Final answer:
The Embecovirus likely acquired hemagglutinin esterase through genetic mutations and natural selection, aiding in adherence and release from host cells. The specifics of when this occurred are unclear without extensive research into Embecovirus evolution. Like influenza viruses, Embecovirus may undergo changes to evade the host immune system.
Step-by-step explanation:
The question of how and when the Embecovirus acquired the hemagglutinin esterase (HE) is rooted in the study of viral evolution. Hemagglutinin esterase is a protein that has both receptor-destroying and receptor-binding functions, which can help a virus both adhere to and later release from a host cell. While the specific timing of this acquisition is difficult to pinpoint without further research into the evolutionary history of coronaviruses, the general mechanism likely involves genetic mutations and natural selection. Viruses such as the influenza virus use their hemagglutinin protein to bind to host cells and neuraminidase to release new virions. Changes in the configuration of these proteins can make them unrecognizable to host immune systems, leading to the potential for outbreaks and epidemics.
The influenza virus, for example, can undergo antigenic shift, resulting in new strains with different hemagglutinin and/or neuraminidase proteins. These shifts can result from a process called reassortment, where two different viruses infect the same cell and exchange genetic material, creating new hybrid viruses with altered surface proteins. The same principles apply to coronaviruses like Embecovirus, where acquisition of HE could provide similar functions critical for viral infection and spread. Ongoing research continues to uncover the complexities of how viruses evolve these mechanisms.