymorphism of the virus itself affects the COVID-19 spread and severity of its course . The genome of the virus accumulates mutations and evolves towards increasing contagiousness, replicative ability and evasion from the host's immune system. Genetic determinants of the COVID-19 infection are potential therapeutic targets. Studying them will provide information for the development of drugs and vaccines to combat the pandemic.
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