Viruses are known to use the genetic machinery of the human cells they invade to make copies of themselves. As part of the process, viruses leave behind remnants throughout the genetic material (genomes) of humans. The virus-like insertions, called “transposable elements,” are snippets of genetic material even simpler than viruses that also use host cell machinery to replicate.

Nearly all these inserted elements have been silenced by our cells’ defense mechanisms over time, but a few, nicknamed “jumping genes,” can still move around the human genome like viruses. Just one, called long interspersed nuclear element 1 (LINE-1), can still move by itself.

As an element type that behaves like the retrovirus HIV, the LINE-1 “retrotransposon” is first copied into a molecule of RNA, the genetic material that partners with DNA, and then the RNA LINE-1 copy is converted back into DNA in a new place in the genome.

Vaccines save millions of lives every year, but there is still an urgent need for more efficient vaccines. Strategies to combat serious outbreaks of viral infections are particularly important. Such infections are initiated at mucosal surfaces, where there is a close association between polarized epithelial cells and immune effector cells. However, vaccines are usually given intramuscularly or subcutaneously, and often do not provide sufficient protection at the actual site of infection.

In Nature Communications, the laboratory of Professor Jan Terje Andersen and collaborators report on a novel vaccine technology platform, in which the subunit antigen is genetically fused to albumin.

Albumin was chosen as a carrier as it is actively transported across the mucosal barrier by FcRn, a receptor found on mucosal epithelial cells.

An investigational gene therapy has successfully restored immune function in all nine children treated with the rare and life-threatening immune disorder called severe leukocyte adhesion deficiency-I, or LAD-I, in an international clinical trial co-led by UCLA.

LAD-I is a genetic condition that affects approximately one in a million people in the world. It is caused by mutations in the gene that produces CD18, a protein that enables white blood cells to travel from the bloodstream to infection sites.

In the absence of this critical protein, individuals with severe LAD-I—most of whom are diagnosed within their first months of life—are left vulnerable to dangerous, recurrent bacterial and fungal infections. Survival beyond childhood is rare without treatment.