Researchers at Hopkins have identified a protein that helps control cytomegalovirus (CMV). This virus, which may seem unrecognizable from its name, causes one of the most common viral infections among humans. In fact, the CMV infection is so common that there is a 50 to 80 percent chance that you will have it by the time you are 40 years old.
CMV is extremely infectious: It can be transferred through any bodily fluid. Before you go rushing to the emergency room and ask for immediate tests, relax. CMV very rarely causes any signs or symptoms. Even if you contract the virus, chances are you will never have to deal with it during your lifetime.
Currently, there are no known cures or treatments for CMV infections. While this may be okay for CMV-infected individuals without symptoms, there is a subset of the population that significantly suffers from this dearth of medicine. The virus can cause serious illness in newborns, especially those who were infected before birth. These infants can present serious complications later in life, such as developmental disabilities and hearing problems. Furthermore, CMV can also affect individuals with immune system disorders or advanced HIV and those taking immunosuppressive drugs.
The CMV-regulating protein discovered by researchers at Hopkins is a cell receptor called NOD2.
It can be found in several types of immune cells and has been linked with the immune system’s defense against bacterial infections. When a bacterial invader enters the body, NOD2 alerts other cells of the bacteria’s presence. This prompts a chemical cascade leading to the destruction of the bacteria.
Ravit Boger, an associate professor of Pediatric Infectious Diseases at Hopkins School of Medicine and the lead investigator of this study, discovered that NOD2 has a similar function when presented with DNA viruses. CMV is similar to these DNA viruses because it can alter the DNA of target cells rather than just the cellular defense mechanism. Because of this similarity, Boger’s team linked NOD2 to CMV infections.
Boger’s research is also especially relevant for the treatment of Crohn’s disease. This condition, which is a form of inflammatory bowel disease, is thought to be caused by the gene that that regulates NOD2. This molecular link could explain a correlation Boger observed years ago between patients with Crohn’s who were receiving immunosuppressive drugs and the increased prevalence of CMV among these patients. A mutation in the NOD2-linked gene apparently leads to decreased resistance to both inflammatory pathogens and those that affected the generalized immune system.
To test the link between NOD2 and CMV, Boger’s team infected immune cells with different types of viruses and then tested the cells’ defense mechanisms. The cells without the NOD2 mutation prevented CMV from replicating its viral DNA. In contrast, the cells with a mutation were virtually ineffective at stopping CMV. A more detailed analysis revealed that a single incorrectly transcribed amino acid in the DNA sequence is responsible for the malfunction of NOD2.
This new insight into the role of NOD2 in preventing disease opens up new approaches for the treatment and prevention of CMV, including the possible development of a vaccine against the infection. Additionally, this research reveals a great deal about the general interaction of pathogens with the immune system and how the body’s defense against something as seemingly mundane as the common cold can be dependent on underlying genetic code.
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