For a long time, this ailment was viewed merely as a typical zoonosis—an infection transmitting from animals to humans that quickly subsides. However, in recent years, the pace of monkeypox virus evolution has sharply accelerated, demonstrating a notable adjustment toward human hosts. Murad Shahmardunov, a professor at the Department of Infectious Diseases and Epidemiology at the Pirogov University’s Institute of Clinical Medicine, shared this perspective with TASS.
The expert clarifies that even back in 2022, during the height of the worldwide outbreak, scientists observed a perplexing situation: despite the virus supposedly mutating slowly (owing to its DNA structure), it unexpectedly began accumulating changes at a surprising rate.
According to Shahmardunov, molecular dating analysis revealed that the evolutionary speed of sublineage IIb had increased five to six times compared to previously identified strains. This finding serves as evidence that the virus has entered a novel environment—the human population—and is actively tailoring itself to it.
The professor emphasized that researchers have identified particular mutations within the viral genome, triggered by the action of the human enzyme APOBEC3. This enzyme is a component of the innate human immune system, designed to “slice” viral DNA in an effort to eradicate it.
Yet, the virus persists, even leveraging the resulting damage to generate novel variants. Expert calculations suggest that this sustained transmission within human populations actually commenced as early as 2016.
The most concerning findings were released in April 2026. Indian specialists, after examining 40 virus samples sourced globally, detected mutations in three critical genes responsible for encoding proteins the virus employs to suppress the human immune response, block warning signals (interferons), and evade attacks by T-cells. In essence, the virus is deliberately refining the tools it uses to hide from, and more effectively neutralize, human defense mechanisms over extended periods.
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