A Good Retrovirus

It’s hard to believe that we’re now taking the same route toward redefining viruses that we took ten years ago, about bacteria that coexist with us. It now appears that most viruses in our environment have effects that are either inconsequential or beneficial. Even obscure herpesviruses can protect us from pathogens and help tune our immune system.

Half our genome consists of long-ago trapped retroviruses, known as “endogenous viruses” because we inherit them forever through the germline. Some are defunct and their sequences decayed by mutation. But a few endogenous retroviruses have evolved to express genes essential for us. A particularly fascinating example is an endogenous retrovirus that expresses “syncitin,” a tongue-twister of an enzyme needed to form the placental syncitium, or “syncitial trophoblast.” A syncitium is a giant multinucleated cell, formed by the fusion of smaller cells into one large impervious cell. For example, our muscle cells are all syncitia. The trophoblast (early stage of the placenta) needs to form a syncitium as an impervious barrier to keep maternal blood cells out of the embryo. So why use a retroviral gene? Perhaps because retroviruses (such as HIV, the cause of AIDS) have the ability to form syncitia out of T-cells. A speculative hypothesis, to be sure, but it’s clear that this endogenous retrovirus–which still releases virions into the blood–is an essential part of all human reproduction.