William E. Collins

Bio: William E. Collins is an academic researcher from Centers for Disease Control and Prevention. The author has contributed to research in topics: Plasmodium vivax & Plasmodium falciparum. The author has an hindex of 52, co-authored 244 publications receiving 9783 citations. Previous affiliations of William E. Collins include United States Department of Health and Human Services & National Institutes of Health.

Genetic Selection of a Plasmodium-Refractory Strain of the Malaria Vector Anopheles gambiae

Abstract: The anopheline mosquito is the target in most malaria control programs, primarily through the use of residual insecticides. A mosquito was studied that is refractory to most species of malaria through a genetically controlled mechanism. A strain of Anopheles gambiae, which was selected for complete refractoriness to the simian malaria parasite Plasmodium cynomolgi, also has varying degrees of refractoriness to most other malaria species examined, including the human parasites P. falciparum, P. ovale, and P. vivax for which this mosquito is the principal African vector. Furthermore, the refractoriness extends to other subhuman primate malarias, to rodent malaria, and to avian malaria. Refractoriness is manifested by encapsulation of the malaria ookinete after it completes its passage through the mosquito midgut, approximately 16 to 24 hours after ingestion of an infective blood meal. Fully encapsulated ookinetes show no abnormalities in parasite organelles, suggesting that refractoriness is due to an enhanced ability of the host to recognize the living parasite rather than to a passive encapsulation of a dead or dying parasite. Production of fully refractory and fully susceptible mosquito strains was achieved through a short series of selective breeding steps. This result indicates a relatively simple genetic basis for refractoriness. In addition to the value these strains may serve in general studies of insect immune mechanisms, this finding encourages consideration of genetic manipulation of natural vector populations as a malaria control strategy.

The evolution of primate malaria parasites based on the gene encoding cytochrome b from the linear mitochondrial genome.

Abstract: We report a phylogenetic analysis of primate malaria parasites based on the gene encoding the cytochrome b protein from the mitochondrial genome. We have studied 17 species of Plasmodium, including 14 parasitic in primates. In our analysis, four species were used for rooting the Plasmodium phylogenetic tree: two from closely related genera (Hepatocystis sp. and Haemoproteus columbae) and two other Apicomplexa (Toxoplasma gondii and Theileria parva). We found that primate malaria parasites form a monophyletic group, with the only exception being the Plasmodium falciparum–Plasmodium reichenowi lineage. Phylogenetic analyses that include two species of non-Plasmodium Haemosporina suggest that the genus Plasmodium is polyphyletic. We conclude that the biologic traits, such as periodicity and the capacity to relapse, have limited value for assessing the phylogenetic relationships among Plasmodium species. For instance, we found no evidence that would link virulence with the age of the host–parasite association. Our studies also reveal that the primate malaria parasites originated in Africa, which contradicts the presently held opinion of Southeast Asia as their center of origin. We propose that the radiation of Asian monkey parasites is a recent event where several life history traits, like differences in periodicity, appeared de novo.

Inhibition of development of exoerythrocytic forms of malaria parasites by gamma-interferon

Abstract: A specific DNA probe was used to study the effect of recombinant rat, mouse, and human gamma-interferon (gamma-IFN) on the course of sporozoite-induced malaria infections. In mice and rats infected with sporozoites of Plasmodium berghei, mouse and rat gamma-IFN's strongly inhibited the development of the exoerythrocytic forms in the liver liver cells of the hosts, but not the development of the erythrocytic stages. The degree of inhibition of the exoerythrocytic forms was proportional to the dose of gamma-IFN administered, but was independent of the number of sporozoites used for challenge. A 30 percent reduction in the development of exoerythrocytic forms in rat liver was achieved when 150 units (about 15 nanograms of protein) of rat gamma-IFN were injected a few hours before sporozoite challenge; the reduction was 90 percent or more with higher doses of gamma-IFN. The effect was less pronounced if the gamma-IFN was administered 18 hours before or a few hours after challenge. Human gamma-IFN also diminished the parasitemia in chimpanzees infected with sporozoites of the human malaria parasite Plasmodium vivax. The target of gamma-IFN activity may be the infected hepatocytes themselves, as shown by in vitro experiments in which small doses of the human lymphokine inhibited the development of exoerythrocytic forms of Plasmodium berghei in a human hepatoma cell line. These results suggest that immunologically induced interferon may be involved in controlling malaria infection under natural conditions.

Plasmodium malariae: Parasite and Disease

Abstract: A review of the life history of Plasmodium malariae, the quartan malaria parasite of humans, is presented. Much of the information is based on data obtained from induced infections in humans who were given malaria therapy for the treatment of neurosyphilis between 1940 and 1963. Prepatent periods (i.e., the time until the first day of parasite detection) fever episodes, and maximum parasitemias as a result of infection with P. malariae were obtained and are presented. Experimental and known vectors of the parasite are also discussed. Splenectomized chimpanzees and New World monkeys are readily infected and serve as sources of parasites and antigens for diagnostic and molecular studies. South American monkeys are naturally infected with a parasite known as Plasmodium brasilianum. This parasite appears to be P. malariae that has adapted from humans to grow in monkeys, probably within the last 500 years. Infection with P. malariae is associated with the production of immune complexes in the kidneys and the associated nephrotic syndrome. The essential lesions are a thickening of the glomerular basement membrane and endocapillary cell proliferation. Studies of monkeys infected with P. malariae indicate the same pathology as that demonstrated in humans.

A monkey's tale: the origin of Plasmodium vivax as a human malaria parasite.

Abstract: The high prevalence of Duffy negativity (lack of the Duffy blood group antigen) among human populations in sub-Saharan Africa has been used to argue that Plasmodium vivax originated on that continent. Here, we investigate the phylogenetic relationships among 10 species of Plasmodium that infect primates by using three genes, two nuclear (β-tubulin and cell division cycle 2) and a gene from the plastid genome (the elongation factor Tu). We find compelling evidence that P. vivax is derived from a species that inhabited macaques in Southeast Asia. Specifically, those phylogenies that include P. vivax as an ancient lineage from which all of the macaque parasites could originate are significantly less likely to explain the data. We estimate the time to the most recent common ancestor at four neutral gene loci from Asian and South American isolates (a minimum sample of seven isolates per locus). Our analysis estimates that the extant populations of P. vivax originated between 45,680 and 81,607 years ago. The phylogeny and the estimated time frame for the origination of current P. vivax populations are consistent with an “out of Asia” origin for P. vivax as hominoid parasite. The current debate regarding how the Duffy negative trait became fixed in Africa needs to be revisited, taking into account not only human genetic data but also the genetic diversity observed in the extant P. vivax populations and the phylogeny of the genus Plasmodium.

Effects of stress throughout the lifespan on the brain, behaviour and cognition

Abstract: Chronic exposure to stress hormones, whether it occurs during the prenatal period, infancy, childhood, adolescence, adulthood or aging, has an impact on brain structures involved in cognition and mental health. However, the specific effects on the brain, behaviour and cognition emerge as a function of the timing and the duration of the exposure, and some also depend on the interaction between gene effects and previous exposure to environmental adversity. Advances in animal and human studies have made it possible to synthesize these findings, and in this Review a model is developed to explain why different disorders emerge in individuals exposed to stress at different times in their lives.

Heritable true fitness and bright birds: a role for parasites?

Abstract: Combination of seven surveys of blood parasites in North American passerines reveals weak, highly significant association over species between incidence of chronic blood infections (five genera of protozoa and one nematode) and striking display (three characters: male "brightness," female "brightness," and male song). This result conforms to a model of sexual selection in which (i) coadaptational cycles of host and parasites generate consistently positive offspring-on-parent regression of fitness, and (ii) animals choose mates for genetic disease resistance by scrutiny of characters whose full expression is dependent on health and vigor.

Phylogenetic Perspectives in Innate Immunity

Abstract: The concept of innate immunity refers to the first-line host defense that serves to limit infection in the early hours after exposure to microorganisms. Recent data have highlighted similarities between pathogen recognition, signaling pathways, and effector mechanisms of innate immunity in Drosophila and mammals, pointing to a common ancestry of these defenses. In addition to its role in the early phase of defense, innate immunity in mammals appears to play a key role in stimulating the subsequent, clonal response of adaptive immunity.