The same can be said about disease research, driven by the number of diseases, both noncommunicable and infectious, that are currently lacking effective treatments options. It is easy to see "finding a cure" as the main goal of disease research, but that future-focused vision excludes individuals suffering in the present. A common trend in disease research now is long-term effects of disease, as in, what will happen when we are exposed to such pathogens or experience a disease for an extended period of time? Additionally, how do one-off infections change our health down the road, after the symptoms have come and gone?
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| Image borrowed from https://alzheimersdiseasebiol2095.wordpress.com/ |
It is especially interesting when pathogens overlap or influence noncommunicable diseases, as seen with HPV and cancer, just to name one example. Recently, a relationship between specific Human Herpes Virus (HHV) strains (6A and 7) and Alzheimer's disease was "accidentally" discovered by researchers at Mt. Sinai's Icahn School of Medicine. Twice as much HHV was detected in brain tissue from individuals with Alzheimer's compared to brain tissue of those without Alzheimer's.
Although a direct link isn't clear, this is still an interesting finding. Yet, not a surprising one...
HHV-6 is a neurotropic virus, meaning it can invade nervous system. There are many viruses that are neurotropic, so it would be interesting to see if any of the others, like Japanese encephalitis virus, polio, and rabies (just to name a few) have similar influence on chronic disease down the road.
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| Image from Mayo Clinic Foundation for Medical Education and Research |
HHV-6 is often acquired at a young age, producing a non-specific febrile illness and a rash, called "roseola". HHV-6 is spread through saliva droplets, similar to how a cold or flu are spread, so it is easy to imagine how so many young children acquire the infection. For many, the symptoms can look a lot like a seasonal flu infection with a rash, but it can also cause febrile seizures, encephalitis or intractable seizures. Many also suspect symptoms of chronic fatigue and extreme malaise.
The interesting thing about many herpes viruses is that after the initial infection, which may or may not cause symptoms, the virus experiences a period of latency, where it hides in a specific type of cell, before reactivation later in life. The type of cell that supports latency of the virus depends on the type of herpes virus, as they all have their own favorite. Some prefer nervous system cells, whereas others prefer cells of the immune system. According to Bjørn Grinde, HHV-6 prefers leukocytes, which play a large roll in inflammatory pathways and immune system function. Leukocytes can be trafficked across the blood brain barrier and into the central nervous system, which may be the way latent HHV-6A found its way into the brains of the Alzheimer's disease study at Mt. Sinai.
HHV-7 is also considered a roseola virus and causes similar symptoms in infants. HHV-7 prefers T-cells for latency (also according to Bjørn Grinde's paper... I am not a herpes researcher!), which are also critical cells for immune response. Similarly to HHV-6A, T-cells can cross the blood brain barrier, which may expose the central nervous system to latent HHV-7 virus.
Regardless of the molecular methods used, these viruses may contribute to the activation or progression of Alzheimer's disease. Pretty interesting!
