condylurus_ in Kenya [24; 25] and Guinea [26] indicates that further investigation into the role that this microbat has in the ecology of ebolaviruses is important. Although _Bombal ebolavirus_ has not been isolated from a wild-caught _M. condylurus_ bat yet, its role as natural reservoir for this virus is highly probable. In this study, we focus our investigations on the potential role of this microbat in the ecology of EBOV. A key component in the filovirus entry process is the integral membrane protein Niemann-Pick C1 (NPC1), found in late endosomes and lysosomes [27] and utilized in the viral entry process by the glycoproteins (GP) of Ebola virus [28; 29; 30], Marburg virus (MARV) [31], and Mengla virus [32], a recently discovered filovirus infecting fruit bats in China. NPC1 knockout cells are refractory to EBOV infection [27; 33]. Additionally, NPC1 was shown to be a genetic determinant of filovirus susceptibility in bat cells; NPC1 polymorphisms found in specific bat species result in reduced interactions between filoviruses and NPC1, influencing the cellular susceptibility of bats to filovirus infection, replication, and virulence [34]. In culture, _M. condylurus_ cells typically have low NPC1 expression levels compared to cells from highly symptomatic hosts, such as humans [35]. Infection of _M. condylurus_ cells with EBOV revealed a potential correlation between NPC1 receptor expression level and virus replication rate [35]. A critical requirement for the identification of a natural reservoir of a given zoonotic virus is evidence of viral persistence at the population level, which can only be determined through longitudinal studies [36]. When elucidating the hypothetical circulation and maintenance of EBOV in a bat species, high population densities in wild bat colonies and metapopulation structures with bat migration between colonies have to be considered. Virus spread within the colony may be rapid and result in a decrease in the number of susceptible individuals (through induction of protective immunity) to a level too low to maintain virus transmission [37]. As viruses are obligate intracellular parasites that must be maintained in a population, RNA viruses have evolved a number of strategies to counteract the dead-end case of depletion of susceptible individuals [37]. One strategy is the establishment of persistent infections in at least some individuals, who maintain the virus for months, years, or even lifelong and can then act as a periodic source of the virus within a host population [37]. This strategy has been observed for several RNA viruses such as Foot and mouth disease virus (FMDV) [38; 39], Borna disease virus (BDV) [40; 41; 42], Bluetongue virus (BTV) [43; 44], Measles morphillivirus (MeV) [45; 46; 47], Hepatitis C virus (HCV) [48; 49; 50], and Zika virus (ZIKV) [51; 52; 53]. Long-term studies with Nipah virus (NiV)-infected _Pteropus vampyrus_ and MARV-infected _Rousettus aegyptiacus_ fruit bats provide evidence for virus persistence in individuals of these reservoir species [54; 55; 56] and MARV has been also shown to establish testicular persistence in macaques [57]. EBOV has been shown to persist in immune-privileged sites such as eye, brain, and testes in humans [58; 59; 60; 61] and rhesus monkeys [62], although this is not a main driver of virus transmission. The resurgence of EBOV in 2021 in Guinea from persistently infected humans [63] underlines the importance to investigate filovirus persistence. The fact that humans can become persistently infected may also reflect the intrinsic ability of EBOV to establish persistence in its natural host [37]. The establishment of a persistent infection in a host requires a supply of susceptible cells dividing at a similar pace as the virus replicates, and the ability to hide from, or subvert the host's immune response [64]. If cells continue to synthesize high levels of viral proteins, cells will likely suffer cytopathic effects, either as a direct consequence of virus replication, or elimination by host immune responses.