Researchers have identified a gene of human origin within a virus closely related to smallpox, marking a potentially unique instance of a virus acquiring a human gene within recent evolutionary history. The discovery sheds light on how viruses can appropriate elements of their hosts’ DNA, possibly to enhance their own infectivity.
The gene, known as BC200, was found in molluscum contagiosum virus, a poxvirus that solely infects humans and typically causes skin lesions that resolve within months. Scientists uncovered the gene during a thorough analysis of viral genetic sequences in public databases. BC200 is notable for its production of an RNA molecule primarily active in the human brain, where it has been proposed to regulate protein synthesis in nerve cells, though its precise function remains uncertain.
Cedric Feschotte, a biologist at Cornell University, and his team estimated that the virus acquired BC200 approximately 100,000 years ago. This timeline was derived from mutations identified in the viral version of the gene, distinguishing it from the human counterpart. The gene’s structure also enables it to integrate into new locations within the host genome, a feature responsible for multiple copies of BC200 present in human DNA — 178 copies have been cataloged, generated over millions of years. Such genetic duplications may similarly underpin how the virus initially incorporated the gene.
The long-term retention of BC200 in the molluscum contagiosum virus genome suggests it confers a selective advantage. None of the viral strains analyzed lacked the gene, indicating it plays a functional role. Evolutionary biologist Nels Elde from the University of Utah, who was not involved in the study, posited that the virus might exploit BC200 to manipulate the host cell’s protein production machinery. Infected cells often respond by shutting down protein synthesis to inhibit viral replication, but poxviruses have strategies to reactivate this process. The BC200 gene could help molluscum contagiosum virus sustain or restore protein synthesis, facilitating its replication.
Viruses typically hijack host cells by injecting their own genes and commandeering cellular mechanisms to propagate their genomes. Occasionally, mistakes occur in this process, causing segments of the host's DNA to become incorporated into viral genomes. This phenomenon has been observed in viruses infecting bacteria, where transferred genes can spread antibiotic resistance.
The discovery opens questions about how frequently viruses acquire human genes and the broader implications for viral evolution and infection strategies. Dr. Feschotte expressed interest in further investigating whether this event is an isolated case or part of a wider, previously underappreciated pattern.
The findings were published recently in the journal Science and highlight a novel dimension of host-virus genetic interplay that could have significant ramifications for understanding viral disease mechanisms in humans.