Crucial immune system proteins are not entirely supportive of the body when dealing with certain viruses, as three new studies find. Some viruses, such as the lymphocytic choriomeningitis virus, or LCMV, used on mice in all three studies, result in the proteins sending out messages destroying antibody-producing immune cells. With the cells depleted, the viruses have it easier avoiding extermination. All three studies blame the type 1 interferons for this, which are responsible for the loss of B cells, delaying greatly the destruction of the virus by T cells, as well as the predicament they present. Interestingly, T cells, which are also an essential part of the immune system, are among the cells used to eliminate B cells prematurely, as directed by type 1 interferons.
The T cells are not the only usually helpful part of the immune system suddenly turning on its compatriots. Type 1 interferons are usually responsible for making cells less hospitable for viruses. Instead of being bad for the virus, they are doing harm unto the body, in these three instances. The reason for this is not known at the moment.
The studies help explain how certain chronic infections evade immune system response, and help point the way for solving this particular issue. The culprit has been identified, though the immediate reason for the actions is not entirely clear. This, at least, presents a clear course of action: to find out what is the cause of the apparent “friendly fire”, and how to stop it. The direct long-term applications of this are unclear, however, as it is unknown whether or not this issue persists in other viral infections. If it does, the potential is immense for treatment. Chronic infections, which can vary from a minor, if lengthy, annoyance to a serious danger, could possibly become inconsequential. They could turn into the equivalent of a minor bruise, if further research is pursued. If not, the issue will be little more than a footnote in medical history. Unfortunately, the studies are not sure if the situation applies to other types of viral infections, or if it even impacts humans. This does not, however, fully invalidate reason for further research into this particular subject. The potential is still present.
Interestingly, the effect of type 1 interferons and the harm it causes is not just limited to long term. When dealing with an infection, B cells receive orders from the type 1 interferons to transform into cells which rapidly produce antibodies for the virus currently plaguing the organism. The cells die off shortly thereafter, leaving the organism more vulnerable for long term infections, but short term ones as well. Once again, more questions arise. Is this course of action voluntary? Is it malicious intent? Is it a side effect of a virus evolving to take advantage of a minor flaw in the immune system? The article does not state why the mice’s immune systems reacted the way they did, though the fun does derive from trying to finding the answer.