Host-parasite interactions with a focus on the Malaria parasite.
Malaria eradication, as defined by the World Health Organisation, is the permanent reduction to zero of the global incidences of malaria caused by malaria parasites because of deliberate activities, no other interventions are needed once eradication has been achieved. In recent years only 8 countries have been certified by WHO as having eliminated malaria and according to the most current World Malaria Report (November 2017), 216 million cases of malaria were seen in 2016, 211 million cases up from 2015 (Malaria, 2018). With the growing resistance Plasmodium falciparum, responsible for cerebral malaria, is displaying to antimalarial drugs combined with the emerging growth of insecticide-resistant mosquitos (Crompton, 2010), it’s imperative that we find new and effective solutions in the form of vector control and vaccines.
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Host-parasite symbiosis can be defined as a relationship between species, where one organism lives in or on another organism; the host (Poulin, 2007). Malaria is an example of such a relationship and is a parasitic infection caused by four species of protozoan parasites: P. falciparum, P. vivax, P. ovale, and P. malariae. Though P.vivax is the more common form of the species in relation to malaria infections P. falciparum is the deadliest of the group and is associated with the highest mortality around the world. The manifestations of malaria vary from patient to patient, ranging from fevers and vomiting to cerebral malaria and renal failure, the latter caused by slow medical intervention in P.falciparum cases.
The life cycle of the malaria parasite [as shown in figure 1] is divided into two stages, three in the mosquito and two in the human host. The parasite is transmitted in the form of a sporozoite, from the salivary glands of infected female mosquitoes in the genus Anopheles . Of the 2,500 species of mosquitos present today only a maximum of 60, and only females, belonging to the genus Anopheles can transmit malaria. The females are the main transporters of the parasite as they require blood meals for reproduction. Once sporozoites have entered the host, they invade hepatocytes where they take approximately 5-15 days to mature into schizonts. It’s possible for malaria to reappear years after what appeared to be “successful” treatment, as at this stage some forms of the parasite remain dormant in the liver and can resume their life cycle later, causing further infection . Each schizont contains 10,000-30,000 daughter parasites called merozoites, which upon release invade erythrocytes, here the merozoites transform back into schizonts each with 32 new merozoites . These erythrocytes then rapture releasing the merozoites and infect surrounding blood cells, this stage highlights the clinical onset of malaria . Some merozoites differentiate into gametocytes, which are needed for sexual reproduction of the next generation of parasites, intended to be absorbed by a female mosquito during a blood meal . Upon ingestion inside the vector, the gametocytes exit the host blood cells and fuse to make a zygote, which elongates to make an ookinete (the motile form of the zygote) . Next, the ookinete penetrates the lining the of the stomach wall in the mosquito and becomes an oocyst, depending on factors such as parasite species the oocyst enlarges into sporozoites. The oocyst splits and the sporozoite move to the salivary glands, to be released into the host bloodstream during a blood feed and the cycle starts again  (Institute of medicine, Oaks, & Mitchell).
Figure 1: life cycle of the malaria parasite. (Institute of medicine, Oaks, & Mitchell)
This review presents ideas on how a lack of understanding about malaria epidemiology, with focus on Plasmodium falciparum, coupled with minimal knowledge on how characteristics such as different infection lengths impact this parasites evolution, hinders our chances of understanding P. falciparum ‘s growing drug resistance. The review highlights how these variations increase the speed and likelihood of beneficial alleles being fixed for the parasite, for example, populations with both short and long infection cycles encourage selection efficiency (Chang, Childs, & Buckee, 2016). The second area that will be covered will be on vector control, and though host malaria virulence has been the focus of many studies, the vectors contribution hasn’t as much. It’s been found that lipids from mosquitos determine host-parasite virulence by controlling the quantity and quality of sporozoites that are produced, it’s also been predicted that parasitic resource exploitation inside the vector can restrict the parasite’s virulence inside the host (G, et al., 2018).
Non-competitive resource exploitation within mosquito shapes host infectivity and virulence
In 2018 G.Costa et al examined the association between parasite-vector resource exploitation and host virulence. Studies have focused primarily on host malaria virulence with some focus on the link between host virulence and vector fitness, however, the vectors contribution to the spread and severity of malaria hasn’t been as explored. They modeled two examples of vector-parasite symbiosis and looked at how they affected parasite transmission and predicted that the relationship of resource acquisition between parasite and vector shaped the virulence inside the host later. In summary, a competitive relationship increased parasite virulence while a non-competitive relationship restricted it. Resources collected after a blood meal are needed for both mosquito eggs and Plasmodium parasites, parasites can either compete for vector nutrients (competition), of course, the parasite would benefit from this and proliferate, or share resources and take advantage of egg developmental processes (oogenesis) from the vector later on and increase chances of producing and passing on offspring.
Mosquito lipids regulate host Plasmodium virulence
To investigate whether restricting resources in the vector affected the parasite’s virulence, the group focused their study on lipids associated with vector-parasite development. Lipid trafficking in adult female parasites was interrupted by depletion of lipid transporter Lipophorin (Lp), which led to large amounts of lipids building in the midgut and stopping ovary development. Mice were exposed to the Plasmodium-berghei infected control group and the Lp depleted mosquito group, and the results showed that Lp depletion greatly reduced parasite infectivity. Only 20% of mice bitten by the Lp depleted group became infected [as shown in figure 2], and only 10% developed symptoms of experimental cerebral malaria (ECM) compared to the 90% in the control group. These results suggested that parasite development inside the vector depends on lipophorin involved in oogenesis, supporting the idea of a parasitic relationship versus a competitive one.
Mosquito lipids shape sporozoite loads and infectivity
Lipid accumulation was measured in growing parasites using Nile Red lipid staining. In the control mosquitos, lipid build-up was seen in vesicles of mature oocysts, but in the Lp depleted group lower levels of Nile Red staining were recorded. There was an increase in the amount of Lp positive oocysts grew from 25%-72 %, 7-13 days after infection. These results supported a parasitic relationship as Plasmodium uses Lp to deliver lipids while proliferating. Reduced numbers of Lp reduced oocyst sporulation, the size of mature oocysts that were available and decreased the number of sporozoites that could be deployed. These results confirmed the group’s theoretical points as the vector lipid environment shaped the quantity and quality of Plasmodium parasites as well as their mitochondrial potential.
Time difference between oogenesis and parasites gaining lipids
Mosquito ovaries collect lipids during the first 2 days after feeding, however, Plasmodium growth begins 1 week after infection. Despite Lp depletion causing lipid accumulation in the midgut, this environment didn’t benefit the sporozoites and reduced infectivity and virulence was noted, even when no competition with egg development was present. The team found that early oocysts didn’t take up lipids, instead of reducing competition with the mosquitos needs, and accumulating lipids after the completion of the vectors oogenesis. The time shift in the vector-parasite oocyst maturation benefits the parasitic non-competitive relationship by allowing timely delegation of resources for both host reproduction and parasite growth.
Figure 2: health status of the subject group, once bitten by the control group (Ctrl) or Lp depleted mosquitos (dsLp).
In conclusion, the data collected demonstrates how the vector environments impact the within-host virulence, and how the malaria parasite has shown great adaption to its vector for its own proliferation. Currently, the mechanisms behind how the parasites acquire lipids are unknown, and future studies on oocysts transcriptional processes would be needed to identify these processes (G, et al., 2018).
Variation in infection length and superinfection enhance selection efficiency in the human malaria parasite
The success of the malaria parasite is considered to be partly due to the unique lifecycle and evolutionary tactics of Plasmodium falciparum. Malaria can present itself in shortly lived infections mainly in young children resulting in death, to non-sterilising immunity in adults that leads to the parasite being in low quantities with asymptomatic infections. The latter group have multiple genotypes and can remain in the host for months contributing to transmission. It is crucial that the role asymptomatic and chronic infections play in drug resistance is understood, to help develop new antimalarial drugs. In an endemic region, there is a mixture of chronic and acute infections of malaria, and these mixed genotypes have been suggested to be more infectious to mosquitos than infections with a single genotype. Hsiao-Han Chang et al model how having variable infection cycles increases the likelihood of the fixation of beneficial alleles, as well as the role superinfection and chronic infections have on overall virulence.
Chronic infections exhibit a higher probability of fixation than acute infections
Idealized models of acute and chronic infections were compared, which contained observations and trends collected from field settings. It’s noted that it was assumed that the prevalence of infection was at equilibrium; that is the number of people infected was the same as the number of people who died or were clear of infection. A comparison was made of the probability that a mutation happening on the same day after infection in both models became fixed in the population, as well as how long it took to reach this fixation. Results showed how fixing beneficial mutations was promoted higher in the chronic model during the growth phase of the infection, and the likelihood of fixing increases with the length of infection.
Superinfection increases selection efficiency
Superinfection is defined as a second infection occurring onto an earlier one so that both infections are still evident (Definition of Superinfection, 2018). Superinfection was found to increase the likelihood of fixation in all selection models and led to increased amounts of infections being acquired by the host. Surprisingly superinfection was found to increase the number of infections being transmitted to different host too and increased the competition between alleles in a host, resulting in the fittest most beneficial alleles being selected. The study found that the time it took for a mutation to be fixed decreased with superinfection, as superinfection brings wild-type and mutant alleles together quicker and causes direct competition.
Infection length variation in the host population enhances selection efficiency
Malaria in endemic regions is characterized by its varying infection lengths, so the probabilities of fixation in populations with equal amounts of infected human hosts but varying chronic infections was investigated. It was found that as the number of infections that are long-lived increased, it promoted competition between alleles in the host and reduced the contribution by individuals with chronic malaria to the infected population. In populations where the infections are majority long-lived, despite promoting high allele competition, newly infected hosts are low as most of the people are already infected. When chronic infections are low there’s an increased probability that a mutation that’s beneficial to the parasite will compete successfully and be passed on more than once during a long infection, plus there will be more hosts because of recovered acute infections. Since the likelihood of fixing is lower in chronic infections and the fact that acute infections have higher parasite densities and potentially are more infections, the group decided to increase the amount acute infections in relation to chronic infections. Despite the acute infections being twice as infectious than chronic infections the probability of fixing did not change, ultimately models with both chronic and acute infections were more efficient at fixing.
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A combination of both chronic and acute infection, as well as superinfection, was shown to increase the speed of fixation of mutations and provide the parasite with an advantage in the host. The probability and speed at which a mutation is fixed are vital in understanding drug resistance in the future (Chang, Childs, & Buckee, 2016).
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