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Biomedical subjects

R M May

Publications and source records attributed to R M May.

At least 73 records · Page 4Linked to original sources
PubMed1990

Distinguishing error from chaos in ecological time series.

Over the years, there has been much discussion about the relative importance of environmental and biological factors in regulating natural populations. Often it is thought that environmental factors are associated with stochastic fluctuations in population density, and biological ones with deterministic regulation. We revisit these ideas in the light of recent work on chaos and nonlinear systems. We show that completely deterministic regulatory factors can lead to apparently random fluctuations in population density, and we then develop a new method (that can be applied to limited data sets) to make practical distinctions between apparently noisy dynamics produced by low-dimensional chaos and population variation that in fact derives from random (high-dimensional) noise, such as environmental stochasticity or sampling error. To show its practical use, the method is first applied to models where the dynamics are known. We then apply the method to several sets of real data, including newly analysed data on the incidence of measles in the United Kingdom. Here the additional problems of secular trends and spatial effects are explored. In particular, we find that on a city-by-city scale measles exhibits low-dimensional chaos (as has previously been found for measles in New York City), whereas on a larger, country-wide scale the dynamics appear as a noisy two-year cycle. In addition to shedding light on the basic dynamics of some nonlinear biological systems, this work dramatizes how the scale on which data is collected and analysed can affect the conclusions drawn.

Chickenpox↗
PubMed1990

Nonlinear forecasting as a way of distinguishing chaos from measurement error in time series.

An approach is presented for making short-term predictions about the trajectories of chaotic dynamical systems. The method is applied to data on measles, chickenpox, and marine phytoplankton populations, to show how apparent noise associated with deterministic chaos can be distinguished from sampling error and other sources of externally induced environmental noise.

Animals↗
PubMed1990

Host-parasitoid associations in patchy environments.

Studies of insect host-parasitoid interactions have contributed much to the consensus that spatial patchiness is important in the regulation of natural populations. A variety of theoretical models predict that host and parasitoid populations, although unstable in the absence of environmental heterogeneity, may persist at roughly steady overall densities in a patchy environment owing to variation in levels of parasitism from patch to patch. Observed patterns of parasitism, however, have a variety of forms (with variation in attack rates among patches depending directly or indirectly on host density, or showing variation uncorrelated with host density). There is some confusion about the dynamical consequences of these different forms. Here we first show how the dynamical effects of all these forms of environmental heterogeneity can be assessed by a common criterion. This 'CV2 greater than 1 rule' states that the overall population densities will remain roughly steady from generation to generation if the coefficient of variation squared (CV2) of the density of searching parasitoids in the vicinity of each host exceeds approximately unity. By partitioning CV2 into components, we show that both direct and inverse patterns of dependence on host density, and density-independent patterns, all contribute to population regulation in the same way. Second, we show how a maximum-likelihood method can be applied to the kind of field data that are usually available (that is, percentage parasitism versus local host density) to estimate the components of CV2. This analysis indicates that heterogeneity is large enough to stabilize dynamics in 9 of 34 published studies, and that density-independent heterogeneity is the main factor in most cases.

Algorithms↗
PubMed1990

The evolutionary dynamics of HIV-1 quasispecies and the development of immunodeficiency disease.

This paper presents a theory to explain the development of immunodeficiency disease after a long and variable incubation period of infection with HIV-1. Two assumptions are central to the theory: (1) mutation via reverse transcription during viral replication can generate viral strains resistant to neutralization by antibodies specific to earlier mutants in a particular host; (2) the virus can kill the CD4-positive lymphocytes that play a role in mounting an immunological attack directed at the virus. The theory is examined via the development of a mathematical model which reveals that an increasing number of antigenically distinct viral strains may overwhelm the immune system of the host. As the viral diversity increases beyond a certain level the immune system is unable to suppress the population growth of all the strains simultaneously. The intuitive explanation of this pattern of model behaviour lies in the assumption that each virus can kill CD4-positive lymphocytes that are specific to any of the viral strains, but each lymphocyte only directs immunological attack against a single viral strain.(ABSTRACT TRUNCATED AT 250 WORDS)

Acquired Immunodeficiency Syndrome↗
PubMed1990

Red cell enzyme and serum protein polymorphisms in the western Cape region of South Africa.

Nine red cell enzyme systems: Acid phosphatase-1 (ACP1), adenosine deaminase (ADA), adenylate kinase-1 (AK1), esterase D (ESD), 6-phosphogluconate dehydrogenase (PGD), phosphoglucomutase first and second loci (PGM1, PGM2), carbonic anhydrase-2 (CA2) and glyoxalase-I (GLO1); and three serum protein systems: haptoglobin (HP), transferrin (TF) and properdin factor B (BF), were examined in four populations--Caucasoids, "Cape Coloureds", Cape Malays and Negroes--in the western Cape region of South Africa. The results show distinct differences between the four groups for several genetic markers.

Black People↗
PubMed1989

Blood group gene frequencies of four population groups in the western Cape.

Blood group gene frequencies of 4 population groups in the western Cape region of South Africa were determined. The ABO, MNSs, Rhesus, Kell and Duffy blood group systems were studied in 2,094 non-Malay Cape Coloureds, 1,181 South African (SA) Negroes, 506 SA Caucasoids and 115 Cape Malays. The gene frequencies of these 4 population groups together with, for comparative purposes, previously published data on 3 others, namely Johannesburg Coloureds, Khoikhoi and San, were used to measure the genetic distances between them. In addition, multivariate analysis was used in an attempt to clarify whether the 2 coloured and the Cape Malay samples resemble each other, and to demonstrate the relationships between the 7 population groups. Although genetic distance measurements suggest that Johannesburg Coloureds have a greater SA Negro contribution to their gene pool than the Cape Coloureds, the results are in accordance with previous studies suggesting that coloureds in southern Africa form a relatively homogeneous group. The allele frequencies in the Rhesus and Duffy blood group systems suggest that Cape Malays, although similar in some respects to the Cape Coloureds, are a genetically distinct group.

ABO Blood-Group System↗
PubMed1989

Paternity exclusion using 18 genetic systems in 2124 cases in four South African population groups.

Using 18 different blood group systems, 2,124 cases of doubtful paternity, unevenly distributed among four different population groups--South African Negroes (Xhosas) 645 (30%); South African Caucasians 264 (13%); Cape Coloureds (non-Malay) 1,156 (54%), and Cape Malays 59 (3%)--were analysed. Tests for red cell antigen, plasma protein, red cell enzyme and HLA polymorphisms were done on all subjects. The overall exclusion rate was 38,23%, i.e. 812 of the 2,124 men were not biological fathers of the children ascribed to them. The capability of the individual systems to exclude a man from specific paternity was also evaluated. The polymorphic HLA system was the most useful and alone--depending on the particular population group--excluded between 93.5% and 97.8% of falsely accused men. The proportion of men excluded also varied between different population groups using the different systems, e.g. the Rhesus system alone excluded 43.9% of South African Caucasian non-fathers and only 14% of the Xhosa non-fathers. This is a reflection of the gene frequencies within a particular population. The analysis showed that the genetic systems tested in this laboratory were extremely efficient in providing evidence in proof of non-paternity.

Black People↗
PubMed1989

Restriction fragment length polymorphism of HLA-DRw53 detected in South African blacks and individuals of mixed ancestry.

The HLA-DRw53 specificity has not until now been shown to demonstrate polymorphism. We have studied 33 DRw53 haplotypes, comprising 19 DR4, 10 DR7, and 4 DR9 haplotypes, from 6 homozygous typing cells, 11 families, and 8 random individuals. All the subjects studied were South African blacks or of mixed ancestry (Cape Coloureds), with the exception of four homozygous typing cells from whites. The DNA was digested with TaqI and, after Southern blotting, was hybridized with a full-length DRB cDNA probe. Fragments correlating with DR4 (5.5 kb), DR7 (4.0 kb), and DR9 (4.1 kb) were observed. Two fragments of 14.5 and 2.8 kb correlated with DRw53. In addition, two pairs of fragments demonstrated a diallelic pattern, which is likely to correlate with a polymorphism of the DRB4 (DRw53) gene, since one or other of the two patterns was observed in all cells carrying the DRw53 specificity. The first allelic pattern, called DRw53a, was characterized by the presence of 7.5- and 2.6-kb fragments, while the second pattern, called DRw53b, had 5.8- and 2.7-kb fragments. DRw53a occurred in 10 of the 19 DR4 haplotypes and 7 of the 10 DR7 haplotypes. All three DR9,DQw2 haplotypes were also associated with DRw53a. These findings may have important implications for disease associations and the use of unrelated donors for organ transplantation.

Alleles↗
PubMed1989

Non-linear phenomena in host-parasite interactions.

The paper examines non-linear dynamical phenomena in host-parasite interactions by reference to a series of different problems ranging from the impact on transmission of control measures based on vaccination and chemotherapy, to the effects of immunological responses targeted at different stages in a parasite's life-cycle. Throughout, simple mathematical models are employed to aid in interpretation. Analyses reveal that the influence of a defined control measure on the prevalence or intensity of infection, whether vaccination or drug treatment, is non-linearly related to the magnitude of control effort (as defined by the proportion of individuals vaccinated or treated with a drug). Consideration of the relative merits of gametocyte and sporozoite vaccines against malarial parasites suggests that very high leves of cohort immunization will be required to block transmission in endemic areas, with the former type of vaccine being more effective in reducing transmission for a defined level of coverage and the latter being better with respect to a reduction in morbidity. The inclusion of genetic elements in analyses of the transmission of helminth parasites reveals complex non-linear patterns of change in the abundance of different parasite genotypes under selection pressures imposed by either the host immunological defences or the application of chemotherapeutic agents. When resistance genes are present in parasite populations, the degree to which abundance can be suppressed by chemotherapy depends critically on the frequency and intensity of application, with intermediate values of the former being optimal. A more detailed consideration of the impact of immunological defences on parasite population growth within an individual host, by reference to the erythrocytic cycle of malaria, suggests that the effectiveness of a given immunological response is inversely related to the life-expectancy of the target stage in the parasite's developmental cycle.

Animals↗
PubMed1989

The influence of different sexual-contact patterns between age classes on the predicted demographic impact of AIDS in developing countries.

A model is developed to describe the spread of HIV within heterosexual communities and the demographic impact of AIDS. The model combines epidemiologic and demographic processes and is designed to mirror the impact of AIDS in sub-Saharan Africa. Refinements on past work in this area include unequal probabilities for transmission from females to males and from males to females, the inclusion of an age- and sex-dependent sexual-partner choice function and distributed incubation plus infectious periods. Numerical studies suggest that unequal transmission probabilities (weighted to a greater probability from males to females than vice versa), and the tendency of males to choose sexual partners of the opposite sex younger than themselves, both act to increase the demographic impact of AIDS over that predicted with equal transmission between the sexes and partner choice restricted within given age classes. Analyses support the conclusions of past work that the epidemic will only have a small detrimental impact on the dependency ratio of a population (the ratio of dependents to working adults) even when a weighting is added to take account of the extra burden imposed by the care of adult AIDS patients. However, a small increase in the ratio can imply a significant rise in the number of dependents within the population. Stimulation studies of the impact of changes in behavior to reduce transmission highlight to the need to induce such changes as early as possible in the course of the epidemic in order to minimize its impact. Directions for future research are discussed emphasizing the need to acquire quantitative data on sexual habits and to construct models to represent heterogeneity in sexual behavior.

Acquired Immunodeficiency Syndrome↗
PubMed1989

Networks of sexual contacts: implications for the pattern of spread of HIV.

This paper examines the influence of sexual contact patterns (mixing matrices) on the pattern of the AIDS epidemic in a male homosexual community via numerical studies of a mathematical model of the transmission dynamics of HIV. A discussion is presented of the range of possible structures of networks of sexual contacts with extremes of assortative (within sexual activity groups) and disassortative (between sexual activity groups) mixing. The assortative mixing extreme is shown to generate the most rapid growth in the incidence of infection in the early stages of the epidemic while the disassortative extreme is shown to generate the epidemic of the largest magnitude over a long period. High within-group mixing (assortative) may generate multi-peak epidemics. The results are discussed in the context of both the interpretation of observed patterns of the spread of HIV and the acquisition of data on sexual contact patterns.

Disease Outbreaks↗
PubMed1988

The transmission dynamics of human immunodeficiency virus (HIV).

The paper first reviews data on HIV infections and AIDS disease among homosexual men, heterosexuals, intravenous (IV) drug abusers and children born to infected mothers, in both developed and developing countries. We survey such information as is currently available about the distribution of incubation times that elapse between HIV infection and the appearance of AIDS, about the fraction of those infected with HIV who eventually go on to develop AIDS, about time-dependent patterns of infectiousness and about distributions of rates of acquiring new sexual or needle-sharing partners. With this information, models for the transmission dynamics of HIV are developed, beginning with deliberately oversimplified models and progressing--on the basis of the understanding thus gained--to more complex ones. Where possible, estimates of the model's parameters are derived from the epidemiological data, and predictions are compared with observed trends. We also combine these epidemiological models with demographic considerations to assess the effects that heterosexually-transmitted HIV/AIDS may eventually have on rates of population growth, on age profiles and on associated economic and social indicators, in African and other countries. The degree to which sexual or other habits must change to bring the 'basic reproductive rate', R0, of HIV infections below unity is discussed. We conclude by outlining some research needs, both in the refinement and development of models and in the collection of epidemiological data.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Epidemiological parameters of HIV transmission.

Epidemiological data on the main determinants of the transmission potential of HIV-1 in specific at risk groups in slowly accumulating, but many uncertainties remain.

Acquired Immunodeficiency Syndrome↗