Why is OC43 BETA a topic of interest in medical news?

In addition to the Coronavirus strain that infects humans, some very pathogenic zoonotic strains such as severe acute breathing syndrome Coronavirus (SARS-COV) in 2002, Middle Eastern Respiratory Syndrome Coronavirus (MERS-COV) in 2011 and Novel Coronavirus Covid -19, infected 8.24 million people and claimed to live more than 446,000 thousand individuals worldwide.

OC43 BETA classification

In the order of the nidiovirul virus is the cornidovirineeae suborder. In Cornidovirineea are two subfamilies known as Letovirinae and Orthocoronairinae. All Coronavirus is in orthocor virinae subfamiliation; However, certain Coronavirus strains can be further classified into one of the four genera, including Alphacoronavirus, Betacoronavirus, Gammacoronavirus, and Deltacoronavirus. While HCOV and HCOV-NL63 were found in the genus Alphacoronavirus, OC43 BETA, and HCOV-HKU1, MERS-COV, SARS-COV and SARS-COV-2 were all classified in the genus betacoronavirus.

How does OC43 BETA enter the cell?

The entry of HCOV-OC43 into human cells is largely achieved through endocytosis pathways that depend on Caveolin-1; However, vesicles containing viruses on the cell surface can also experience SCIS to penetrate human cells.

In particular, while host-induced interferon (iFITMS) transmembrane proteins often prevent Coronavirus entry such as HCOV-229E, -NL63, SARS-COV and MERS-COV from entering cells through various antivirus functions, IFITM2 and IFITM3 promoting subsequent entries and infections From OC43 BETA to human cells.

After HCOV-OC43 entered the cell, the infection was mainly due to a stress response by the endoplasmic reticulum (ER). Under normal circumstances, ER is responsible for modifying synthesis, fold and post-translation of many proteins; However, when the ER processing capacity is reached, the accumulation of wrong proteins or open will occur, resulting in stress response by this vital organ. If not referred to as a protein (UPR) response that is not folded, the ER voltage response by HCOF specifically activates Inositol, which requires enzyme 1 (IRE1) and induces protein x-box 1 (XBP1) splicing mRNA.

Furthermore, the HCOV-OC43 protein can introduce a two-point mutation of H183R and Y241H into human cells, both of which contribute further to the mRNA XBP1 splicing and overall infected apoptotic deaths. Cell apoptosis caused by OC43 BETA has also been proven because of the mitochondrial translocation of protein X associated with BCL-2 (Bax).

In addition to the direct role in inducing ER voltage response, HCOV-OC43 has also been proven to reduce regulating more than 30 genes involved in the default immune response, some of which include map kinases, receptors such as toll, interleukin, interleukin, and signal transduction proteins.

Conclusion

In addition to the most prominent effect on the upper respiratory tract and the possibility of neuron infiltration, OC43 BETA outbreaks in Normandy, France, found that this virus can also cause various digestive problems. More specifically, this plague found that up to 57% of patients with HCOV-OC43 experienced vomiting, diarrhoea, and abdominal pain.

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