The COVID-19 pandemic has affected the world in unprecedented ways, leaving researchers and medical professionals scrambling for answers to an ever-growing list of questions. One of the most critical areas of study has been the transmission of the SARS-CoV-2 virus from cell to cell. Recent findings suggest that protein OCLN plays a crucial role in this transmission process, shedding new light on the mechanisms that make this virus so infectious. In this article, we will explore the latest research on protein OCLN and its implications for combatting the spread of COVID-19.
A recent study published in the journal PNAS has shed light on the role of the tight junction (TJ) protein occludin (OCLN) in the cell-to-cell transmission of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus inside a host. The study found that OCLN is a critical host factor involved in SARS-CoV-2 entry and subsequent cell-to-cell viral transmission. The researchers examined the effect of SARS-CoV-2 on TJ proteins, specifically OCLN, and found that the virus-induced fusion of virus-infected cells with neighboring cells and the creation of syncytia requires breaking the intercellular barrier, thus the TJ proteins may be involved in the spread of SARS-CoV-2 via cell-to-cell transmission.
The study used infected Vero-E6 cells expressing enhanced green fluorescent protein (eGFP) and SARS-CoV-2 S (rVSV-eGFP-S) and confirmed that OCLN levels became undetectable 48 hours post-infection in infected Vero-E6 cells. The researchers discovered that OCLN served as a host-origin internalization factor for SARS-CoV-2 entry and confirmed its interaction with the SARS-CoV-2 S protein through the co-immunoprecipitation assay. The team also determined that the endosomal entry pathway was engaged in OCLN-mediated SARS-CoV-2 cell-to-cell transmission.
The study pointed out that OCLN-mediated SARS-CoV-2 internalization and subsequent cell-to-cell transmission decreased immediately upon its knockdown but markedly enhanced both internalization and replication upon its overexpression. However, OCLN could not be considered a receptor or coreceptor for SARS-CoV-2 entry, although its function has been established as a vital host factor for the entry of several viruses inside a human host, such as rotavirus and hepatitis C virus. The study found that SARS-CoV-2 only degraded OCLN but had minimal impact on other TJ proteins, such as claudin-1.
The study provided insights into SARS-CoV-2 entry and its subsequent spread inside a human host, proving the crucial role of OCLN in cell-to-cell viral transmission. Further studies should investigate the mechanisms underlying the mechanisms of SARS-CoV-2-induced down-regulation of the synthesis and stability of the OCLN protein in TJs. The researchers presented robust substantiation of OCLN-driven cell-to-cell transmission of WA-1 and all other SARS-CoV-2 variants examined in this study.
In conclusion, the discovery of the role of protein OCLN in facilitating the spread of SARS-CoV-2 between cells could offer new opportunities for therapeutic interventions to combat the COVID-19 pandemic. As researchers continue to delve deeper into the intricate mechanisms of the virus, we are hopeful that groundbreaking discoveries such as these will eventually lead to the development of effective treatments and ultimately, a cure for this global health crisis. Until then, it is vitally important that we continue to follow public health measures and do our part to slow the spread of the virus. Together, we can get through this challenging time and emerge stronger and more resilient than ever.
