Could interaction with other viruses stop SARS-CoV-2 replication?
The coronavirus responsible for the ongoing COVID-19 pandemic, SARS-CoV-2, is susceptible to mutations or changes in its genetic sequence. Such mutations have resulted in the emergence of new, more transmissible SARS-CoV-2 variants.
SARS-CoV-2 is most transmissible through the first 8 daysTrusted Source of the virus entering your body. Variants of the virus differ within their transmissibility, and this could be due to distinctions in the body’s capability to respond to them during this time period.
The body’s initial response to the SARS-CoV-2 infection involves the activation of the innate immune response, which is rapid rather than specific to any particular virus.
Thus, to comprehend the differences in transmissibility of SARS-CoV-2 variants, it is vital to characterize the interaction between your virus and the innate immune system.
After entering your body, SARS-CoV-2 initially replicates in the upper respiratory system. This replication triggers an antiviral response involving interferons, a family of proteins that are likely involved in the innate immune response. Interferon production, in turn, switches on the expression of interferon-stimulated genes (ISG) that inhibit viral replication.
Although a robust interferon response might help combatTrusted Source viral infections, studies advise that SARS-CoV-2 inhibits and delays the interferon response.
Dr. Ellen Foxman, an assistant professor at Yale School of Medicine in New Haven, CT, led a recent study that sought to clarify the power of the interferon response to restrict SARS-CoV-2 replication.
The study discovered that as the viral load, or amount, of SARS-CoV-2 in organoids made from upper respiratory system tissue rose and fell, the expression degrees of ISG also increased and declined. Furthermore, the results recommend that the timing and magnitude of the interferon response, that your team measured using ISG expression levels, could influence the progression of the SARS-CoV-2 infection.
Talking to Medical News Today, Dr. Foxman explained that the interactions between your virus and the disease fighting capability might also make clear why a lot of people develop serious illness, whereas others have mild or no symptoms.
Dynamics of the interferon response
To comprehend the interplay between SARS-CoV-2 replication and the interferon response, the researchers collected nasopharyngeal swabs from patients at various stages of COVID-19.
The researchers measured SARS-CoV-2 levels in the swab samples by quantifying viral RNA levels, whereas they measured the degrees of a protein called CXCL10 to track ISG expression levels. This was possible because CXCL10 levels in the upper respiratory system had a positive correlation with ISG expression levels.
As the CXCL10 levels correlated with upper respiratory system virus levels in persons with SARS-CoV-2, CXCL10 production started a few days following the onset of viral replication.
To delineate the time span of changes in SARS-CoV-2 and the interferon response in greater detail, the scientists used laboratory cultures called organoids, which comprise human epithelial cells that line the respiratory system. They used a 3D culture system to create the organoid, that is a way of investigating the behavior of a collection of cells that simulate the human respiratory tract in the laboratory.
The researchers infected the organoid cells with SARS-CoV-2 and measured the viral load and the CXCL10 and ISG expression levels.
The cell culture data showed that SARS-CoV-2 replicated exponentially during the initial 72 hours and plateaued. The viral load doubled in approximately 6 hours during this period.
On the other hand, CXCL10 protein levels and ISG expression levels slowly but surely increased through the initial 72 hours before rapidly increasing over another 24 hours.
These data suggest that SARS-CoV-2 levels rose rapidly after entering your body and gave rise to a strong interferon response that lagged by a few days.
Source: www.medicalnewstoday.com
