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Viruses help the immune system

16.01.2015

Antibodies are needed by the immune system to catch foreign molecules, and with them their carriers, viruses and bacteria. It would be strange to expect pathogens themselves to help immune cells produce weapons against them. But nothing is impossible for nature - researchers from the University of Texas Southwestern Medical Center, led by Nobel laureate Bruce Beutler, have figured out how endogenous retroviruses help B cells synthesize antibodies.

The genome of retroviruses is represented by RNA, and when the virus enters the cell, it first synthesizes DNA on the RNA template using the reverse transcriptase enzyme. This viral DNA is integrated into the cellular genome, after which a mass of viral RNA molecules are synthesized on it, which, in turn, serve as templates for the production of viral proteins. It all ends with the RNA being packaged into viral particles that come out.

But it happens that the cell suppresses the synthesis of viral RNA, so that the virus, having integrated into the host's DNA, loses the ability to multiply. Its genome becomes a kind of cargo that will pass from the parent cell to the daughter cell. And if you analyze, for example, the mammalian genome, you can find many retroviral sequences that are mostly inactive - after the cells are forbidden to synthesize RNA on them, they also mutate many times, so that, in the end, they become completely safe and inactive genetic debris.

However, B cells appear to be able to capitalize on junk viral DNA. The benefit is associated with so-called TI-2 antigens. An antigen is any molecule that arouses suspicion in the immune system and forces it to take appropriate action. This may be a foreign protein, or the lipopolysaccharide shell of a bacterial cell or viral particle. But the immune system "sees" different antigens differently. When it comes to a protein, the production of antibodies against it requires the help of special T-helper cells: they take a dubious protein and literally show it to B-cells, which trigger the synthesis of antibodies against the molecule demonstrated to them.

However, antigens of TI varieties, including TI-2, which are large polysaccharide fragments with repeating regions in the molecular structure, can be sensed by B cells themselves, without intermediaries. It is known that TI-2 interacts at many points with B-cell receptors, but what happens next, how the synthesis of immunoglobulins is triggered, has not yet been understood.

Beutler and colleagues' research began by looking for mutations in mice whose immune system did not see TI-2 antigens. It turned out that in such animals the signaling pathways that react to foreign RNA and DNA in the cytoplasm were damaged. But why do B cells need RNA and DNA signals to make antibodies? In an article in Science, the authors write that TI-2 antigens turned on RNA synthesis on all retroviral sequences dormant in the cellular genome. A lot of viral RNA appeared in the cell, on which DNA was synthesized. The synthesis of viral nucleic acids and the synthesis of antibodies were directly related. If the enzyme reverse transcriptase (which makes DNA on an RNA template) was turned off in B cells, the synthesis of immunoglobulins dropped dramatically. But even then, there was still a spare activation pathway: one mitochondrial antiviral protein was triggered, which was sensed by RNA, and gave a signal for the synthesis of antibodies. That is, even without retroviral DNA, the cell could respond to the antigenic signal.

The experiments were carried out on the immune system of mice, and if the results are confirmed in humans, this will have great implications for medicine. After all, for example, anti-HIV therapy involves suppressing the reverse transcriptase of the immunodeficiency virus - but then the reverse transcriptase of B-cells is also turned off, which, as we see, is very important for the response to infection. It is possible that assisting in the synthesis of antibodies is not the only function of endogenous retroviruses dormant in DNA, and further research may reveal other ways in which our cells and animal cells have learned to use former parasites to their advantage.

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