Impact of joint interactions with humans and social interactions with conspecifics on the risk of zooanthroponotic outbreaks among wildlife populations

Abstract

Pandemics caused by pathogens that originate in wildlife highlight the importance of understanding the behavioral ecology of disease outbreaks at human–wildlife interfaces. Specifically, the relative effects of human–wildlife and wildlife-wildlife interactions on disease outbreaks among wildlife populations in urban and peri-urban environments remain unclear. We used social network analysis and epidemiological Susceptible-Infected-Recovered models to simulate zooanthroponotic outbreaks, through wild animals’ joint propensities to co-interact with humans, and their social grooming of conspecifics. On 10 groups of macaques (Macaca spp.) in peri-urban environments in Asia, we collected behavioral data using event sampling of human–macaque interactions within the same time and space, and focal sampling of macaques’ social interactions with conspecifics and overall anthropogenic exposure. Model-predicted outbreak sizes were related to structural features of macaques’ networks. For all three species, and for both anthropogenic (co-interactions) and social (grooming) contexts, outbreak sizes were positively correlated to the network centrality of first-infected macaques. Across host species and contexts, the above effects were stronger through macaques’ human co-interaction networks than through their grooming networks, particularly for rhesus and bonnet macaques. Long-tailed macaques appeared to show intraspecific variation in these effects. Our findings suggest that among wildlife in anthropogenically-impacted environments, the structure of their aggregations around anthropogenic factors makes them more vulnerable to zooanthroponotic outbreaks than their social structure. The global features of these networks that influence disease outbreaks, and their underlying socio-ecological covariates, need further investigation. Animals that consistently interact with both humans and their conspecifics are important targets for disease control.

Effects of captive and primate-focused tourism on the gut microbiome of Tibetan macaques

“…Most members of the Streptococcus and Sarcina are potential pathogenic bacteria in humans and animals (Wyder et al, 2011;Tintara et al, 2019). The prediction results of wide-scale phenotypic properties KEGG pathways also support that the captive breeding may cause the increase of potential pathogens in gut of these macaques (Amato et al, 2016;Balasubramaniam et al, 2022). In particular, the loss of diversity in gut microbiome will increase the risk of opportunistic infection (Arrieta et al, 2014;Malard et al, 2021).…”

Intragroup sociality drives individual participation in intergroup competition in an urban-dwelling nonhuman primate

“…Moreover, social proximity EC and multilayer affiliative centrality were better predictors of participation compared to grooming EC. Greater proximity to conspecifics might encourage animals to take more risks, for example jointly interact with humans [137] or participate in IGC (this study, [6,78]). Moreover, coalitionary support ties within groups may better ‘prime’ animals to participate in IGC, given the links between participation and intragroup cooperation and conflict resolution [55].…”

“…Another explanation is that in macaques, and in other group-living animals that show similar organizations, males spend more time in the periphery and tend to disperse away from their natal groups, and may therefore face greater intergroup encounters than females [102,154,155] Moreover, limited research on wildlife populations in anthropogenically-impacted environments has to-date revealed that males more so than females tend to engage more frequently with humans (e.g. African elephants, Loxodonta africana [156]; macaques: [91,119] and/or jointly aggregate around anthropogenic factors (macaques [137]). Thus, participation by males in IGC might be an artefact of participation in human-wildlife interactions over food, or vice versa, due to which, males may be more likely to encounter members of other groups than females.…”

"A Note on the COVID-19 Pandemic Evolution Debate: What is Next?"

“…Although the mechanism that determines the emergence of new VOCs, such as Omicron [26,27], remains unknown, it is clear that the virus is transmitted via infected individuals and replicates within their organs, giving rise to mutations in the SARS-CoV-2 genome. Only a few mutations can enhance the virus's functions and its degree of infectivity (i.e., the capacity of the virus to enter human host cells), transmissibility (the capacity of the virus to move from one host to another) and immune escape, giving rise to VOCs.…”