Roy M. Anderson

Population biology of infectious diseases: Part II.

In the first part of this two-part article (Nature 280, 361–367), mathematical models of directly transmitted microparasitic infections were developed, taking explicit account of the dynamics of the host population. The discussion is now extended to both microparasites (viruses, bacteria and protozoa) and macroparasites (helminths and arthropods), transmitted either directly or indirectly via one or more intermediate hosts. Consideration is given to the relation between the ecology and evolution of the transmission processes and the overall dynamics, and to the mechanisms that can produce cyclic patterns, or multiple stable states, in the levels of infection in the host population.

Population biology of infectious diseases

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Coevolution of hosts and parasites

The coevolution of parasites and their hosts has both general biological interest and practical implications in agricultural, veterinary and medical fields. Surprisingly, most medical, parasitological and ecological texts dismiss the subject with unsupported statements to the effect that ‘successful’ parasite species evolve to be harmless to their hosts. Recently, however, several people have explored theoretical aspects of the population genetics of host-parasite associations; these authors conclude that such associations may be responsible for much of the genetic diversity found within natural populations, from blood group polymorphisms (Haldane, 1949) to protein polymorphisms in general (Clarke, 1975, 1976) and to histocompatibility systems (Duncan, Wakeland & Klein, 1980). It has also been argued that pathogens may constitute the selective force responsible for the evolution and maintenance of sexual reproduction in animal and plant species (Jaenike, 1978; Hamilton, 1980, 1981, 1982; Bremermann, 1980).

Epidemiology and Genetics in the Coevolution of Parasites and Hosts

Recent studies suggest that parasites (interpreted broadly to include viruses, bacteria, protozoans and helminths) may influence the numerical magnitude or geographical distribution of their host populations; most of such studies focus on the population biology and epidemiology of the host-parasite association, taking no explicit account of the genetics. Other researchers have explored the possibility that the coevolution of hosts and parasites may be responsible for much of the genetic diversity found in natural populations, and may even be the main reason for sexual reproduction; such genetic studies rarely take accurate account of the density- and frequency-dependent effects associated with the transmission and maintenance of parasitic infections. This paper aims to combine epidemiology and genetics, reviewing the way in which earlier studies fit into a wider scheme and offering some new ideas about host-parasite coevolution. One central conclusion is that ‘successful’ parasites need not necessarily evolve to be harmless: both theory and some empirical evidence (particularly from the myxoma-rabbit system) indicate that many coevolutionary paths are possible, depending on the relation between virulence and transmissibility of the parasite or pathogen.

Epidemiological determinants of spread of causal agent of severe acute respiratory syndrome in Hong Kong

Summary Background Health authorities worldwide, especially in the Asia Pacific region, are seeking effective public-health interventions in the continuing epidemic of severe acute respiratory syndrome (SARS). We assessed the epidemiology of SARS in Hong Kong. Methods We included 1425 cases reported up to April 28, 2003. An integrated database was constructed from several sources containing information on epidemiological, demographic, and clinical variables. We estimated the key epidemiological distributions: infection to onset, onset to admission, admission to death, and admission to discharge. We measured associations between the estimated case fatality rate and patients’age and the time from onset to admission. Findings After the initial phase of exponential growth, the rate of confirmed cases fell to less than 20 per day by April 28. Public-health interventions included encouragement to report to hospital rapidly after the onset of clinical symptoms, contact tracing for confirmed and suspected cases, and quarantining, monitoring, and restricting the travel of contacts. The mean incubation period of the disease is estimated to be 6.4 days (95% Cl 5.2–7.7). The mean time from onset of clinical symptoms to admission to hospital varied between 3 and 5 days, with longer times earlier in the epidemic. The estimated case fatality rate was 13.2% (9.8–16.8) for patients younger than 60 years and 43.3% (35.2–52.4) for patients aged 60 years or older assuming a parametric γ distribution. A non-parametric method yielded estimates of 6.8% (4.0–9.6) and 55.0% (45.3–64.7), respectively. Case clusters have played an important part in the course of the epidemic. Interpretation Patients’age was strongly associated with outcome. The time between onset of symptoms and admission to hospital did not alter outcome, but shorter intervals will be important to the wider population by restricting the infectious period before patients are placed in quarantine. Published online May 7, 2003 http://image.thelancet.com/extras/03art4453web.pdf

Averting a malaria disaster

Estimates for the annual mortality from malaria range from 0·5 to 2·5 million deaths. The burden of this enormous toll, and the concomitant morbidity, is borne by the world’s poorest countries. Malaria morbidity and mortality have been held in check by the widespread availability of cheap and effective antimalarial drugs. The loss of these drugs to resistance may represent the single most important threat to the health of people in tropical countries. Chloroquine has been the mainstay of antimalarial drug treatment for the past 40 years, but resistance is now widespread and few countries are u n a f f e c t e d . 1 Pyrimethamine-sulphadoxine (PSD) is usually deployed as a successor to chloroquine. Both these antimalarials cost less than US

Sexual mixing patterns and sex-differentials in teenage exposure to HIV infection in rural Zimbabwe

0.20 per adult treatment course, but the drugs required to treat multidrug-resistant falciparum malaria (quinine, mefloquine, halofantrine) are over ten times more expensive and cannot be afforded by most tropical countries— especially those in Africa, where it is estimated that more than 90% of the world’s malaria deaths occur. Resistance to chloroquine is widespread across Africa and resistance to PSD is increasing. 2 A health calamity looms within the next few years. 3 As treatments lose their effectiveness, morbidity and mortality from malaria will inevitably continue to rise. Can this disaster be prevented? Can we really “roll back malaria”, as the new Director-General of WHO has demanded? 4

Regulation and stability of host-parasite population interactions: II - Destabilizing processes

BACKGROUND HIV-1 prevalence typically rises more rapidly at young ages in women than in men in sub-Saharan Africa. Greater susceptibility to infection on exposure in women is believed to be a contributory factor as is greater exposure to previously infected sexual partners of the opposite sex. We investigated the latter hypothesis using data from a field study in rural Manicaland, Zimbabwe. METHODS Quantitative data on onset and degree of sexual activity, numbers of partners, concurrent partnerships, condom use, and partner characteristics were used in conjunction with epidemiological data on age and sex specific prevalence of HIV infection to do statistical analyses of association between key variables. Mathematical models and qualitative data were used to aid analysis and interpretation. FINDINGS Older age of sexual partner was associated with increased risk of HIV-1 infection in men (odds ratio 1.13 [95% CI 1.02-1.25]) and women (1.04 [1.01-1.07]). Young women form partnerships with men 5-10 years older than themselves, whereas young men have relationships with women of a similar age or slightly younger. Greater number of lifetime partners is also associated with increased risk of HIV (1.03 [1.00-1.05]). Young men report more partners than do women but infrequent coital acts and greater use of condoms. These behaviour patterns are underpinned by cultural factors including the expectation that women should marry earlier than men. A strong gender effect remains after factors that affect exposure to infected partners are controlled for (6.04 [1.49-24.47]). INTERPRETATION The substantial age difference between female and male sexual partners in Manicaland is the major behavioural determinant of the more rapid rise in HIV prevalence in young women than in men. Theoretical studies have suggested that this difference is an important determinant of observed epidemiological patterns but the study reported in this paper provides clear empirical evidence of association.

HIV-1 Transmission, by Stage of Infection

SUMMARY (1) Three categories of biological processes are shown to have a destabilizing influence on the dynamical behaviour of model host-parasite associations: parasite induced reduction in host reproductive potential, parasite reproduction within a host which directly increases parasite population size and time delays in parasite reproduction and transmission. (2) The importance of parasitic species as regulators of host population growth is examined in light of empirical evidence. Data from two particular laboratory studies used to indicate the magnitude of this regulatory influence. Suggestions are made concerning the type of information required from field studies to facilitate critical assessment of theoretical predictions.

Helminth Infections of Humans: Mathematical Models, Population Dynamics, and Control

BACKGROUND The epidemiological impact of public health interventions targeted at reducing transmission of human immunodeficiency virus type 1 (HIV-1) during early or late-stage infection depends on the contribution of these disease stages to transmission within a particular epidemic. METHODS Transmission hazards and durations of periods of high infectivity during primary, asymptomatic, and late-stage infection were estimated for HIV-1-serodiscordant heterosexual couples in Rakai, Uganda, by use of a robust probabilistic framework. RESULTS Primary infection and late-stage infection were estimated to be 26 and 7 times, respectively, more infectious than asymptomatic infection. High infectiousness during primary infection was estimated to last for approximately 3 months after seroconversion, whereas high infectiousness during late-stage infection was estimated to be concentrated between 19 months and 10 months before death. CONCLUSIONS Primary and late-stage HIV-1 infection are more infectious than previously estimated, but for shorter periods. In a homogeneous population, the asymptomatic stage of infection will typically contribute more to the net transmission of HIV-1 over the lifetime of an infected individual, because of its longer duration. The dependence of the relative contribution of infectious stages on patterns of sexual behavior and the phase of epidemics is discussed.