Update of the current knowledge on genetics, evolution, immunopathogenesis, and transmission for coronavirus disease 19 (COVID-19)

Abstract

In December 2019, an acute respiratory disease caused by novel species of coronavirus (SARS-CoV-2), emerged in China and has spread throughout the world. On 11 th March 2020, the World Health Organization (WHO) officially declared coronavirus disease 19 (COVID-19) a pandemic, severe coronavirus-mediated human disease. Based on genomic and phylogenetic studies, SARS-CoV-2 might originate from bat coronaviruses and infects humans directly or through intermediate zoonotic hosts. However, the exact origin or the host intermediate remains unknown. Genetically, SARS-CoV-2 is similar to several existing coronaviruses, particularly SARS-CoV, but differs by silent and non-silent mutations. The virus uses different transmission routes and targets cells and tissues with angiotensin-converting enzyme 2 (ACE2) protein, which makes it contagious. COVID-19 shares both the main clinical features and excessive/dysregulated cell responses with the two previous Middle East respiratory syndrome coronavirus (MERS) and severe acute respiratory syndrome coronavirus (SARS) epidemics. In this review, we provide an update of the current knowledge on the COVID-19 pandemic. Gaining a deeper understanding of SARS-CoV-2 structure, transmission routes, and molecular responses, will assist in the prevention and control of COVID-19 outbreaks in the future.

Can Echinacea be a potential candidate to target immunity, inflammation, and infection - The trinity of coronavirus disease 2019

“…SARS-CoV-2 enters into the host cells through interaction and binding with ACE2 receptors, and the virus pathogen-associated molecular pattern (PAMP) signals induce innate immune cells, antiviral effectors such as T CD8+ cells, NK cells, neutrophils, monocytes, and macrophages in the presence of the invading virus. The innate immune cells, which possess PRRs such as TLRs, retinoic acid-inducible gene I RIG-I-like receptors (RLRs), and nucleotide-binding and oligomerization domain NOD-like receptors (NLRs), detect PAMPs and induce a suitable immune response against the invading pathogen [ 118 , 119 , 120 ]. The interaction between the PRR and PAMP triggers phagocytosis and elicits the synthesis of proinflammatory cytokines, such as type I interferon (IFNα/β) and type II interferon (IFN-γ), and chemokines, such as CXCL-10 and CCL-2, producing an antiviral response [ 34 ].…”

Investigating the first stage of the COVID-19 pandemic in Ukraine using epidemiological and genomic data

“…Even well after a year since the epidemic started, fundamental questions regarding the effects of isolation and lockdown measures [16][17] and the genomic evolution of SARS-CoV-2 [18][19][20][21] during the first epidemic wave remain. Additionally, recent modeling efforts aimed at shedding light on those questions have mostly focused on China [1][2][3][4], the rest of Asia [22][23][24], Western and Central Europe [25][23][26], and North America [27][28][29][30][5], largely neglecting Africa, the Middle East, and Eastern Europe.…”

The Role of Immunogenetics in COVID-19

“…Since the emergence of the first documented cases in December 2019, it soon became evident that subjects infected by SARS-CoV-2 experience a disease promptly named coronavirus disease 2019 (COVID-19) with dramatic interindividual variability in its clinical manifestations. In fact, COVID-19 may arise as an asymptomatic state as well as a panel of respiratory conditions ranging from mild flu-like symptoms (fever, fatigue and dry cough) to a severe respiratory disease (including pneumonia and dyspnoea) that may require hospitalization and may be exacerbated by cytokine storm, acute respiratory distress syndrome (ARDS), multi-organ and respiratory failure, with potentially fatal consequences [ 1 , 2 , 3 , 4 ]. In contrast to the SARS-CoV (-1)-caused SARS pandemic (2002/2003), recorded as the first pandemic of the 21st century, the SARS-CoV-2-caused COVID-19 pandemic was not stopped by public health preventive measures in its first season 2019/20.…”

“…Epidemiological data demonstrated that clinically relevant variables like sex, age and comorbidities, as well as viral genome variants were not enough in explaining why subjects with apparently similar clinical history and pre-existent status develop such a different group of symptoms [ 2 , 4 ]. Thus, other factors must contribute to the pathogenesis of the disease, determining which patients will develop an asymptomatic infection and how serious the disease will be in symptomatic subjects [ 4 , 7 ]. Defining these factors will be especially advantageous to detect patients who may benefit from an early hospitalization and therapeutic intervention [ 2 , 3 ].…”