COVID-19 Pathophysiology, Clinical Manifestations, and Drug Treatment
Authors: Manzur Sandoval Daniel , Rojas-Velasco Gustavo , Melano Carranza Efren , Cruz Rodr´ıguez Camelia , Arzate Ram´ırez Arturo , avier Gonzalez Ruiz Francisco J , Arteaga Cardenas Gerardo , Lopez Polanco Mar´ıa Alexandra , Gonzalez Escudero Eduardo Alberto , Garc´ıa Cruz Edgar , Baeza Herrera Luis Augusto , Santos Mart´ınez Luis Efren 
Published: September 2022

COVID-19 is caused by a single-stranded RNA encapsulated betacoronavirus, known
as SARS-CoV-2, implicated in the pandemic that started in China in 2019. Viral replication
consists of five stages that culminate in the release of the new virion. The exaggerated
inflammatory response of COVID-19 is characterized by an elevation of acute phase reactants such
as C-reactive protein and ferritin. It is associated with an unfavorable clinical course, intensified&nbsp;by abnormal activation of the protein complex called the inflammasome. When the immune
response does not control the virus, lung tissue damage occurs that leads to the massive release of
proinflammatory cytokines, producing acute respiratory failure syndrome. Vascular permeability
is increased; interaction with coagulation factors develops disseminated intravascular coagulation
and multiorgan failure. Up to 33% of cases can be asymptomatic. Clinical manifestations can
be mild or severe and involve various organs and systems. Among the most commonly affected
are: respiratory, cardiovascular, renal, and hematological and coagulation systems. Among the
most representative laboratory data are: elevation of inflammatory markers (CRP, inflammatory
cytokines, tumor necrosis factor), high levels of D-Dimer, elevation of troponin I, lymphopenia,
thrombocytopenia, alteration of liver enzymes and kidney function. There are risk factors and
comorbidities that contribute to the severity of the clinical picture (mainly cardiovascular and
metabolic diseases): diabetes mellitus, high blood pressure, obesity, chronic lung diseases,
cancer, and chronic kidney failure. There are also other genetic factors associated with the
host’s immunopathogenesis and response to SARS COV-2 infection. There are various imaging
methods that allow adequate identification and involvement of the pulmonary and cardiovascular
systems with great sensitivity and specificity (computed tomography and echocardiography). The
pandemic imposed decisions with very little information regarding what may be useful as a
therapeutic strategy. This uncertainty applies to the treatment indicated in the prevention phase, as
well as to the different stages of severity of the disease. In many cases, treatments were applied
without having gone through a trial phase but only with the theoretical support of its probable
benefit. However, over time, controlled studies showed that they did not provide any benefit and
that they could even have a deleterious effect. Other therapies still in use have shown contradictory
results in the different clinical trials where they were tested. Very few therapeutic options have
shown undisputable benefit so far. The only ones that can modify the presentation or course of
the disease are vaccines, which have also been developed in record time and in controlled trials,
and all those that have been approved showed a decrease in the risk of infection and in the risk of
presenting a severe manifestation of the disease.<br>