In the summer of 1958, an epidemic of smallpox-like skin infections occurred in macaque monkeys at the Statens Serum Institut in Copenhagen, used for polio research and vaccine production. Analysis revealed the existence of a new virus of the orthopox genus of the poxvirus family, related to that of human smallpox. It was named monkeypox virus. In the following years, it caused further epidemics in primates at various research institutes in France, the US and the Netherlands, but its origin could not be traced.
Its misleading name reveals one of its characteristics. It is a zoonotic virus capable of infecting several animal species, including the Gambian rat, the striped African squirrel and the red-legged sun squirrel, species of African tree-dwelling rodents that could constitute its source. Monkeys are thought to be infected only occasionally.
The monkeypox virus, renamed mpox in 2022, is a DNA virus, which immediately distinguishes it from RNA viruses such as SARS-CoV-2 (responsible for Covid-19), the influenza virus or HIV owing to the slowness of its evolution, with a mutation rate a thousand times lower. There are two branches, or clades 1 and 2, present in Central and West Africa respectively, with genomes ranging from 4% to 5%. They are thought to have diverged 560 years ago, a period of climate change that may have affected the geography of tropical forests.
The monkeypox virus also stands out for its size. Its genome of around 200,000 base pairs contains the genes for some 200 proteins, compared with just 10 for HIV. Some of these are known from studies carried out on the vaccinia virus, used until 1980 in the smallpox vaccine. They serve to multiply the viral genome in infected cells and build viral particles. Others are accessory and present in variable numbers (67 in monkeypox virus vs. 53-55 in smallpox virus). Their role is poorly understood, but they appear to be important for the interaction between the virus and its hosts.
"When the smallpox virus adapted to the human species from its animal source, it lost many accessory genes. This is a complex and poorly understood process, and questions remain open regarding their role in modulating the immune response and in the spectrum of species that viruses can infect," said Alex Sigal of the South African Health Research Institute in Durban. "But they do seem to be important for affinity to a given host. It's not like with SARS-Cov-2, where this affinity depends very much on the receptor. These viruses are more complex."
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