## 1 Introduction
It plays a central role in the transmission of viral pathogens in honeybee populations, particularly facilitating the spread of Deformed Wing Virus (DWV) and Acute Bee Paralysis Virus (ABPV) [14; 35]. The mite worldwide invasion process and its strict relationship with honeybees have intensified viral infections, contributing to its diffusion through honeybee colonies and subsequent increases in the viral load [36]. Varroa mites feeding on the hemolymph of honeybees not only results in the bees becoming physically weakened but also acts as a mechanical vector, injecting viruses directly into the bee systems [37]. This transmission mode circumvents the honeybees' natural immune defenses, leading to a rapid increase in viral loads and the development of more severe symptoms, such as wing deformities, paralysis, and colony collapse [35]. Without effective management, these mites can decimate honeybee colonies through their dual impact of parasitism and virus transmission. However, the potential role of _V. destructor_ in transmitting viruses to wild bees is not yet fully understood and remains the subject of ongoing investigations. The current evidence indicates that while varroa mites have a specific impact on honeybees, they directly parasitize wild bees, including species such as the social _Bombus_ (bumblebees) or some solitary Apoidea. Other viruses, such as the Chronic Bee Paralysis Virus (CBPV), can easily spread within colonies, with infected bees showing symptoms such as tremors, hair loss, swollen abdomens, and flight inability, often leading to widespread mortality. Despite its efficient transmission within colonies, CBPV has not been linked to _V. destructor_ infestations, as it is not associated with this parasite. Indeed, transmission appears to be primarily determined by direct contact between infected and healthy bees, as infected individuals are often attacked or nibbled by their nest mates [38]. In addition, it has been hypothesized [19; 39] that wild bees may contract honeybee viruses such as DWV through the sharing of foraging environments rather than through direct interactions with varroa mites. Similarly, ref. [40] highlighted that although the mites cause significant virus amplification in honeybee colonies, their ability to affect wild bee populations is likely to be related to the indirect amplification of viral loads in honeybee colonies, thus increasing the likelihood of highly infected honeybees interacting with wild pollinators that share the same niche. The detection of different viruses in glandular secretions of worker bees and in colony resources such as pollen, honey, and bee feces [41; 42] highlight the potential transmission pathways, including food-borne and fecal-oral routes. Such indirect transmission could occur via contaminated floral surfaces and, in detail, through pollen and nectar contamination, feeding in the same flowers, through trophallaxis, and by a fecal route [42; 43; 44]. DWV was found to be a frequent component of pollen pellets and was also present in bee feces, suggesting that honeybee foragers and colonies could facilitate horizontal virus transmission to the broader pollinator community [45]. Infected foragers may consequently contaminate pollen, nectar, and floral organs with pathogens, further increasing the risk of transmission [17]. Spillovers could also involve species that are not expected to come into direct contact with bees, such as wasps, which predate the infected bees and cannibalize their carcasses [17; 46; 47]. In urban gardens where bee populations may be artificially concentrated, the risk of disease transmission is heightened due to the increased contact and proximity of bees with other pollinators [5; 12]. These dynamics underscore the importance of studying disease transmission in urban environments to mitigate the threat to managed and wild bee pollinator populations while promoting biodiversity conservation and/or urban bekeeping.