A narrative review of coronavirus disease 2019 (COVID-19): clinical, epidemiological characteristics, and systemic manifestations

Abstract

Coronavirus disease 2019 (COVID-19) is an emerging infectious disease which has had a rapid surge in cases and deaths since it is first documented in Wuhan, China, in December 2019. COVID-19 is caused by the Betacoronavirus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). SARS-CoV-2 uses angiotensin-converting enzyme 2, which is highly expressed in the human lower respiratory tract but also in other tissues, as the cellular entry receptor. Thus, COVID-19 mainly affects the respiratory system but can cause damage to other body systems, including the cardiovascular, gastrointestinal, hepatobiliary, renal, and central nervous systems. We review the pathogenesis and clinical manifestations of the infection, focusing on our current understanding of the disease mechanisms and their translation to clinical outcomes, as well as adverse effects on different body systems. We also discuss the epidemiology pathogenesis, clinical, and multi-organ consequences, and highlight some of the research gaps regarding COVID-19.

Analytical Performance of COVID-19 Detection Methods (RT-PCR): Scientific and Societal Concerns

“…A bewildering viral diversity has been found even in single patients, with a median number of four/five intra-individual variants [38,42]. It should be stressed that such heterogeneity in viral RNAs not only could help explaining differences in intra-individual immunological response and clinical pathophenotype [43] but can also undermine the accuracy of RT-PCR detection [44]. Consequently, it is currently assumed that about 10-15% of SARS-CoV-2 variants were not detectable by at least one of the commercialized primers [45].…”

Mild COVID-19 manifestation in multiple risk factor patient on methotrexate, who had been treated with UVB phototherapy and had sufficient plasma 25-OH-vitamin D3 level

“…According to the current knowledge, the basic pathogenetic mechanisms responsible for the propensity to severe COVID-19 course in the patients at risk could be reduced to a common denominator relating to facilitation and reinforcement of inflammatory processes. Inappropriately excessive and uncontrolled inflammation more likely can result with the development of autodestrucitive cytokine storm, which is considered to be the final effector mechanism of tissue damage 4,6,10,11 . Obesity, insulin resistance and diabetes mellitus, as well as hypertension, are characterized by the presence of persistent low-intensity inflammation, which may be decisive underlying factor amplifying and perpetuating viral-induced inflammatory response [4][5][6][7][8][9][10][11] .…”

“…Some authors also suggest pathogenetic involvement of immunogenic damage-associated molecular patterns (DAMPs), released as a consequence of preexisting disease 29 . Immunosuppression is thought to favor more severe disease development by permitting faster viral replication resulting in extensive direct viral-mediated tissue damage 4,6,11 . In the other hand, immunosuppression can mitigate excessive inflammation.…”

“…Such chronic proinflammatory state can arises either due to hypersecretion of proinflammatory adipokines in obese patients 7 , lack of anti-inflammatory signaling in diabetic and insulinresistant patients 7,8 or dysregulation of renin angiotensin system (RAS) with increased proinflammatory angiotensin II (Ang II) production in hypertensive patients 6,9,10 . Patients on immunosuppressive therapy are considered to be at risk due to the facilitated viral multiplication and dissemination during the initial phase, enabling in turn more vigorous ignition of hyperinflammatory phase 6,10,11 . In the other hand, hyperactive inflammatory processes could be, in some extent, kept under control by immunosuppressants 12 , but conclusions and recommendations on their use in COVID-19 patients are inconsistent and unclear.…”

Chest CT and Clinical Features of COVID-19 Patients in the Early Stage of the Epidemic: An Observational Study from China

“…We performed a statistical analysis of radiological ndings of all enrolled patients (Table 2). The median time interval from the rst Chest CT after admission to the symptom onset was 18 [13][14][15][16][17][18][19][20][21][22][23][24][25][26][27][28][29] days, and the time of the last CT examination was 41.5 [33-52.75] days. According to imaging examination, 94% patients showed bilateral pneumonia, and about half showed peripheral distribution.…”