Spillover is a common event; in fact, more than two-thirds of human viruses are zoonotic.^[4][5] Most spillover events result in self-limited cases with no further human-to-human transmission, as occurs, for example, with rabies, anthrax, histoplasmosis or hydatidosis. Other zoonotic pathogens are able to be transmitted by humans to produce secondary cases and even to establish limited chains of transmission. Some examples are the Ebola and Marburg filoviruses, the MERS and SARS coronaviruses and some avian flu viruses. Finally, some spillover events can result in the final adaptation of the microbe to humans, who can become a new stable reservoir, as occurred with the HIV virus resulting in the AIDS epidemic and with SARS-CoV-2 resulting in the COVID-19 pandemic.^[5]

If the history of mutual adaptation is long enough, permanent host-microbe associations can be established resulting in co-evolution, and even permanent integration of the microbe genome with the human genome, as is the case of endogenous viruses.^[6] The closer the two target host species are in phylogenetic terms, the easier it is for microbes to overcome the biological barrier to produce successful spillovers.^[1] For this reason, other mammals are the main source of zoonotic agents for humans. For example, in the case of the Ebola virus, fruit bats are the hypothesized zoonotic agent.^[7]

During the late 20th century, zoonotic spillover increased as the environmental impact of agriculture promoted increased land use and deforestation, changing wildlife habitat. As species shift their geographic range in response to climate change, the risk of zoonotic spillover is predicted to substantially increase, particularly in tropical regions that are experiencing rapid warming.^[8] As forested areas of land are cleared for human use, there is increased proximity and interaction between wild animals and humans thereby increasing the potential for exposure.^[9]

Commercially bred bumblebees used to pollinate greenhouses can be reservoirs for several pollinator parasites including the protozoans Crithidia bombi, and Apicystis bombi,^[10] the microsporidians Nosema bombi and Nosema ceranae,^[10][11] plus viruses such as Deformed wing virus and the tracheal mites Locustacarus buchneri.^[11] Commercial bees that escape the greenhouse environment may then infect wild bee populations. Infection may be via direct interactions between managed and wild bees or via shared flower use and contamination.^[12][13] One study found that half of all wild bees found near greenhouses were infected with C. bombi. Rates and incidence of infection decline dramatically the further away from the greenhouses where the wild bees are located.^[14][15] Instances of spillover between bumblebees are well documented across the world, particularly in Japan, North America, and the United Kingdom.^[16][17]

Zoonotic spillover is a relatively uncommon but incredibly dangerous natural phenomenon—as is evidenced by the Ebola epidemic and Coronavirus pandemic. For zoonotic spillover to occur, several important factors have to occur in tandem.^[1] Such factors include altered ecological niches, epidemiological susceptibility, and the natural behavior of pathogens and novel host or spillover host species.^[29] By suggesting that the natural behavior of pathogens and host species impacts zoonotic spillover, simple Darwinian theories are being referenced. As with all species, a pathogen's main goal is to survive. When a stressor puts pressure on the survival of the pathogenic species, it will have to adapt to said stressor in order to survive.^[30] For example, the ecological niche of the novel host may be subject to a lack of food which leads to a decrease in the novel host population. In order for a virus to replicate, it must invade a eukaryotic organism.^[31] When the novel eukaryotic organism is not available for the virus to infect, it must jump to another host.^[30] In order for the virus to make the jump to the spillover host, the spillover host must be epidemiologically susceptible to this virus. Although it is not well understood what makes one spillover host "better" than another host, it is known that the susceptibility has to do with the shedding rate of the virus, how well the virus survives and moves while not within a host, the genotypic similarities between the novel and spillover hosts, and the behavior of the spillover host that leads to contact with a high dose of the virus.^[1]

• European Center for Disease Prevention and Control
• U.S. Centers for Disease Control and Prevention,
• Infectious Disease Society of America (IDSA)