Corona virus, SARS or Ebola – some particularly problematic viruses originally developed in bats. But why of all things in these animals? A study provides an explanation for this: According to this, bats breed sharp viruses, as it were. They have an immune system that keeps the pathogens at bay – and in return, the viruses upgrade. With these aggravated pathogens, the comparatively weak immune defense of humans is then rather overwhelmed, the explanation.
It is not uncommon for viruses to sometimes cross species boundaries: most of the newly emerging viral diseases in humans originally come from animals. In the case of influenza, birds, pigs or rodents are often the source of pathogens. But many particularly dangerous viruses such as Ebola, Marburg, Sars or the new coronavirus Sars-CoV-2 originally developed as a reservoir host in bats, according to studies. Through contact of humans with bats or through another animal as an intermediary, these pathogens made the leap onto humans.
Infection test on bat cells
The researchers around Cara Brook from the University of California at Berkeley have investigated why bat viruses are so particularly aggressive and reproductive. “Bats can harbor viruses that are highly virulent for non-flying mammals for a long time without showing any obvious symptoms of the disease,” says Brook. What made the animals so resistant and how this could influence the aggressiveness of the pathogens, she and her colleagues have investigated in cell cultures of the black fruit bat (Pteropus alecto) and the Nile fruit bat (Rousettus aegyptiacus). Both are known to be natural reservoirs for aggressive viruses. In the experiment, the researchers infected the cell cultures and control cultures from cells of the Vervet Monkey with various Marburg and Ebola-like viruses.
It turned out that the viruses took the monkey cells away within a few days. However, this was not the case with bat cell cultures: the progression of the infection slowed down significantly. Although many cells were infected, some seemed to be able to successfully defend themselves against the attack: they remained healthy and not infected even after several days. “It’s like a fire that burns through a forest,” Brook explains. “Some trees – here bat cells – have protective blankets so that the fire rushes past without harming them.” At the same time, glowing coals remain in the forest, from which a new fire can start at any time. In cell culture, this corresponds to bat cells that still carry active viruses.
Strong defense breeds “turbo viruses”
A model of the bat immune system that the researchers used to simulate the infection then clarified what the bat cell’s protection strategy is based on: the first time the virus is in contact, the entire system is flooded with the messenger substance interferon-alpha. This activates the cellular defense and causes the cells to isolate themselves from the pathogen. At the same time, the messenger prevents an excessive inflammatory reaction and thus dampens the symptoms of the disease. “If our immune system tried the same antiviral strategy, it would trigger a system-wide inflammation,” explains Brook. Because we humans and most other mammals lack the strong interferon-alpha release and the strong anti-inflammatory immune response. Ultimately, the immune system of the bats is up-regulated and acts accordingly effectively against pathogens, the researchers sum up.
The results explain why bat viruses can be so dangerous for us. “If you have a strong immune response and some cells are protected from infection, the virus can up-regulate its multiplication without its host dying,” Brook explains. This makes the viruses more pathogenic, but still preserves their reservoir hosts. “Our study thus demonstrates how the bats’ immune system can boost the virulence of such pathogens,” says Brook. If a corresponding virus spreads to humans or other mammals, it can develop a threatening potential. Because their much weaker immune system can hardly counter this “turbo virus”.
Source: University of California – Berkeley, Technical article: eLife, doi: 10.7554 / eLife.48401