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What Human Diseases Have No Animal Vectors

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The Brute Origin of Major Human Infectious Diseases: What Can Past Epidemics Teach Usa Nigh Preventing the Next Pandemic?

Writer(s): , * , , 2 , iii , four , five , 2 , vi , 7 , 8 , 9 , 10 , two , * ,

Publication appointment (Electronic):

Journal: Zoonoses

Publisher: Compuscript

Keywords: affliction environmental, emerging infectious disease, pathogen, parasite, zoonoses

Emerging infectious diseases are one of the greatest public health challenges. Approximately three-quarters of these diseases are of animal origin. These diseases include classical zoonoses maintained in humans only via transmission from other vertebrates (e.g., rabies) and those initiated by a successful i-off zoonotic consequence (host-switch) in conjunction with efficient human-to-human transmission (east.g., H1N1 influenza). Here, we provide a systematic review, in conjunction with a meta-analysis and spatial hazard modeling, to identify the major characteristics of past epidemics of animal origin and predict areas with high future disease emergence risk. Countermeasures against time to come pandemics of animal origin must focus on several fundamental mechanisms. First, the eco-epidemiological contexts favoring spillover events must exist clearly plant. Second, pathogen surveillance must be scaled up, particularly in taxa and/or eco-geographic areas with high disease emergence adventure. Third, successful spillover take a chance must be mitigated through proactive strategies to interrupt animate being-to-homo transmission chains. Quaternary, to decrease epidemic potential and preclude epidemics from becoming pandemics, improved source identification and real-time spatial tracking of diseases are crucial. Finally, because pandemics practice not respect international borders, enhancing international collaboration is critical to improving preparedness and response.

INTRODUCTION

Human history has been punctuated by many pandemics, including the bubonic plague (fourteenth century), the Spanish flu (20th century), HIV/AIDS (twentythursday and 21st centuries), and coronavirus disease 2019 (COVID-19). Having infected more than than 238 million people and caused more than iv.eight million deaths since its emergence in Dec 2019 [i] (Fig 1), COVID-19 has underscored the devastating, long-lasting societal and economical consequences of emerging infectious diseases. Peculiarly alarmingly, the risk of novel disease emergence in human populations is increasing because of the confluence of numerous drivers of global ecology change, including those associated with climate, land-use (e.g., urbanization), and the agronomical industry (e.g., large commercial beast farms). Moreover, this risk is aggravated by the e'er-increasing resistance to antimicrobial drugs and insecticides used for disease vector control [2,3], and the growing potential for the rapid spread of diseases with increased global transport [four–7].

Figure 1 |

Major diseases of animal-origin affecting human health.

A timeline of emergence of diseases of animal-origin which are considered to be a threat to global wellness or which require urgent research as identified by the Globe Health System, including: (a) Crimean-Congo hemorrhagic fever; (b) Dengue fever; (c) Marburg virus disease; (d) Lassa fever; (eastward) Rift Valley fever; (f) Hendra virus disease; (g) Highly Pathogenic Asian Avian Influenza A subtype H5N1; (h) Nipah virus disease; (i) HIV/AIDS; (j) Zika fever; (thousand) Ebola virus illness; (l) Sudden Acute Respiratory Syndrome (SARS); (chiliad) Flu A virus subtype H1N1; (north) Middle E Respiratory Syndrome (MERS); (o) Coronavirus Disease 2019 (COVID-19). For each disease the yr of initial identification (round symbols on time line) or declaration of a public health emergency of international business concern (square symbols on time line) are shown. The spatial extent of each disease is besides given as a map highlighting with areas where transmission is reported (red areas) and the location from where the pathogen was first reported (blueish symbol). Also, depicted are the major routes of transmission in the zoonotic source population (dark-green arrows), master zoonotic event (red arrows) and manner of maintenance in the human population (light-green arrows). Diseases include those that are strictly zoonotic and maintained in the homo population only through transmission from a vertebrate animal host (e.grand., Rift Valley fever and Hendra virus illness), diseases that are primarily maintained past zoonotic spillover but which can also exist transmitted directly betwixt humans (eastward.g., Ebola/Marburg virus diseases and MERS), and diseases of animal-origin which show very efficient human-to-human transmission (e.chiliad., HIV infection, H5N1/H1N1 influenza). Several diseases are suspected to be of zoonotic origin but the vertebrate brute reservoir remains unconfirmed (e.m., Ebola virus affliction, SARS and COVID-xix). See Supplemental Cloth for references to source information used to produce the figure.

From a public health perspective, considering approximately three-quarters of all emerging infectious diseases are caused past pathogens originating from domestic or wild animal species [viii], concerns regarding the threat of human being infectious diseases of beast origin have grown. These pathogens vary considerably in terms of the conditions favoring spillover events and the resultant public health consequences. For instance, strictly zoonotic diseases cannot be maintained in human populations without new spillover events from a vertebrate reservoir, because human-to-human transmission does not occur (e.g., echinococcosis, toxoplasmosis, and rabies). Other infections, such as bubonic plague (caused by Yersinia pestis), Lyme affliction (acquired by Borrelia burgdorferi), and West Nile fever (acquired past the W Nile virus) are transmitted by arthropod vectors but do not show long-term man-to-human transmission. Other diseases are primarily maintained in human populations through spillover from vertebrate reservoirs, but exercise bear witness rare (e.chiliad., hantavirus affliction and hepatitis-E infection) or inefficient (due east.g., pneumonic plague) human-to-homo transmission. Finally, some diseases are initiated by a successful ane-off zoonotic event (host-switch) with such efficacious rates of long-term human-to-human transmission that a new human pathogen is created de facto, and the original animal reservoir is no longer essential to maintaining recurring infections in humans. Many recent emerging infectious diseases have been caused by pathogens whose ancestors were maintained in vertebrate reservoirs but at present are efficiently transmitted between humans via aerosol/respiratory droplets (e.g., H1N1 flu), exchange of bodily fluids (e.chiliad., HIV/AIDS), or arthropod vectors (e.g., Zika virus fever). Although SARS-CoV-2 may also exist a virus of animate being origin, the bodily source of the virus in human populations remains enigmatic [9]. Interestingly, many modern human pathogens take zoonotic origin. One classical example of such a affliction is measles, which probably diverged from rinderpest approximately 900 years ago [x]. Additionally, human malaria caused by both Plasmodium falciparum and P. vivax is the consequence of successful historical host switching between African apes and humans [11]. Currently, macaque monkeys are a major reservoir of P. knowlesi, an of import emerging man malaria pathogen in parts of southeast Asia [12,13].

Host switching events leading to the creation of a new homo pathogen tin occur directly from the original fauna reservoir (e.grand., non-human primates in the case of HIV) or via an intermediate step with amplification/adaption (e.one thousand., recombination) in other species, including domestic animals (east.g., domestic swine for H1N1 influenza) [14]. Although whatsoever zoonotic disease tin accept serious public wellness consequences, the risk of a pandemic is profoundly enhanced after efficient man-human transmission is established. The currently high connection among human populations [15] farther facilitates the geographical spread of novel viruses, particularly respiratory syndrome diseases such every bit COVID-19 [ane]. The potential for geographical spread of novel viruses in human populations is exemplified by the emergence of respiratory syndrome diseases in the 21st century, particularly coronaviruses, such as those causing sudden acute respiratory syndrome (SARS), Heart Eastward respiratory syndrome (MERS), and COVID-nineteen (Fig 1). Epidemics of these diseases have shown rapid spatial and temporal spread. For example, SARS (2002–2003) affected countries across five continents (Africa, Asia, Australia, Europe, and Northward America), MERS (2012–2020) affected four continents (Africa, Asia, Europe, and Due north America), and COVID-nineteen has spread to all continents [1].

To mitigate the persistent threat of emerging and re-emerging diseases, several global wellness security frameworks have been established, such as the International Heath Regulations [16]. These frameworks aim to protect individuals and societies from acute public health events and to support global preparedness and responses to emerging infectious diseases [17]. For instance, in the past few decades, the Globe Health Organization (WHO) has declared six Public Health Emergencies of International Concern—health emergencies that "potentially require a coordinated international response" [16]. 5 of the six have been associated with pathogens of animal origin: the H1N1 influenza virus in 2009, Ebola virus in 2014 and 2018, Zika virus in 2016, and SARS-CoV-ii in 2020 (Fig 1). To advance the power to fight futurity pandemics, identifying the major characteristics, sources and conditions for emergence of previous diseases of fauna origin is critical. To this aim, we performed a systematic review in conjunction with a meta-analysis and spatial modeling to identify the major characteristics associated with by epidemic outbreaks of animal origin and to predict areas with high future affliction emergence gamble (details on the methods used to identify, extract, and analyze these data are described in the Supplementary Online Materials).

Discussion

Key drivers of pathogen spillover

The initial transmission of pathogens originating from animals to humans requires specific ecological barriers to be overcome (Fig ii). The manual route acts every bit an initial barrier by limiting the pathogens that humans can run into from specific vertebrate animals. Zoonotic diseases can be maintained in human populations through manual of a pathogen from a vertebrate animal host through various routes [4], including direct contact with infected animal tissues or body fluids through wounds or abraded skin; animal bites and scratches (due east.g., Brucella abortus and rabies virus); indirect contact with a contaminated environment or fomites (e.thou., Burkholderia pseudomallei and Leptospira interrogans); air-borne transmission via aerosols or grit particles (e.m., MERS-COV and H1N1 influenza viruses); oral manual (e.thousand., Toxoplasma gondii and Giardia spp.); and vector-borne manual (e.1000., Yersinia pestis and Borrelia burgdorferi). Diseases of creature origin with efficient human-to-homo manual can too initially enter the man population through any of the routes described to a higher place. However, zoonotic events introducing infections into humans may issue from unusual manual routes that differ from the normal transmission route in the animal reservoir as well as the normal manual route in humans. For example, HIV is efficiently transmitted through sexual contact among humans, but the original spillover was probable to accept occurred through repeated exposure of humans to simian immunodeficiency virus through cuts received during butchering meat or contact with the blood of infected wild primates [eighteen–20]. Similarly, plague is transmitted among rodents and from rodents to humans by flea bites or sometimes the consumption of infected meat [21,22]; however, man-human manual occurs through pneumonic manual or lice [23].

FIGURE two |

An eco-evolutionary risk assessment framework of zoonotic disease emergence.

Risk of zoonotic disease emergence (EID risk) can be viewed every bit a function of threats (the animal host and pathogen pool), vulnerabilities (the ecological barriers that pathogens need to overcome to sally in human populations) and the focal asset (i.e., homo health). To emerge a pathogen first needs to overcome manual barriers, which depend on the pathogen transmission road, and include: (A) Directly contact; (B) Indirect contact; (C) Airborne transmission; (D) Oral ingestion; (East) through bites of arthropod vectors. The pathogen then has to overcome species barriers, which can be influenced by: (F) Phylogenetic distance between the brute species and humans; (One thousand) Spatial distance between the animal species and humans; (H) Pathogen multifariousness hosted by the animal species. In each panel, the histograms betoken the overall pool of pathogen propagules hosted by the animal with pathogens with higher risk of emergence in humans being depicted past increased numbers. The zoonotic pool indicates the sample of propagule pool that can emerge in humans, and is afflicted past the overall frequency of the pathogen in the propagule pool and the pathogen'south risk of emergence.

For a novel pathogen to emerge in humans from some other vertebrate species, the pathogen must too successfully overcome the species barrier (Fig 2). Although host switching events are inherently stochastic, past zoonoses have revealed that creature species with a high take a chance of harboring potentially zoonotic pathogens are characterized past at least one of three key features. Kickoff, hosts that are phylogenetically related are more than likely to share pathogens [24–26]. Thus, not-homo primates (specifically great apes) are a major source of potential zoonotic diseases [24,27,28], and 21% of non-human primate species (77/365) have been identified every bit hosts [6] for zoonotic pathogens. This increased risk of pathogen sharing between humans and non-human primates is likely to be driven past the underlying coevolutionary relationships between primates and their pathogens [29–31].

Second, spatial overlap with humans appears to exist an even more important driver than phylogenetic proximity in influencing the extent of pathogen sharing betwixt humans and non-human primates [32]. Indeed, species in close contact with humans are more than likely to be sources of emerging zoonotic pathogens, because a higher frequency of interspecific contacts leads to greater pathogen transmission risk. High contact rates with domestic animals, which are regularly near humans, are besides expected [33]. The number of diseases that these species share with humans increases with the time after domestication [34]. Additionally, synanthropic species (e.one thousand., brown rats, Rattus norvegicus) accept been estimated to be 15 times more than likely to be sources of emerging infectious diseases than other species [35]. Critically, contempo evidence has demonstrated that hosts that tend to thrive in human being-modified landscapes also tend to harbor a higher diversity of zoonotic pathogens [36]. This relationship is likely to be driven by specific traits (e.one thousand., fast pace of life) that increment susceptibility to infection and facilitate survival in man-dominated landscapes [36].

Third, the risk of emergence of novel pathogens is expected to be greater with increasing multifariousness of the pathogens harbored by a particular species [25]. This relationship occurs considering a diverse "zoonotic pool" [37] has a college probability of harboring specific pathogen lineages that tin potentially infect humans (with or without boosted mutations). A recent written report has revealed that the zoonotic viral diversity of a particular taxonomic guild is proportional to the total viral richness, which in turn depends on the species richness of the order [31]. Thus, the 2 almost specious orders of mammals, Rodentia (2020 species) and Chiroptera (1100 species), harbor the highest proportion of zoonotic viruses [6,28,33]. Rodents and bats can transmit various viruses (due east.g., Ebola, Hendra, Nipah, and Lassa fever viruses) and bacteria (e.g., Y. pestis and Francisella tularensis). Thus, these 2 taxa are of special interest from a human disease perspective, considering of the diversity of pathogens that they harbor [28,38–45] and because they commonly are constitute in homo-modified landscapes [36].

Importantly, host and vector ecology and host physiology (e.g., immune strategies) can regulate the genetic diversity of pathogens [46] and thus the zoonotic risk posed past a host species [43,47–49]. For example, the transmission efficiency of plague (Y. pestis) appears to be affected past the bacterium'due south ability to grade a biofilm blockage in the flea gut, thus causing fleas to bite more frequently. This extended flea phenotype is caused past selection for mutations in the rpoZ gene in the bacterium under wet and common cold climate conditions [45]. Some other critical attribute affecting the "zoonotic pool" is the blazon (i.e., genetic variability) of pathogens harbored by a specific host species. For instance, the standing genetic variation (associated with population size) and mutation charge per unit of the pathogen critically affect the risk of a zoonotic event. Thus, RNA-viruses, which mutate more quickly than DNA-viruses, can adapt more chop-chop to a novel host [50,51]. Interestingly, pathogen evolution rates may themselves be affected by host immune responses, and increased selection for mutations tin can evolve under stressful environments of immunity accelerating the rate of adaptation [52,53]. For example, the stomach bacterium Helicobacter pylori produces mutation bursts during the astute phase of infection, which facilitate faster accommodation against host immunity [54].

What will drive the next pandemic of animal origin?

An understanding of past zoonoses enables informed predictions to exist made regarding where the side by side pandemic of animate being origin is likely to originate. For example, climate is recognized to critically influence illness dynamics in multiple ways. Climate tin affect the seasonal dynamics of many diseases [55,56] by influencing electric current and future pathogen [57], host [58,59], and vector [60] distributions [61–63]. Additionally, climate, in conjunction with anthropogenic disturbances, too affects host species diversity [64] and is some other critical driver of zoonotic disease spillover risk worldwide. Host species diversity affects disease risk because high pathogen diversity provides a larger genetic pool of novel pathogen lineages with the potential to spill over into human populations [65]. Thus, illness spillover has been hypothesized to be more mutual in relatively undisturbed areas of the world with high biodiversity [8,66]. Still, the preponderance of empirical testify indicates that illness spillover adventure is mostly elevated in areas with high levels of anthropogenic disturbance and thus relatively depression levels of biodiversity [5,half dozen,36,67–72].

The enhanced adventure of illness spillover in disturbed areas may exist driven by two mechanisms interim independently or in concert. Outset, anthropogenic disturbance tin increment spillover by increasing the spatial overlap between wildlife and humans, as humans invade natural habitats or wild species invade anthropogenic habitats [73,74]. Second, human being disturbance can affect illness adventure by negatively influencing biodiversity—a response termed the "dilution effect," which occurs because diversity in many systems increases the proportion of hosts with depression pathogen competence, thus "diluting" the adventure of infection beyond the entire host customs [75,76]. Although not universal [77,78], recent meta-analyses have revealed wide testify of the dilution effect in many host-pathogen systems [79,fourscore] and at multiple spatial scales [81]. Critically, both species richness and composition are probable to play roles in disease spillover dynamics [36]. For example, anthropogenic disturbance can pb to the biotic homogenization of natural communities in which many highly specialized species are replaced by several widespread generalists [82,83], because generalist species are relatively less sensitive to disturbance and tend to exist "r-selected" (i.e., their populations are governed past their reproductive ability) [73,84]. Additionally, rapid reproduction favors the epidemic spread of disease, because a constant supply of susceptible individuals hinders adequate herd immunity in these populations [85]. Importantly, as described above, generalist species that are more than likely to invade anthropogenic habitats may also be more competent hosts for pathogens [86], particularly zoonotic pathogens [36,72,87].

At finer spatial scales (i.e., at the private host level), host switching, as with any invasion process, is facilitated past propagule pressure [88,89], and the affliction spillover risk increases as interspecific contacts increase. In such situations, ample opportunities exist for spillover infections that originate in the reservoir host (off-the-shelf) or that successfully adapt to humans and thus undergo a true host-switch (i.eastward., tailor-fabricated) [90]. Consequently, commercial farms housing many animals in restricted spaces can be major sources of novel pathogens [91]. For case, the 2009 "swine flu" epidemic was caused by a novel influenza virus (H1N1) that was a product of reassortment amidst three viruses (H3N2, H1N2, and Eurasian avian-like swine viruses) circulating in domestic pigs [14]. As large-scale commercial animal operations increase globally, these "melting pots" are likely to go along to be major sources of novel pathogens [92]. High spillover risk besides exists at alive-beast markets (often referred to as "moisture markets"), which sell wild and/or domestic animals [93,94]. The recent SARS epidemics associated with novel coronaviruses (SARS-CoV-ane in 2002–2003 and SARS-CoV-2 in 2019–2021) have been suspected to be associated with such markets in China at the kickoff of the outbreaks [93,95,96]. Notwithstanding, solid prove of the specific sources remains elusive [97]. Although SARS-CoV-2 itself does not appear to exist a recombinant of any currently known sarbecoviruses [98], coronaviruses by and large do show high recombination rates [99], and such viral recombination tin can increase the risk of emergence of novel zoonotic pathogens. Consequently, the real run a risk associated with live-fauna markets might exist that they provide opportunities for viruses, particularly generalist viruses, from unlike animals to meet and recombine, thus enhancing the gamble of emergence of novel viruses.

Future countermeasures

Most emerging and novel zoonoses are due to stochastic host switching (or spillover) events that are inherently unpredictable. Therefore, numerous challenges exist in understanding the emergence and control of diseases of animal origin (Box 1). Preventing spillover into human populations will primarily depend on establishing the association betwixt eco-epidemiological contexts and transmission mechanisms. We contend that the prevention of future pandemics must be based on a holistic approach comprising the following countermeasures:

  1. Establish eco-epidemiological contexts: Spillover events are inherently stochastic and unpredictable, given the complex eco-epidemiological contexts in which diseases are transmitted via multiple mechanisms and are modulated by various drivers. In this example, clarifying the eco-epidemiological contexts in which these stochastic events are almost likely to occur is a key scientific countermeasure. As indicated in a higher place, the development of a pandemic episode is highly associated with a sequential probability of pathogen-human see, infection, and transmission. These probabilities are essentially determined by several factors that modulate human exposure to novel pathogens. Amongst these factors, agricultural intensification dramatically increases disease emergence risk in human populations through the increased use of chemicals (due east.chiliad., antibiotics, pesticides, and fertilizer), changes in land use (e.g., conversion of forest to agronomical or pastural lands), and increased contact between humans and domestic animals. Indeed, agricultural drivers have been estimated to be associated with approximately 25% of all diseases and fifty% of zoonotic diseases that accept emerged in human populations [3]. Understanding the complex and interacting effects of such eco-epidemiological drivers in affecting disease spillover risk is of import, and modern modeling approaches can provide robust predictive risk cess frameworks [100,101]. Additionally, recent advances in model-inference frameworks are expected to substantially contribute to contextualizing disease dynamics in diverse eco-epidemiological settings and to provide powerful assessment tools to identify regions with loftier affliction spillover gamble [102,103].

  2. Scale up surveillance at human-animal interface: Scaling up active surveillance at human-domestic creature interface, with a focus on high-hazard human populations (e.g., veterinarians, subcontract workers, and workers in dairy or meat processing plants), is critical to rapidly identify spillover events. With respect to wildlife, the selection of species and locations for surveillance may be more challenging. Kress et al. [104] have argued that, with the advent of modern genomic tools, merely a small fraction of the resources allocated to suppressing COVID-19 would be needed to identify every zoonotic pathogen hosted past birds and mammals. However, surveillance efforts are likely to need to exist focused in terms of both the species surveyed and the geographic regions targeted. We propose that species could be targeted according to underlying ecological traits that bear upon their potential to harbor zoonotic pathogens. For example, in wild mammals, three variables are significantly associated with a species harboring at least one zoonotic pathogen, as explained above: the phylogenetic proximity to humans, the spatial overlap between the species distribution and human populations, and the diversity of non-man pathogens that the species harbors (Fig 3A). This framework should enable the identification of species that accept a loftier likelihood of harboring zoonotic or potentially zoonotic pathogens but are poorly surveilled. Unfortunately, a disquisitional weakness in the to a higher place approach is that the number of host species with good data on pathogen variety remains limited. This limitation could be addressed through modeling approaches using phylogenetic data to predict zoonotic pathogen risk in poorly surveyed species, on the basis of information from well surveyed species (for example, ref. [36]). Alternatively, wildlife surveillance programs could besides focus on specific eco-geographic areas according to the chance of transmission of pathogens between wild animals and humans. One way to effectively target geographic areas for surveillance is to prioritize them according to both the diverseness of hosts known to harbor zoonotic pathogens and human density. Thus, for mammals, poorly surveyed areas in eastern and southeastern Asia would take college priority than poorly surveyed areas in Australia (Fig 3B). Additionally, this framework could also help inform which taxa should be prioritized in unlike geographic regions (Fig 3C-F). For example, this framework indicates a need to prioritize the surveillance of bats beyond much of India and Prc. Critically, as in previous studies [5,36], our framework emphasizes the need to focus surveillance on global regions undergoing rapid land-utilise change. In many cases, these regions are too the most socio-economic challenged and therefore the virtually vulnerable to the effects of outbreaks [8]. Recently, researchers take advocated for a "pandemic interception" platform to proactively address pandemic risks, consisting of global genomics-based bio-surveillance programs [104], such as the Earth BioGenome Projection, the Global Virome Projection, BIOSCAN, and the PREDICT project [105,106]. Critically, the interaction of these international programs with regional programs focusing on biodiversity and ecological change (e.g., Mexico's Commission for Biodiversity) tin help develop a global surveillance synergy well poised to accost the urgent need for proactive measures, in low-cal of the pandemic risks in the Anthropocene.

  3. Reduce spillover frequency: The current arroyo to combat zoonotic pandemics is reactive, focusing on successful host switching events (i.east., pathogens that have already emerged in the homo population). Withal, successful host switching events represent merely a small-scale proportion of the preceding unsuccessful host switching opportunities. Thus, a more proactive approach to preventing futurity pandemics would be to subtract host switching opportunities by shifting focus toward interrupting animal-human spillover and subsequent transmission chains. The successful interruption of such transmission chains critically depends on decreasing the contact rates betwixt humans and zoonotic reservoirs, on the basis of a better understanding of illness environmental and pathogen transmission dynamics. For example, to decrease the risk of spillover of pathogens transmitted by straight contact or droplets transmission, focus must be placed on high-run a risk locations where close contact betwixt humans and potentially infected animal tissue or alive animals is common (e.1000., locations where hunted wildlife are trafficked or traded, live animal markets, or high-intensity commercial livestock farms) [74,92,107]. Alternatively, in the example of orally transmitted diseases, attention should be focused on populations at high risk of exposure to these pathogens, such as local communities that consume bush meat [108–111]. Finally, integrated vector management (e.one thousand., WHO's Global Vector Command Response 2017–2030) remains a key strategy to disrupt the manual, and thus combat the ever-increasing burden, of vector borne diseases [112–114].

  4. Decrease epidemic potential: For newly emerging infectious diseases, identification of the pathogen and manual routes remain critical for constructive epidemic control. Although the identification of the animal source of a pathogen is disquisitional to prevent future spillover events, it often is a highly challenging undertaking [115]. For example, more than xl years afterwards the discovery of the Ebola virus, the actual natural reservoir remains unknown, although strong evidence supports the interest of bats [116]. For the SARS outbreak in 2002–2003, researchers took several months to identify the pathogen just did not identify the potential source for more than a decade [117]. For the COVID-nineteen pandemic, in 2019–2020, scientists took but several weeks to identify the pathogen, and have identified horseshoe bats as a potential source of the ancestral virus; other intermediate host(s) are suspected only remain unconfirmed [97]. In many cases, the potential source of novel pathogens has been identified through spatial associations. For example, live creature markets selling domesticated species have been identified every bit sources of numerous pathogens in humans (e.g., swine-origin flu A viruses) [118]. However, the risks of novel zoonoses are particularly high in live animal markets that sell wildlife, because these markets bring humans and wild animals into proximity, frequently under conditions of poor hygiene [106,119]. In the case of the recent SARS-CoV-2 outbreak, the Chinese Center for Disease Command and Prevention detected SARS-CoV-two RNA in 33 of 585 environmental samples from the Huanan Seafood Market in Wuhan. Moreover, 93.9% (31/33) of the positive samples were from the western end of the market, where booths selling wildlife were concentrated [120]. However, the exact role of wildlife in maintaining or amplifying the virus in the Huanan Seafood Market remains unclear; for example, the market environment might accept amplified the pathogen subsequently it had already entered the human population [121]. Given the existent risks of novel zoonoses entering homo populations through live animate being markets selling wild animals, governments worldwide must decrease the nutritional dependency of local populations on meat procured from wild animals and ban the merchandise of wildlife species [122]. The regulation of live creature markets must as well be improved to subtract the risks of zoonotic disease transmission by segregating live animals of unlike species from 1 another and from humans, improving slaughter techniques to meet international standards of ideals and safety, and improving sanitation and hygiene [107,123]. Still, until these biosecurity measures are in place, improved surveillance of potentially loftier-take chances locations, such every bit alive animal markets, will be disquisitional [122].

    Genetic and genomic analyses have demonstrated highly efficient in surveillance, and the identification of origins and routes for the spread of pathogens [110,124,125]. Surveillance of known pathogens is easily performed with PCR tests (to find ongoing infections) or antibiotic-based tests (to test for past infections) in the human population. Because viruses and leaner have small genomes, complete genomic studies of many samples tin exist performed at loftier speed and depression cost with NGS techniques [110,126]. This capability has provided unprecedented access to detailed information on the origin, migratory routes, and critical mutations, all of which are crucial for understanding the changes in pathogen transmission efficiency [110]. Genomic information tin also be effectively leveraged to develop improved diagnostics (due east.one thousand., PCR-based assays) and control measures (e.m., vaccines) [127]. Genomics has provided an unparalleled ability to place the causative agents of by pandemics through emerging ancient Deoxyribonucleic acid approaches [128], as well equally to finer track affliction outbreaks, better empathise manual chains and elucidate population dynamics, as seen in the COVID-19 pandemic [129].

  5. Meliorate time to come preventive measures: Effective inter-sectoral collaboration and mutual benefits of joint actions of international communities with respect to the Sustainable Development Goals tin be leveraged for constructive preparedness and response to epidemics. A particularly urgent need exists for global governments to recognize the value of biodiversity protection in pandemic prevention [130]. Consideration of environmental determinants, climate changes and related risks to man health, and ecosystem integrity and relevant direction systems will exist critical. In proactively addressing future emergencies, a disquisitional need exists to understand that human being health is inextricably associated with animal health, equally well every bit ecosystem structure and role (eastward.g., OneHealth). Thus, cross-sector collaboration must exist strengthened, specially as it relates to emergency preparedness and response, including the harmonized translation of policy guidance (WHO, OIE, and FAO) into action. Specific programs such as the Global Virome Project and BIOSCAN (described to a higher place) are examples of such collaborations. International collaboration is also highly of import for source tracing [131]. For example, in the 2002–2003 SARS epidemic, civets were initially suspected as the source; however, continual international collaborations determined that the source of SARS-CoV was most probable to be bats [117]. COVID-xix is a disease currently straining international political relationships and economic development, and international and multi-disciplinary collaborative teams are urgently needed to mitigate the pandemic's effects, such as the team mobilized past the WHO to place the source of SARS-CoV-2 [121]. The unprecedented rapid response to SARS-CoV-two has demonstrated that international collaborations have facilitated the 2 pillars of disease direction: non-pharmaceutical interventions and vaccine development. Non-pharmaceutical interventions, such as case isolation, contact tracing, travel restrictions, and cancellation of mass gatherings, were crucial in the early response to the rapid diffusion of the pandemic [132–136]. These measures have collectively decreased the manual, and the fourth dimension required for vaccine development and for designing general intervention frameworks [137] and prototypical pathogen approaches [138] to pandemic preparedness. Indeed, as the hazard of zoonotic disease emergence increases globally, an urgent need remains for strategies to forbid future zoonotic pandemics. Such strategies volition crave an interdisciplinary inquiry agenda, as well as robust intra- and international collaboration at the interface of science, policy and society.

BOX 1 | Major challenges relating to the emergence and control of diseases of beast origin.

I. Structure and dynamics of disease systems: For all systems, the following must be better understood:

  1. The combined roles of diverse drivers of global change (e.g., climate, land use, global transport, and socio-economical factors) on zoonotic risks, particularly in landscapes undergoing rapid climatic (due east.chiliad., high elevation areas) and/or habitat (e.chiliad., peri-urban areas) modifications.

  2. The relative pandemic potential of endemic pathogens (i.e., emergence driven by local country-employ and/or socio-economic factors) vs. exotic pathogens (i.e., emergence driven past alterations in global send and/or altered distribution due to climate change).

  3. How the interaction betwixt host and pathogen diversity affects disease gamble across ecological systems and spatial scales. For instance, exercise macroecological differences in host and/or pathogen diverseness beyond ecosystems bear on infection gamble in like ways to human-mediated alterations in biodiversity inside ecosystems?

  4. How do the population size and density of hosts and pathogens influence the emergence of new host-pathogen combinations, and what are the relative effects of human population density vs. altered host community construction in anthropogenic habitats?

2. Surveillance and command: For all zoonotic systems, the following must exist developed:

  1. Effective surveillance efforts directed at both at-risk human populations and high-risk animal populations

  2. Reliable techniques to identify "competent" vs. "non-competent" hosts of zoonotic pathogens in a community, and better frameworks to narrate how community competence varies with human-mediated changes to the environment

  3. Optimal measures to minimize zoonotic disease emergence (due east.m., ban of wildlife sale and improved sanitation in live-animal markets) and spread (e.g., contact tracing and improved border control), respecting socio-cultural norms and economical needs at the local and global scales

Figure 3 |

A framework to prioritize species and geographical areas for zoonotic disease surveillance.

(a) The likelihood of a wildlife species being a zoonotic host (equally measured past the binomial odds ratio) significantly depends on various species characteristics, including the phylogenetic distance betwixt the animal species and humans (Phylogeny), hazard of spatial overlap betwixt the host species and humans (Spatial) and the richness of the pathogen community hosted by the species (Patho. Rich.). Analyses restricted to mammalian species simply and error bars are 67% (red lines) and 95% (black lines) quantiles obtained from non-parametric bootstrap or Bayesian regression analyses (see Supplementary Online Methods for details). (b) Zoonotic disease emergence adventure depends on the diversity of hosts that harbor zoonotic pathogens and the density of humans in the area. The map shows the joint distribution of zoonotic mammalian host diverseness and human being population density. Areas with high diversity of zoonotic hosts and high human density (black areas) need to exist prioritized over those with simply high zoonotic host multifariousness (light light-green areas) or high human being density (light blue areas), which in plough need to exist prioritized over areas with low zoonotic host diversity and human density (low-cal cyan areas). Priority areas for surveillance also depend on the specific mammalian orders considered. Maps are shown for four major orders that accept loftier numbers of zoonotic hosts: (c) Non-homo primates; (d) Rodentia; (eastward) Chiroptera; (f) Carnivora. Encounter Supplemental Material for details.

The authors declare they have no actual or potential competing interests.

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Contributors

Guha Dharmarajan:

ORCID: https://orcid.org/0000-0001-8500-0429

Nils Chr. Stenseth:

ORCID: https://orcid.org/0000-0002-1591-5399

Journal

Periodical ID (publisher-id): Zoonoses

Title: Zoonoses

Abbreviated Title: Zoonoses

Publisher: Compuscript (Shannon, Ireland )

ISSN (Print): 2737-7466

ISSN (Electronic): 2737-7474

Publication date (Electronic): 01 April 2022

Volume: two

Issue: ane

Affiliations

[1 ]Segmentation of Science, Schoolhouse of Interwoven Arts and Sciences, Krea University, Sri Urban center, Andhra Pradesh, India

[2 ]Centre for Ecological and Evolutionary Synthesis, Department of Biosciences, University of Oslo, Oslo, Norway

[iii ]Catching and Non-Infectious disease Cluster, World Wellness Organization Regional Role for Africa, Brazzaville, Republic of Congo

[4 ]Norwegian Veterinarian Institute, Oslo, Kingdom of norway

[five ]Department of Biology and Woods Institute for the Environs, Stanford Academy, Stanford, CA, U.s.a.

[6 ]Section of Biology, Ashoka Academy, Sonepat, India

[7 ]Evolutionary Ecology Grouping, Department of Biological science, University of Antwerp, Wilrijk, Kingdom of belgium

[8 ]CAS Primal Laboratory of Special Pathogens, Wuhan Constitute of Virology, Wuhan, China

[9 ]Metabiota, 425 California Street, Suite 1200, San Francisco, CA, USA

[10 ]State Central Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, China

Author notes

Edited past: Wei Wang, Jiangsu Institute of Parasitic Diseases, China

Reviewed by: Cao Chen, National Institute for Viral Disease Control and Prevention, China

Aaron Irving, Zhejiang Academy-University of Edinburgh Institute, China

The third reviewer chose to remain anonymous.

Article

DOI: 10.15212/ZOONOSES-2021-0028

And then-VID: 75a8204b-8825-4f76-a51d-b505bb891885

Copyright statement: Copyright © 2022 The Authors.

License:

This is an open access commodity distributed nether the terms of the Creative Eatables Attribution License (CC BY) 4.0, which permits unrestricted use, distribution and reproduction in any medium, provided the original writer and source are credited.

Page count

Figures: 3, References: 138, Pages: xiii

Product
Funding

Funded by: "Researcher Project for Young Talents" from Research Quango of Kingdom of norway (RCN)

Award ID: 325041

Funded by: "COVIDOSE - Determining infectious dose for SARS-CoV-2 and assessing contact/proximity adventure"

Accolade ID: 312751

Funded past: Ministry of Science and Engineering science of China

Honor ID: 2020YFC0848900

Funded by: "COVID-nineteen Seasonality Project"

Award ID: 312740

We give thanks L.S. Shashidhara and members of the International Union of Biological Sciences (IUBS) for initial discussions and ideas. R.50. acknowledges funding from "Researcher Project for Young Talents" from Research Council of Norway (RCN) (reference number 325041). E.C. acknowledges support from the World Health Organization Regional Office for Africa. R.D. was supported by Stanford'south H&Southward and Woods Constitute for the Environment. M.S.J. acknowledges funding from "COVIDOSE - Determining infectious dose for SARS-CoV-2 and assessing contact/proximity take a chance" (reference number 312751) from RCN. I.K. acknowledges support from Ashoka University and Early Career Research (ECR) Laurels, Science and Applied science Research Board (SERB), India. H.50. acknowledges support from the VAX-413 IDEA Consortium of Excellence at the University of Antwerp and the BiodivERsA BIODIV-AFREID and BioRodDis projects. R.Y. acknowledges support from Ministry of Science and Technology of China (no. 2020YFC0848900). N.C.S. acknowledges support from the "COVID-nineteen Seasonality Projection" (reference number 312740) from RCN. The other authors declare no specific funding back up for this research. The funders had no role in the study pattern, information collection and analysis, decision to publish, or grooming of the manuscript.

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