Researchers Find New Therapeutic Target Against Chronic Viral Infections


Researchers offer more insight on the role of IFN-I and find a potential therapeutic target that may be able to protect against chronic viral infections.

There are a number of things that can impact our immune system’s ability to eliminate a virus; the expression levels of particular proteins—specifically interferon proteins—is one of them. In the past, human type I interferons (IFNs), a large subgroup of interferon proteins, were thought to be a key player in inducing antiviral immune response. However, as new research comes to light, it is becoming clear that IFN-I may also play a role in persistent viral infections—such as those caused by hepatitis C virus (HCV) or human immunodeficiency virus (HIV)—and it’s not a positive one.

A team of researchers at the INRS-Institut Armand-Frappier Research Centre (INRS) have delved deeper into the role that IFN-I plays when it comes to chronic viral infections. Their findings may help inform new therapeutic measures that can be taken to fight these harmful infections.

Over 1.2 million individuals are living with HIV in the United States alone and the Centers for Disease Control and Prevention estimates that 2.7 to 3.9 million individuals in the United States have chronic hepatitis C. Researchers from around the world are working towards advancing currently available knowledge of these viruses, as well as developing novel therapeutic approaches to reduce these staggering numbers. By closely examining IFN-I, the INRS researchers contribute to this collaborative effort.

To understand the researchers’ work, one first has to understand what IFN-I are and how they have worked in the past to fight acute viral infections. IFN-I are pleiotropic cytokines that are able to encourage antiviral response through the use of signaling pathways. According to a recent INRS press release, “During a typical virus infection, the virus replicates in the infected cell and induces IFN-I expression through pattern recognition receptors (PRRs) signaling. The cytokine then binds a specific receptor (IFNAR) to adjacent cells, which usually triggers reactions that stimulate the host’s immune defenses.” However, it seems that when it comes to chronic infection, “prolonged exposure” to IFN-I can negatively influence immune response, turning IFN-I “from friend[s] [into] foe[s].”

HCV, HIV, and lymphocytic choriomeningitis virus (LCMV) are some known causes of chronic viral infections. Most recently, INRS researchers have been working on analyzing the “molecular mechanisms” that work to inhibit immune system response during chronic viral infections. They take their research a step further by taking a closer look at how IFN-I negatively impact immune system response. According to the press release, the team noted an increased amount of TFH (a subpopulation of CD4+ T-cells), which they found prompted non-specific B lymphocytes expansion. Furthermore, an increased amount of TFH also works to diminish the amount of other T-cells that are essential to fighting infection.

In addition, the team was also able to show that IFN-I signaling has a “direct” effect on humoral immune response. By blocking B cell IFN-I receptors the researchers were able to reestablish antigen-specific immune responses; this means that “IFN-I acts directly on B cells to increase non-specific responses while impairing antigen-specific responses.” For LCMV’s chronic phase, the team was able to pinpoint the IFN-I signaling pathways that lead to humoral immune response disruption. Therefore, it is apparent that IFN-I is a key player in humoral response disruption, but the question of whether IFN-I production is a cause or effect of chronic viral infection remains unknown. Nonetheless, IFN-I’s role in humoral response disruption can provide researchers with a new therapeutic target that can be used against chronic viral infections.

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