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Advances in biochemistry, molecular biology, virology, and structural biology have enabled the researchers in veterinary medicine to make many exciting discoveries that have, in some cases, conceptually revolutionized our understanding of the discipline.
Emerging Trends in Veterinary Virology is a review of selected topics about viral infections in animals. 11 chapters cover recent findings about specific viruses that infect a variety of hosts. The contents cover several types of veterinary infections in birds (Infectious laryngotracheitis (ILT), avian leucosis), cats (feline rabies), dogs (canine distemper), bovines (viral leukemia) and equines (hendra virus disease). Additionally, special topics such as the epidemiology of veterinary zoonoses and SARS are also covered.
The book provides updated information for researchers (virologists, microbiologists), students and veterinarians, alike.
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Seitenzahl: 252
Veröffentlichungsjahr: 2022
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Emerging Trends in Veterinary Virology presents some emerging aspects and general principles in the field of veterinary virology. Recently, new advances in molecular biology, virology, biochemistry and structural biology have enabled the field of veterinary virology to make many exciting discoveries that have, in some cases, conceptually revolutionized our understanding of the topic. The book will provide useful information to virologists, microbiologists, students, and researchers.
Emerging infectious diseases are causing outbreaks with loss of human and animal lives and may have huge economic and societal impacts. There may be both natural and anthropogenic drivers behind the emergence of viral diseases. Zoonotic diseases are more commonly emerging, and the inborn tendency of RNA viruses to mutate makes these over-represented among the emerging diseases. A thorough understanding of the molecular biology, immunology, and pathogenesis of viruses that cause diseases is necessary for the rationale design of vaccines and diagnostics to control diseases.
In this book, eleven chapters are showcased to illustrate some of the most important findings made in the field of veterinary virology. Our first chapter starts with discussing viral evolution and moves towards discussing global changes and the impact on diseases, with a particular focus on vector-borne viruses. The second chapter is Infectious laryngotracheitis (ILT), an economically important respiratory disease of chickens that is prevalent throughout the world.
The third chapter covers avian leukosis viruses, which are the ancient RNA viruses that are notorious for causing oncogenesis in birds, especially in poultry. The purpose of this chapter is to understand the various aspects of ALV biology as well as to provide a comprehensive account of emerging trends in research for its diagnosis as well as control.
Our next chapter covers a neglected area; rabies lyssavirus (RABV) is the chief lyssavirus involved in rabies, a 100% lethal zoonotic acute encephalitis. Cats, like other mammals, are susceptible to the disease, and this is an emerging concern regarding feline health and Public Health as rabid cats might transmit the disease to humans. The next chapter covers an emerging virus, Bovine Leukemia, which is becoming a zoonotic threat.
Another chapter covers Hendra, which is a newly emerged disease of horses and humans. Paramyxoviridae family of viruses infect numerous species but with host specificity. Hendra virus, earlier called Horse morbillivirus, cause disease in horses but also have zoonotic importance.
The next chapter covers the West Nile virus (WNV), in which infected horses suffer from lethargy and nervous disorder. WNV causes West Nile virus disease in humans, which is characterized by skin rash, fever, vomiting, and sometimes neurological disorder.
Chapter 10 covers SARC-CoV and MERS-CoV, which belong to the group of betacoronavirus of the family Coronaviridae, the largest of RNA viruses. First emerged from China in 2003, it spread to other parts of the world in the following year. MERS-CoV is closely related to SARS and was reported in 2013 with 30-90% fatality.
The book ends with an updated chapter on advances in rabies research from its epidemiology, transmission, immunopathology, clinical disease, patient management and prophylaxis measures. This chapter will also discuss the technical framework for rabies control through advanced strategies of vaccination, surveillance, laboratory diagnosis, animal movement monitoring and research. The last chapter is linked to emerging potential zoonotic issues related to virology and contains key information in detail.
Emerging infectious diseases are causing outbreaks with loss of human and animal lives and may have large economic and societal impacts. There may be both natural and anthropogenic drivers behind the emergence of viral diseases. Zoonotic diseases are more commonly emerging, and because RNA viruses have an inherent tendency to change, they are overrepresented among emerging diseases. Apart from the naturally occurring changes in the pathogens, humans also contribute to disease emergence by contributing to changes in land use and climate, which in turn affects ecosystems and biodiversity. This chapter reviews the different mechanisms behind viral disease emergence, as well as presents a framework evaluating the spill-over of zoonotic diseases at the human-wildlife-livestock interfaces. The chapter starts with discussing viral evolution and moves towards global changes and the impact on diseases, with a particular focus on vector-borne viruses.
Emerging infectious diseases in both animals and humans cause major economic and health burdens in every part of the world. On average, a new human disease appears every four months, and around 75% of emerging diseases are zoonotic [1].
Most originate from wildlife, and the study of disease emergence has a strong focus on wildlife. However, economically important emerging diseases often involve domestic animals. For example, between 1997 and 2009, six major emerging diseases have together cost at least $80 billion; the Nipah virus outbreak in Malaysia, West Nile fever in the US, severe acute respiratory syndrome (SARS) (starting in Asia), highly pathogenic avian influenza (HPAI, starting in Asia), bovine spongiform encephalopathy (BSE) and RVF in East Africa [2]. In five of these six high-impact diseases, livestock or animals for human consumption were a reservoir or a bridge to carry disease to people. Later outbreaks of emerging infectious diseases, such as the Middle East Respiratory Syndrome (MERS) and the Ebola outbreak in West Africa, were also caused by viruses with an animal reservoir; while bats seem the most important reservoir, in the case of MERS, livestock (camels) are an amplifying host, and in the case of Ebola, a livestock interface has been suspected [3-5]. The 2020 pandemic of coronavirus disease-19 (Covid-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-cov2), likely originated from food markets, where both animal products and live domestic and wild animals are sold for consumption [6, 7]. The origin of this virus is believed to be bats, likely through an intermediate host, like in the case of the closely related coronavirus that caused the SARS outbreak [8-11].
The burden of infectious diseases is not evenly distributed, and in low-income countries, zoonotic diseases and diseases that have recently evolved from animals account for a higher proportion of diseases than in high-income countries [12]. In Africa, diseases affect poor people disproportionally and further contribute to their poverty in a vicious circle. Zoonotic diseases have the potential to harm both the livelihoods and health of those depending on livestock [13]. Africa is also the continent where more than half of all outbreaks verified by WHO between 1996 and 2009 occurred, and where the time lags between outbreak and detection and public alerts are the longest [14].
Moreover, while populations globally are stabilizing, demographic growth is predicted to remain high in Africa, with the continent's population predicted to reach 4 billion in 2100, from 1 billion in 2014 [15]. This rapid population growth is likely to drive equally rapid changes in ecosystems, including expansion of crop agriculture into marginal areas, irrigation, deforestation, urban sprawl, road building, mining, and bushmeat harvesting [16]. Depending on how these changes affect the number of susceptible animals and humans, the risks of exposure, and the infectiousness of infected individuals, they may either increase or decrease disease incidence [17]. Disease is frequently caused by land-use change; it has been estimated to be responsible for more than 20% of the disease emergence on the island continent of Australia [18]. In addition, the risks of land use-associated diseases are often exacerbated by climate change and variability, and the poor adaptive capabilities of communities.
The fact that the emergence of viral diseases depends on factors from molecular levels to global politics (Fig. 1) not only means that it is difficult to predict or study, it will also require scientists from different fields to understand it, and the engagement of policymakers and stakeholders from different areas to manage it.
Fig. (1)) Examples of various factors affecting viral emergence at a different scale.The changes occurring within a virus can have different effects. By mutations or re-assortment events, the virus can develop new epitopes, which may change the antigenic properties. This can cause the reemergence of a virus in a population that was partly immune, either by vaccination or by natural previous infections. An example is influenza outbreaks, where a large outbreak may occur, such as H1N1, when significant changes in antigenic properties result in most people lacking sufficient immunity. Changing epitopes can also make a virus able to infect new host species and thus cause an emergence event.
Genetic changes within the virus may also mean that the virus becomes more pathogenic for the same host by changing cell predilection or increasing the viral reproduction capacity. Even though changed pathogenicity not necessarily means the virus is emerging, it may give rise to emerging disease, and instead of sub-clinically infected people, an outbreak may occur.
Single-stranded RNA viruses are usually prone to emergence due to rapid replication and frequent mutation, with almost one error per replication [19]. However, the increasing evolutionary pressure of adapting to both vertebrate and invertebrate hosts makes arbovirus slower in mutations than non-vector-borne viruses [20].
There are, however, examples of how small mutations can have dramatic influences on epidemiology. Chikungunya virus (CHIKV), causing a febrile illness with arthralgia and rashes in humans, has been known since the 1950s. Due to a non-synonymous point mutation in the genome, the virus suddenly started to infect Aedes albopictus in addition to Aedes aegypti, which might be the reason behind the outbreak from 2004 onwards [21-23]. Aedes albopictus is a highly invasive mosquito species [24, 25], and thus the virus can easily emerge where the vector spreads.
For most avian influenza viruses to be pathogenic for humans, there needs to be a change in receptor affinity, which may occur in the many re-assortment events expected when poultry mix at markets or when they mix with wild birds, but other genetic changes may be necessary for human disease emergence [26].
Cross-species events may also be a factor behind zoonotic emergence, and the risk for disease transmission to a new host depends on how often the species are in contact (Fig. 2). For example, although hantaviruses seem to evolve together with a specific mammalian host, phylogenetic analyses suggest that cross-species transmission (host switching or host jump) has occurred between more distantly related rodent hosts during the evolution of several hantaviruses [27]. Often, it seems that mutations allowing species jumping are associated with some drawbacks or costs for the viruses, which explains why not more viruses can infect different species [28]. For many zoonotic viruses, the capability to infect humans seems accidental, and humans are often dead-end hosts, not developing a high enough viremia for further spread. Examples of this would be the Japanese encephalitis virus, a zoonotic flavivirus transmitted by mainly Culex mosquitoes, and the Rift Valley fever virus, a bunyavirus transmitted by a wide range of mosquitoes. The reservoir of the Japanese encephalitis virus seems to be ardeid birds, although it has been suggested that potentially bats or reptiles could also harbor the virus [29, 30] (Fig. 3). The reservoir of RVF, on the other hand, is presumed to be eggs of Aedes mcintoshi mosquitoes, but a lot of work is being done to determine whether there is a mammalian reservoir for this virus [31-33]. For all cross-species transmission, changes that move a species into the habitats of other species increase the risks for emergence. One noteworthy example of this was the Nipah virus outbreak in Malaysia, where habitat destruction for bats caused bats and swine to live closer to each other, whereby transmission of the virus from bats to pigs, and subsequently to humans, could occur [34-36].
Fig. (2)) Framework for the disease transmission and spill-over of infectious diseases at the interface between humans, wildlife, and livestock. The more the habitats overlap, the higher the risk for spill-over events becomes. Fig. (3)) The epidemiology of Japanese encephalitis virus [37].The dependence of arthropod vectors on the surrounding environment makes them susceptible to change. Arthropods are exothermic, and thus their life cycles, as well as possible pathogen replication within them, are affected by temperature [38, 39]. Vectors are also dependent on suitable habitats for breeding, with suitability determined by factors such as soil, land use, temperature, moisture, rainfall patterns, and vegetation. When climate changes, the consequence may be that a vector expands or decreases its range and increases or reduces its active seasons [40-42]. Climate change may also result in changes in precipitation with varying effects on vectors [40]. For example, drastically increased precipitation may flush out larval habitats reducing vector populations [38, 43, 44], but the long-term effect might be the establishment of more breeding grounds. Pathogens that emerge are seldom completely new; more commonly, an established pathogen may acquire new features and become more pathogenic or spread more easily, or a pathogen may move to an area where the population is naïve, or a population may intrude into new areas and encounter new pathogens, or the pathogen evolves and infects a new host species or a new vector species.
Transmission of virus by invertebrate vectors is dependent on the vector capacity [45], defined as the number of potentially infective bites an individual is exposed to for one day from one particular vector species [46]. Extrinsic and intrinsic factors needed to be estimated for the calculation of vector capacity include:
• The vector density concerning the host density, where there are many hosts relative to the number of vectors; this reduces the likelihood that a vector would feed on a viremic host;
• The probability that a vector feeds on a specific host, which depends on the feeding frequency and the proportion of meals from that host; High biodiversity can have a dilution effect since it decreases the likelihood that vectors feed on the same host;
• The probability that the vector survives depends on many climatic factors, of which the microclimate may be very important and hard to assess;
• The vector competence, which is the proportion of vectors given an infected meal that become infected and can transmit the infection to the next host; while this is to a large extent given by the vector species and the virus characteristics, the temperature may play a role in changing this as well;
• The duration of the vector's life after the incubation period of the pathogen in the vector is again dependent on the environment and climate.
Climate changes have direct and indirect impacts on vector-borne disease transmission. Temperature changes can change the vector competence and thus cause mosquito species that are minor or insignificant vectors to become more important [47, 48]. This is because whether an arthropod can act as a vector, and how efficient it is, depends on many factors, of which some are dependent on temperature, such as longevity of the vector and the time required by the virus to reproduce and spread within the vector [39]. In addition to temperature, humidity and wind will influence the longevity and dispersal of the vector, and precipitation affects the breeding grounds.
So, how will vector-borne diseases be affected when climate changes? The complex vector-borne transmission makes prediction difficult, and in addition to understanding the effects of climate change on the vectors, it is important to understand the impact of climate change on other environmental factors that may influence vector dynamics [49]. It is thus an over-simplification to equate increases in vector-borne transmission change with temperature increases. Temperature affects the intrinsic factors of the arthropods, such as longevity, the pathogen incubation period within the vector (extrinsic incubation period (EIP)), abundance, behavior, and reproduction. Increased temperature, within defined biological limits, speeds processes up within the arthropods and thus decreases both the incubation period in the vectors and their longevity [39, 48]. In general, all factors contributing to increased vector abundance, shorter incubation periods, and increased vector survival are likely to increase the disease transmission, but also factors contributing to an increased proportion of suitable hosts.
The indirect effects of climate change on ecosystems may also be important, also for diseases that are not vector-borne. Decreased surface water availability may cause large numbers of potential hosts to aggregate closer to the water sources, which could intensify transmission, and reduced water bodies could negatively impact the predators that feed on mosquito larvae [50]. In addition, even when an increase in disease incidence is observed after climate changes, there are confounding factors. Any negative impact on the nutritional status in a community, such as droughts affecting the crop yield, interrupted infrastructures, which may, for example, make vaccination campaigns or health care impossible, or decreased social and health services, may cause a subsequent increase in disease incidence.
Due to these complexities, there are uncertainties as to how the different vector-borne diseases will be affected by the different aspects of climate change. Each combination of vector-pathogen has a different range of tolerated temperatures, with optimal transmission within a narrow range [47]. It has been suggested that minimum temperatures will change more than maximum temperatures, therefore, the effects on vector-borne disease transmission are more likely to go from suboptimal to more optimal than from optimal to above the higher range of transmission [51]. As an example, the lower temperature that will allow malaria transmission is estimated to be around 14-18°C, whereas the upper limit is around 35-40°C. Similarly, analyses of seasonal dynamics of dengue fever in Southeast Asia suggest that controlling for other confounders, an increase in the minimum temperature significantly increases dengue incidence. When changes occur in those borderline regions, it is likely to affect disease transmission more than when there are changes in already suitable ranges [40], although all changes around the temperature range that makes transmission more optimal in the local setting are likely to have an impact. Cold season temperatures affect how long breeding season mosquitoes have, and different species may continue breeding at lower temperatures than others [52]. Temperature increases could also lead to the life span of the mosquito getting shorter than the incubation period or the mosquito mortality getting too high; however, the capacity of mosquitoes to find themselves suitable microhabitats to avoid heat makes this less likely.
Another aspect is if the changes in transmission caused by climate change will be observable. If the transmission of vector-borne diseases is already very high, it may not be possible to notice small increases in transmission, and this could be the case, especially in tropical low-income countries [53]. The opposite scenario may occur in developed countries, where socioeconomic factors may prohibit the increased spread of diseases, despite a climate becoming more permissive. Mosquitoes capable of transmitting malaria are present as far north as Scandinavia, but in connection with changed household sizes, changed livestock keeping, and improved standards, the incidence of malaria disappeared in the 20th century [54, 55], and similar dynamics may also affect the incidence of arboviral disease. The determination of infectious disease risk, therefore, should use a vulnerability framework that considers biophysical and vulnerability drivers [56]. Vulnerability represents the predisposition of a community or individuals to disease. It represents a range of socioeconomic and demographic factors, including institutional and cultural indicators.
Climate changes are not responsible for all changes in the distribution of vector-borne diseases. Although climate changes can be a contributor to the spread of different mosquito species, most of the new introductions of invasive mosquito species have not been related directly to climate change [57]. Vectors have different requirements for their breeding grounds, and these are often, but not always dependent on meteorological factors. One of the major vectors for RVF in West Africa, Aedes vexans,