COVID‐19 as a trigger of Guillain‐Barré syndrome: A review of the molecular mechanism

Severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) caused a pandemic with serious complications. After coronavirus disease 2019 (COVID‐19), several post‐acute COVID‐19 syndromes (PACSs) and long‐COVID sequels were reported. PACSs involve many organs, including the nervous, gustatory, and immune systems. One of the PACSs after SARS‐CoV‐2 infection and vaccination is Guillain‐Barré syndrome (GBS). The incidence rate of GBS after SARS‐CoV‐2 infection or vaccination is low. However, the high prevalence of COVID‐19 and severe complications of GBS, for example, autonomic dysfunction and respiratory failure, highlight the importance of post‐COVID‐19 GBS. It is while patients with simultaneous COVID‐19 and GBS seem to have higher admission rates to the intensive care unit, and demyelination is more aggressive in post‐COVID‐19 GBS patients. SARS‐CoV‐2 can trigger GBS via several pathways like direct neurotropism and neurovirulence, microvascular dysfunction and oxidative stress, immune system disruption, molecular mimicry, and autoantibody production. Although there are few molecular studies on the molecular and cellular mechanisms of GBS occurrence after SARS‐CoV‐2 infection and vaccination, we aimed to discuss the possible pathomechanism of post‐COVID‐19 GBS by gathering the most recent molecular evidence. Due to the importance of Guillain−Barre syndrome as a long‐COVID disease, this review performs information about the molecular mechanism of post‐acute severe acute respiratory syndrome coronavirus 2.

Severe Acute Respiratory Syndrome Coronavirus Type 2: Insight Into Challenges for Cell Therapy.

Coronavirus disease 2019 has affected more than 4 million people throughout the world since December 2019. It seems this infection has been the most insidious virus of the coronavirus family. This virus causes severe respiratory failure and symptoms in patients and can result in death. Designing a restrict protocol to deal with infections from severe acute respiratory syndrome coronavirus type 2 is critical in cell therapy institutes. In this review, we present the important aspects related to this virus in cell therapy protocols.

Susceptibility to Metabolic Diseases in COVID-19: To be or Not to be an Issue.

Despite the passage of more than 17 months from the beginning of the COVID-19 pandemic, challenges regarding the disease and its related complications still continue in recovered patients. Thus, various studies are underway to assay the long-term effects of COVID-19. Some patients, especially those with severe symptoms, experience susceptibility to a range of diseases and substantial organ dysfunction after recovery. Although COVID-19 primarily affects the lungs, multiple reports exist on the effect of this infection on the kidneys, cardiovascular system, and gastrointestinal tract. Studies have also indicated the increased risk of severe COVID-19 in patients with diabetes. On the other hand, COVID-19 may predispose patients to diabetes, as the most common metabolic disease. Recent studies have shown that Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) binds to Angiotensin-Converting Enzyme 2 (ACE2) receptors, which are expressed in the tissues and organs involved in regulating the metabolic status including pancreas, adipose tissue, gastrointestinal tract, and kidneys. Therefore, SARS-CoV-2 may result in metabolic disturbance. However, there are still many unknowns about SARS-CoV-2, which are required to be explored in basic studies. In this context, special attention to molecular pathways is warranted for understanding the pathogenesis of the disease and achieving therapeutic opportunities. Hence, the present review aims to focus on the molecular mechanisms associated with the susceptibility to metabolic diseases amongst patients recovered from COVID-19.

Covid-19 pathogenesis in prostatic cancer and TMPRSS2-ERG regulatory genetic pathway.

Members of Coronaviridae family have been the source of respiratory illnesses. The outbreak of SARS-CoV-2 that produced a severe lung disease in afflicted patients in China and other countries was the reason for the incredible attention paid toward this viral infection. It is known that SARS-CoV-2 is dependent on TMPRSS2 activity for entrance and subsequent infection of the host cells and TMPRSS2 is a host cell molecule that is important for the spread of viruses such as coronaviruses. Different factors can increase the risk of prostate cancer, including older age, a family history of the disease. Androgen receptor (AR) initiates a transcriptional cascade which plays a serious role in both normal and malignant prostate tissues. TMPRSS2 protein is highly expressed in prostate secretory epithelial cells, and its expression is dependent on androgen signals. One of the molecular signs of prostate cancer is TMPRSS2-ERG gene fusion. In TMPRSS2-ERG-positive prostate cancers different patterns of changed gene expression can be detected. The possible molecular relation between fusion positive prostate cancer patients and the increased risk of lethal respiratory viral infections especially SARS-CoV-2 can candidate TMPRSS2 as an attractive drug target. The studies show that some molecules such as nicotinamide, PARP1, ETS and IL-1R can be studied deeper in order to control SARS-CoV-2 infection especially in prostate cancer patients. This review attempts to investigate the possible relation between the gene expression pattern that is produced through TMPRSS2-ERG fusion positive prostate cancer and the possible influence of these fluctuations on the pathogenesis and development of viral infections such as SARS-CoV-2.