Ecological Factors of VE Popularity Speed in West-Africa

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1		Olalekan Chris Akinsulie	--	2360	2023-09-20 13:19:07	\|
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This entry is adapted from the peer-reviewed paper 10.3390/idr15050050

Encephalitis is an inflammation of the brain, often caused by an autoimmune reaction, or in most cases because of a direct viral, bacterial, or parasitic infection. Viral encephalitides (VE) presents a significant public health concern globally, especially in West Africa. There are more than five hundred known arthropod-borne viruses (arboviruses), with over a hundred of them identified to cause encephalitic diseases in humans and animals, giving rise to a tremendous burden of the diseases and socioeconomic strains in tropical and subtropical regions worldwide.

viral encephalitides West Africa ecological factors climate land use change animal reservoirs vertical viral transmission

1. Introduction

With numerous emerging and re-emerging zoonotic viral infections that cause serious neurological consequences and have recently gained global attention, viral encephalitides (VE) has become a particularly significant public health concern in West Africa ^[1]^[2]^[3]. It is essential to develop a thorough understanding of the molecular inter-relatedness and the transmission dynamics of these infections in order to properly address future danger. There are several crucial elements which potentiate the establishment and transmission cycle of these plethora of pathogens causing VE generally ^[4]. Firstly, depending on the particular infection, different viruses that cause encephalitis ideally have arthropod or animal reservoirs ^[1]^[5]^[6]. For instance, arthropod-borne viruses (arboviruses), like chikungunya virus (CHIKV), West Nile virus (WNV), Rift Valley fever virus (RVFV), and yellow fever virus (YFV), predominantly exploit infected animals, including birds, livestock, and wild mammals, as the virus’s amplification hosts ^[7]^[8]. Furthermore, zoonotic viruses, like Lassa fever virus (LFV) have particular animal reservoirs, including the Mastomys rat, which helps transmit LFV with the accompanying encephalitis ^[9]. Ticks and mosquitoes are important carriers of arboviruses, like WNV and CHIKV ^[10]^[11]. Aedes mosquitoes, especially Aedes aegypti and Aedes albopictus, are well established carriers of these viruses ^[11]. In most West African countries, especially Nigeria and Ghana, these mosquitoes typically reproduce primarily in urban and peri-urban environments, where people use artificial water storage containers ^[12]. By feeding on cattle and animals, ticks, especially those from the genus Hyalomma, contribute to the spread of encephalitis-causing viruses, like the Crimean–Congo hemorrhagic fever virus (CCHFV) ^[13]. Secondly, there is a substantial role humans play in the VE transmission cycle. Through the bites of infected ticks or mosquitoes, which act as hosts for the viruses, humans get infected ^[14]. Working in the veterinary, agricultural, or health sector exposes certain occupational groups to an increased risk of contracting zoonotic viruses, such as LFV, through contact with body fluids ^[15]. Thirdly, environmental factors are also important in the transmission dynamics of VE. Peak transmission occurs during the rainy season, when mosquito populations are at their highest, and climate and seasonality have a significant impact on tick and mosquito populations ^[16]. Rapid urbanization and changes in land use encourage mosquito breeding, which amplifies the spread of viruses that cause encephalitis. The spread of Aedes mosquitoes in urban settings is further aided by poor waste management procedures ^[17]. Alongside vector-borne viruses, other encephalitic viruses include enteroviruses and lyssaviruses. Currently, there are no specific treatments or vaccine options for most of these encephalitic viruses; hence, infected humans and animals often require symptomatic treatments. Generally, successful implementation of targeted remedies and control strategies requires an understanding of the intricate drivers of VE transmission.

Environmental and human factors seem to have a role in the rising prevalence of vector-borne illnesses. Changes in the climate, urbanization (particularly in altered urban environments), human actions, large-scale gathering events, human and animal movement, expansion of air travel, and large-scale farming practices have all been implicated in the swiftly expanding world epidemic of vector-borne illnesses ^[18]. Finally, growing human population density, widespread land use change, and the emergence of human commensal vectors may exert selection pressure on viruses to develop and take advantage of novel habitats ^[18].

Several of these ecological factors have been briefly overviewed in the following sections.

2. Climate: Climatic Factors and Climate Change

Changes in the climate, such as increases in temperature and rainfall, can create more favorable conditions for the survival, reproduction, and spread of arthropods, which increase their population and the risk of disease transmission. For example, evidence from the literature suggests that in regions where temperatures are regularly between 25 °C and 29 °C, essentially a greater part of West Africa, a warming climate will become less suitable for malaria, which is endemic in those areas, and more suitable for DENV, CHIKV, YFV, and other arboviruses ^[19]. Climate change, according to the 2014 Climate Change Report, can promote the propagation of vector-borne infections by modifying the biology of the vectors, their level of abundance and distribution over space, including their territorial expansion into new areas, and changes in the infectious agents’ extrinsic incubation period. Environmental modifications aimed to offset the consequences of climate change, such as flood protection and more urban green space, might raise the risk of illnesses spread by vectors ^[20].

Ambient temperature has been known for some time to influence viral replication rates and transmission of WNV, influencing the extrinsic incubation period, the seasonal characteristics of the vector mosquito populations, and the regional variability of human cases ^[21]^[22]^[23]. Increased ambient temperatures boost vector population rise ^[24], shorten the time between blood feeds, and hasten viral development ^[21]^[23]. Several experimental discoveries have demonstrated a link between temperature changes and the survival and competency of the WNV mosquito vectors. Although the quantity of precipitation (rain) might alter the disease prevalence patterns, the response may vary across vast geographic regions due to changes in the mosquito vector’s ecology ^[25]. Above-average rainfall may enhance mosquito numbers as well as the risk for epidemics of diseases ^[26]. For instance, the frequency of WNV in the tropics should be highest during the rainy season, when mosquitoes are most prevalent ^[27], but published data on the epidemiology of WNV in the tropical regions are scarce. While precipitation promotes mosquito population emergence in temperate regions ^[28], increasing rainfall in a humid environment may have minimal effect if undeveloped mosquito habitats are already numerous. Nevertheless, mosquitoes in dry regions, such as the climate of the Mediterranean type, may benefit from more rain, as it increases the number of undeveloped habitats, particularly when heavy rainfall during the spring promotes stagnant reservoirs at the start of the hot season ^[24]. The ecologies of the numerous possible mosquito vectors of RVFV contribute to the link between these severe rains and epidemic incidents ^[29]. Over four years, researchers discovered that above-average rainfall for 85–152 days preceded RVF epidemics in seven out of nine locations in South Africa ^[30]. Human outbreaks caused by CHIKV occur at unpredictable intervals, ranging from three to twenty years, and frequently coincide with extremely wet times. Outbreaks in rural areas are typically on a limited scale and are reliant on sylvatic mosquito numbers, which rise during periods of intense precipitation ^[31]. In contrast, certain epidemics in coastal East Africa in 2004 were linked to drought and poor socioeconomic development. In these situations, it was thought that the infrequent replenishment of water reserves and mosquito hatching in storage containers near humans potentiate CHIKV transmission ^[31].

3. Human Population Growth and Global Travel

The substantial expansion of the human population in West Africa has resulted in greater urbanization and expanding agriculture, potentially creating a new medium for the transmission of disease. For instance, the pattern, trend, and characteristics of urbanization in Nigeria is somewhat interesting. Several cities and towns are growing with a remarkable pace in urbanization at an extraordinary high rate of about 5–10% annually, giving a rapid expansion of Nigerian cities’ area to more than 10-fold their previous point of growth ^[32]. Particularly in urban settings, the more populous and the closer together they are distributed, the more hosts and easier accessibility available for blood-feeding mosquitoes. Higher population numbers also indicate more garbage, which produces habitats for receptacle breeders, like Aedes, or dirty pools and streams for Culex, typically in the poorer and less hygienic metropolitan regions where family finances do not afford effective personal mosquito protection. Rapid and huge population expansion is being accompanied by rising urbanization and global migration ^[33]. Most sub-Saharan African populations are expected to expand twice the current size ^[34], resulting in greater human mobility into ancient, wooded regions to obtain access to more land and, hence, exposure to the many arboviruses that exist in wild cycles. It is obvious that increased population, greater urbanization, and increased worldwide travel will create a huge opportunity for the transmission and expansion of mosquitoes, viruses, and related arboviral illnesses. Furthermore, the travel and relocation of humans and animals have accelerated the spread of arthropod-borne viruses to new territories. The transnational and intercontinental movement of infectious vector mosquitoes or their eggs are one of the most significant mechanisms for fast geographical shifts in arbovirus populations. Transport of Aedes aegypti in ships centuries ago allowed for the transmission of yellow fever from Africa to South America, which is still happening today ^[35], and in the case of Aedes albopictus, principally through the used-car tire export trade ^[36]. Dengue, chikungunya, Zika, and other viral diseases have all become major threats to global public health due to this characteristic of global spread through human-facilitated means ^[37], which has elevated Aedes aegypti and Aedes albopictus to their current status as arguably the two most significant disease carriers on the planet. West Nile virus, a Culex-associated arbovirus that uses birds as an amplifying host, has also made the journey to North America ^[38], possibly from Africa or the Middle East, as genetic evidence suggests, and is thought to have arrived by mosquitoes on board airplanes ^[38]. Such disease movement is not limited to trade and tourism, as there is a growing amount of people visiting friends and relatives, pilgrimages, humanitarian and other volunteer work, and large numbers of politically and economically affected refugees, all of which contribute to the potential for infected people to carry infectious agents to other locations and infect native vectors ^[39].

4. Land Use Change

Several land use activities, such as deforestation or urbanization, alter arthropod habitats and create new avenues and opportunities for increased arthropod–human contact, which ultimately facilitate the spread of diseases and increase their risk. The effect of man on the planet, such as modern infrastructure, irrigation, and vast solid waste generation, favors vector growth. Finally, urbanization in impoverished areas with an insufficient water supply and rubbish disposal might encourage mosquito breeding ^[18]^[40]. For example, previous reports have indicated that there has been substantial changes in land use in several southwestern states in Nigeria and Cameroon from 2000 to 2015 for the built-up land, forestland, farmland, and mixed land in those areas ^[41]^[42]. Conversely, water body and rock outcrop land have shown less important land use changes. Other forms of land significantly reduce as the built-up land increases. These findings suggest that animals, like rats, monkeys, and rabbits, that have their natural homes in the forest and farmland could be displaced, making them dwell among humans, which implies that humans in those areas in Cameroon and Nigeria might become susceptible to vector-borne diseases, like yellow fever, Ebola, and others. In the case of JEV, although not endemic in West Africa, the processes of propagation in Asian countries are linked to changes in land use and agricultural activities ^[43]. Increased chances for mosquito breeding arise when the economy develops and the rice sector thrives at the price of deforestation, as rice paddy areas are regarded as an excellent condition for mosquito reproduction and growth. Furthermore, rice fields entice migrating birds, further complicating the intricate interplay of elements that characterize JEV propagation and dissemination ^[43].

5. Animal Reservoirs

Most arthropod-borne encephalitis viruses have animal reservoirs and perhaps amplifying hosts, which can serve as a source of infection for vectors and, in turn, humans. Rift Valley fever virus has been demonstrated in experiments to multiply in a wide range of species of mammals; however, their response to environmental infections varies greatly. Sheep, cattle, goats, and camels are the most commonly connected with severe epizootics, partly because they outnumber other possible hosts in disease-affected areas. There is now strong convincing proof that WNV spreads widely and is largely unharmful among humans, birds, horses, and a variety of other animals in Africa, Europe, many parts of Asia, and Australasia. This is based on serological investigations, virus isolation, and polymerase chain reaction sequencing using samples taken from healthy birds, horses, mosquitoes, and ticks ^[44]. Pigs serve as the amplifying host for JEV ^[43]. In addition to pigs and birds, several domesticated animals that may be sub-clinically ill, but are not likely to aid in the spread of JEV, include horses and other equids (donkeys), cattle, sheep, goats, dogs, cats, chickens, ducks, wild mammals, reptiles, and amphibians ^[45]. However, further studies are required to rule out alternative host animal roles in the JEV transmission cycle ^[46].

6. Vertical Viral Transmission and Desiccation-Resistant Eggs

Horizontal transmission of the virus occurs between mosquitos, birds, humans, and other vertebrates, but there is also a trans-generational, vertical transfer of viruses within some vector species, allowing the infectious virus to travel from adult mosquitos to their offspring ^[47]. Vertical viral transmission from one generation of mosquitos to the next appears to be unusual in mosquito-borne enteroviruses, but widespread in flaviviruses, and prevalent in bunyaviruses ^[48]. Having the capacity to pass the virus on from one mosquito generation to the next via infected eggs (vertical transmission) is a significant adaptive benefit that helps enhance the probability of virus survival in the environment, reducing the chances of the local extinction of the virus at a specific geographical focus. However, a mix of this ability with eggs that are also desiccation tolerant or resistant adds a truly strong dual framework not only for virus survival, but also for spatiotemporal spread. The ability of some mosquitoes to lay eggs that can withstand varying amounts of complete drying out and hatch when the next surges of rain, flood, or human irrigation of a garden occur, or even have staggered hatching events spread over multiple rainfall surges, is likely the most significant biological trait of all that contributed to the efficient transcontinental dissemination of Ae. aegypti and Ae. albopictus, as well as other viruses, such as DENV, CHIKV, YFV, and others that have been linked therewith ^[18]. How RVF virus continues to exist between epidemics that may have more than a decade between such occurrences has long been a mystery. It has been hypothesized that transovarial-infected Aedes eggs, that are drought-resistant and thrive for several decades, may be to blame or assist such inter-epidemic existence ^[49]^[50].

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