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Do you know? Why is the secret connection between the JC virus and the brain able to cross the blood-brain barrier?
JC virus, human polyomavirus type 2, was first discovered in 1965 and is now widely recognized as a causative agent affecting the central nervous system. The complexity of this virus lies not only in its route of transmission and infective effects, but also in how it successfully crosses the blood-brain barrier and affects the human body. Recent studies have shown that JC virus can reactivate when the immune system is suppressed and cause serious diseases such as progressive multifocal leukoencephalopathy (PML).
The initial infection site of JC virus infection may be the tonsils or intestines, and then it lurks in the intestines and can infect tubular epithelial cells in the kidneys.
The virus is spread mainly through contact with contaminated water sources or other environmental media. Eventually, when the body's immune system is low, the JC virus may cross the blood-brain barrier and directly invade the central nervous system. The specific mechanism of this process is still under study, but researchers believe that it may be infection through the 5-HT2A serotonin receptor.
Once the virus enters the central nervous system, it enters oligodendrocytes and astrocytes and continues to multiply. Relevant studies have pointed out that the DNA of JC virus can be detected in the brain tissue of PML patients, and the promoter sequences of these viruses are different between healthy individuals and PML patients. These differences may make the virus more viable in the central nervous system, leading to the development of PML.
Immune deficiency or immunosuppression can promote the reactivation of JC virus and cause fatal progressive multifocal leukoencephalopathy (PML) in the brain. The mechanism remains to be further explored.
It is estimated that in the general population, 70% to 90% of people are likely to be infected with JC virus. Most people get the virus during childhood or adolescence. With high concentrations of JC virus in urban sewage around the world, researchers suspect this is a major transmission route for the virus. Through genotypic analysis, researchers have identified 14 subtypes, some of which are associated with specific geographic areas, helping to understand human migration patterns.
Some studies suggest that JC virus may also be associated with colorectal cancer, as the virus has been detected in some malignancies, but these results remain controversial.
In addition to PML, JC virus is also thought to cause other conditions, such as JC granular cell neuropathy (JCV GCN) and aseptic meningitis (JCVM). Studies have shown that specific mutant strains of JC virus can cause severe damage to cerebellar granule cells, and meningitis is aseptic meningitis caused by JC virus infection.
Because the power of JC virus cannot be underestimated, it is clinically associated with the side effects of a variety of immunosuppressive therapies, including the occurrence of PML in patients with stem-like lymphocytoma when using drugs such as rituximab. This raises urgent questions about JC virus and its interactions with medications, and requires healthcare professionals to be more vigilant when using immunosuppressants.
As the research on JC virus deepens, the correlation between different geographical areas and subtypes of the virus provides a new perspective on human history and migration.
Currently, the need for a deeper understanding of JC virus and its behavior in the central nervous system is becoming increasingly apparent, which has also led to broader exploration. The existence of JC virus and the mechanism of its reactivation in an environment with a low immune system deserve in-depth exploration by the medical community. Is it possible to seek effective preventive methods to reduce the harm caused by JC virus, which has become an important direction of current research?
