Evidence for recent changes in sexual behaviour in homosexual men in England and Wales

Over 80% of cases of Acquired Immune Deficiency Syndrome (AIDS) in England and Wales have occurred in homosexual men. Changes in sexual behaviour in this group may have a substantial influence on the incidence of Human Immunodeficiency Virus (HIV) infection and will therefore be crucial in determining future cases of AIDS. This paper critically weighs the indirect and direct evidence for changes in behaviour in homosexual men since the advent of the AIDS epidemic. The paper reports on falling incidence of gonorrhoea, hepatitis B and syphilis in homosexual men, the changes being most marked from 1985 onwards. Data on temporal trends in HIV prevalence and incidence in homosexual men are reviewed. These suggest that the maximum incidence of HIV infection occurred in 1982-84 and may have fallen since then. Evidence for a concomitant change in sexual behaviour is reported from several sources. This points towards a recent change in sexual behaviour characterized by reduction in the numbers of partners and adoption of safer sexual practices. In some places change may have occurred as early as 1983. A change became apparent generally in 1985 and this appears to have been sustained in 1986-87. Nevertheless, a substantial proportion of homosexual men studied continue to practice high risk sexual practices, such as anal intercourse, including relationships with casual partners.     

Estimation of HIV infection and incubation via state space models

By using the state space model (Kalman filter model) of the HIV epidemic, in this paper we have developed a general Bayesian procedure to estimate simultaneously the HIV infection distribution, the HIV incubation distribution, the numbers of susceptible people, infective people and AIDS cases. The basic approach is to use the Gibbs sampling method combined with the weighted bootstrap method. We have applied this method to the San Francisco AIDS incidence data from January 1981 to December 1992. The results show clearly that both the probability density function of the HIV infection and the probability density function of the HIV incubation are curves with two peaks. The results of the HIV infection distribution are clearly consistent with the finding by Tan et al. [W.Y. Tan, S.C. Tang, S.R. Lee, Estimation of HIV seroconversion and effects of age in San Francisco homosexual populations, J. Appl. Stat. 25 (1998) 85]. The results of HIV incubation distribution seem to confirm the staged model used by Satten and Longini [G. Satten, I. Longini, Markov chain with measurement error: estimating the 'true' course of marker of the progression of human immunodeficiency virus disease, Appl. Stat. 45 (1996) 275].     

The transmission dynamics of the human immunodeficiency virus type 1 in the male homosexual community in the United Kingdom: the influence of changes in sexual behaviour

This paper examines the transmission dynamics of human immune deficiency virus type 1 (HIV-1) in the male homosexual population in the U.K. via numerical studies employing a mathematical model representing the principal epidemiological process. The model is based on an assumption of proportionate mixing between different sexual-activity classes (defined by the rate of sexual partner change per unit of time) and incorporates heterogeneity in sexual activity, distributed infection and incubation periods and the recruitment of susceptibles to the sexually active population. The sensitivity of model predictions to various assumptions and parameter assignments is examined. Numerical studies of model behaviour focus on the influence of changes in the magnitudes of the transmission parameters, associated with three periods of infectiousness during the incubation period of acquired immune deficiency syndrome (AIDS), on the magnitude and duration of the epidemic and on the level of the endemic equilibrium state. Predicted temporal trends in the incidence of AIDS are shown to be particularly sensitive to changes in the intensities and durations of the stages of infectiousness. Most of the paper addresses the influence of changes in sexual behaviour on the magnitude and duration of the epidemic. Numerical simulations show that the manner in which behavioural changes occur and who is influenced by such changes (i.e. infecteds or susceptibles, the sexually active population or new recruits to this population) have a major impact on the future timecourse of the epidemic. The greatest reduction in the incidence of AIDS over the coming decades is induced by changes in the rate of sexual-partner change among the sexually active population, particularly those currently infected. The time periods at which changes in behaviour occur, in relation to the starting point of the epidemic (assumed to be 1979), are also of particular significance to the future pattern of the incidence of disease and infection. Changes in behaviour early on in the timecourse of the epidemic have a much greater impact than equivalent changes at latter time points. On the basis of limited data on the pattern of change in sexual behaviour among the male homosexual community in the U.K., numerical studies of model behaviour tentatively suggest that the epidemic is at, or near to, a period of peak incidence of the disease AIDS. Analyses suggest that, following the peak in incidence, there will be a period of slow decline over many decades provided recent changes in behaviour are maintained in the coming years.(ABSTRACT TRUNCATED AT 400 WORDS)     

Is human immunodeficiency virus/acquired immunodeficiency syndrome decreasing among Brazilian injection drug users? Recent findings and how to interpret them

We briefly review findings from Brazilian settings where the human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS) epidemic among injection drug users (IDUs) seems to be decreasing, highlighting recent findings from Rio de Janeiro and discussing methodological alternatives. Former analyses using serologic testing algorithm for recent HIV seroconversion have shown that HIV incidence has been low in IDUs recruited by two different surveys carried out in Rio, where low injection frequencies and infection rates have been found among new injectors. The proportion of AIDS cases among IDUs in Rio has been fairly modest, compared to S?o Paulo and especially to the southernmost states. Notwithstanding, the interpretation of findings from serial surveys constitutes a challenge, magnified in the assessment of HIV spread among IDUs due to the dynamic nature of the drug scenes and limitations of sampling strategies targeting hard-to-reach populations. Assessment of epidemic trends may profit from the triangulation of data, but cannot avert biases associated with sampling errors. Efforts should be made to triangulate data from different sources, besides exploring specific studies from different perspectives. In an attempt to further assess the observed trends, we carried out original analyses using data from Brazilian AIDS databank.     

Changes in sexual behaviour and the fall in incidence of HIV infection among homosexual men.

To investigate the epidemiology and normal course of infection with HIV the prevalence and incidence of the infection were studied among two cohorts of homosexual men in Amsterdam in 1980-7. The cumulative incidence of infection increased from a weighted 2.2% in 1980 to 39.0% in 1987. The estimated yearly incidence of HIV was 3.0% in 1981, rose to 8.8% in 1984, and fell gradually to 0% in 1987. During the study the sexual behaviour of the cohorts was examined. The number of men with whom anopenetrative intercourse was practised fell from a mean of 10.6 to 1.4 for those positive for HIV antibody, whereas the number with whom anoreceptive intercourse was practised fell from a mean of 3.7 to 0.5 for those negative for the antibody. In addition, there was a reduction in the number of cases of hepatitis B and syphilis among men in general. The decline in infection with HIV was assumed to be linked to changes in sexual behaviour. Such changes practised early in the course of the epidemic probably had a strong effect on the number of cases of AIDS among homosexual men in Amsterdam.     

A simulation model of AIDS in San Francisco: I. Model formulation and parameter estimation.

A model is formulated for the spread of the human immunodeficiency virus (HIV) and the subsequent development of acquired immunodeficiency syndrome (AIDS) in the population of homosexual men in San Francisco. The dynamic simulation model includes sexually very active and active subpopulations, migration, and a staged progression of HIV-infected persons to AIDS and death. Numerous data sources are used to estimate parameter values in the model. In a companion paper, simulations using the model and parameter estimates are found that are consistent with HIV and AIDS incidence data.     

Clinical picture of primary HIV infection presenting as a glandular-fever-like illness.

The clinical symptoms and signs were assessed in 20 consecutive patients developing infection with the human immunodeficiency virus (HIV). All were male homosexuals and all presented with a glandular-fever-like illness. Changes in laboratory values were compared with findings in 40 HIV negative male homosexual controls. In the 10 patients for whom date of exposure to the virus could be established the incubation period was 11-28 days (median 14). One or two days after the sudden onset of fever patients developed sore throat, lymphadenopathy, rash, lethargy, coated tongue, tonsillar hypertrophy, dry cough, headache, myalgia, conjunctivitis, vomiting, night sweats, nausea, diarrhoea, and palatal enanthema. Twelve patients had painful, shallow ulcers in the mouth or on the genitals or anus or as manifested by oesophageal symptoms; these ulcers may have been the site of entry of the virus. During the first week after the onset of symptoms mild leucopenia, thrombocytopenia, and increased numbers of banded neutrophils were detected (p less than 0.0005). The mean duration of acute illness was 12.7 days (range 5-44). All patients remained healthy during a mean follow up period of 2.5 years. Heightened awareness of the typical clinical picture in patients developing primary HIV infection will alert the physician at an early stage and so aid prompt diagnosis and help contain the epidemic spread of AIDS.     

Determination of the spread of HIV from the AIDS incidence history

The relation between the incidence of HIV in the general population, the number of AIDS cases, and the incubation period for the disease is examined. The number of AIDS cases can be expressed in terms of a convolution integral over the incubation period distribution and the temporal history of HIV incidence. In order to determine the level of HIV incidence it is necessary to invert the convolution. In this manner, it is possible to determine the spread of HIV up to the present time from knowledge of the AIDS incidence history and the incubation period. We describe the inversion of the convolution in terms of a Laplace transform technique that is applicable for any given incubation period distribution. Substantial simplifications in the technique are found in the case of an Erlang distribution for the probability density. The spread of HIV infections in the United States is charted through 1988 using AIDS incidence data that are corrected for both the revised AIDS case definition and reporting time delays. The results are consistent with current estimates of the HIV incidence in the United States and show no evidence of saturation in the rate of new infections. Indeed, the rate of new infections still appears to be climbing as of that date. While the technique is unable to predict the future course of the epidemic, it may provide a useful benchmark for comparison with mathematical models of the epidemic. The techniques are conceptually applicable to diseases other than AIDS.     

Framing Thai sexuality in the age of AIDS -- introduction

Four of the papers presented at a panel on acquired immunodeficiency syndrome (AIDS) at the 1994 conference of the Australian Anthropological Society focused on Thailand, which is widely regarded as the epicenter of the epidemic in Southeast Asia. In his introduction to these papers, Lyttleton notes that the discourse on AIDS in Thailand has been characterized by a medical, hierarchical approach. Unlike the situation in countries such as the US, where homosexuals have engaged in collective activism to prevent the further spread of AIDS, Thailand's high-risk groups (e.g., prostitutes and injecting drug users) lack the group identification essential for the development of a culture of safe sex practices. Any discussion of AIDS in the Thai context must include an examination of the role of social drinking in framing men's public sexuality and male identity. Moreover, the homophobic nature of Thai culture has led to a dismissal of the reality of homosexual transmission.     

The chemical bases of the various AIDS epidemics: Recreational drugs,anti-viral chemotherapy and malnutrition

In 1981 a new epidemic of about two-dozen heterogeneous diseases began to strike non-randomly growing numbers of male homosexuals and mostly male intravenous drug users in the US and Europe. Assuming immunodeficiency as the common denominator the US Centers for Disease Control (CDC) termed the epidemic, AIDS, for acquired immunodeficiency syndrome. From 1981-1984 leading researchers including those from the CDC proposed that recreational drug use was the cause of AIDS, because of exact correlations and of drug-specific diseases. However, in 1984 US government researchers proposed that a virus, now termed human immunodeficiency virus (HIV), is the cause of the non-random epidemics of the US and Europe but also of a new, sexually random epidemic in Africa. The virus-AIDS hypothesis was instantly accepted, but it is burdened with numerous paradoxes, none of which could be resolved by 2003: Why is there no HIV in most AIDS patients, only antibodies against it? Why would HIV take 10 years from infection to AIDS? Why is AIDS not self-limiting via antiviral immunity? Why is there no vaccine against AIDS? Why is AIDS in the US and Europe not random like other viral epidemics? Why did AIDS not rise and then decline exponentially owing to antiviral immunity like all other viral epidemics? Why is AIDS not contagious? Why would only HIV carriers get AIDS who use either recreational or anti-HIV drugs or are subject to malnutrition? Why is the mortality of HIV-antibody-positives treated with anti-HIV drugs 7–9%, but that of all (mostly untreated) HIV-positives globally is only 1–4%? Here we propose that AIDS is a collection of chemical epidemics, caused by recreational drugs, anti-HIV drugs, and malnutrition. According to this hypothesis AIDS is not contagious, not immunogenic, not treatable by vaccines or antiviral drugs, and HIV is just a passenger virus. The hypothesis explains why AIDS epidemics strike non-randomly if caused by drugs and randomly if caused by malnutrition, why they manifest in drug- and malnutrition-specific diseases, and why they are not self-limiting via anti-viral immunity. The hypothesis predicts AIDS prevention by adequate nutrition and abstaining from drugs, and even cures by treating AIDS diseases with proven medications.     

On transient effects in the HIV/AIDS epidemic

During the initially exponential spread of the human immunodeficiency virus (HIV—the causative agent of AIDS) the growth rate of the number of AIDS cases decreases from plus infinity to the growth rate of HIV infections. A sensitivity analysis shows that for all reasonable values of the parameters of the HIV epidemic (incubation period, initial doubling time, etc.) the effect of this positive transient becomes negligible when the annual number of AIDS cases reaches a few dozen. Necessary and sufficient conditions are given for the growth rate of the number of AIDS cases to be monotonically decreasing during the positive transient. A mildly pathological density function for the incubation period of AIDS provides an example of a growth rate of AIDS that does not decrease monotonically, even though HIV is spreading exponentially. A negative transient occurs when the growth rate of HIV begins to decrease. In this context a somewhat surprising result emerges under the assumption that the growth rate of HIV is non-increasing: the growth rate of AIDS is at all times larger than the growth rate of HIV. A logistic HIV epidemic illustrates this result, and implications for the growth of the HIV epidemic in the United States and Europe are discussed. In particular, it is shown that the positive transient must have passed by 1982 in the United States and by 1986 or 1987 for the five European countries with the largest caseloads.     

A stochastic model for the development of an AIDS epidemic in a heterosexual population.

A non-age-dependent model, describing the evolution of a bisexual population, is developed in this paper and applied to projecting an AIDS epidemic in a heterosexual population. Included in the formulation are frequency- and non-frequency-dependent rules of partnership formation as well as five states of HIV disease, affecting the probability of infection per sexual contact. Results from computer experiments, designed to study the development of an AIDS epidemic in a heterosexual population fed by single males with a 50% prevalence of HIV infection prior to becoming active in heterosexual partnerships, are reported. In these experiments, the only source of HIV infection for females was sexual contacts with infected males within partnerships. Data on the probability of infection per sexual contact with an infected partner and the number of sexual contacts per month were incorporated into the model. However, the numbers used for the initial population of singles, couples, and those becoming sexually active per month were hypothetical. Even though the prevalence of HIV infection among males entering heterosexual partnerships was high, after 30 years the projected prevalence of HIV infection among females ranged from about 10 to 15% depending in part on the expected duration of partnerships and on whether the frequency- or non-frequency-dependent model was used. In these experiments, solutions of the embedded, nonlinear, deterministic equations for the incidence of HIV infection and the cumulative number of deaths due to AIDS proved to be good measures of central tendency for the sample functions of the stochastic population process.     

The Vancouver Lymphadenopathy-AIDS Study: 5. Antecedent behavioural,clinical and laboratory findings in patients with AIDS and HIV-seropositive controls.

In a group of homosexual men in Vancouver studied prospectively since November 1982, 26 cases of acquired immune deficiency syndrome (AIDS) have arisen. To identify behavioural, clinical and laboratory findings that might predict the development of AIDS in people with antibody to human immunodeficiency virus (HIV), we compared data for 25 patients with AIDS with corresponding data for 80 controls serologically positive for HIV selected from the cohort. The clinical and laboratory data for the patients with AIDS preceded the diagnosis of the syndrome by a mean of 17.5 months. The controls had been both seropositive and AIDS-free for a mean of 16.7 months after acquisition of their data. We detected significant differences between the patients with AIDS and the controls in IgG and IgA levels, absolute number of helper T cells and ratio of helper to suppressor T cells but not in lifetime number of male sexual partners, frequency of receptive anal intercourse or receptive fisting, illicit drug use or history of infectious disease. We also detected an increased risk of AIDS among those who had an elevated number of sexual contacts in AIDS-endemic areas in the 5 years before enrollment. A history of increased early sexual contact in AIDS-endemic areas is likely to be associated with early infection and with an increased risk of AIDS among men with HIV infection of unknown duration. Thus, although our analysis had limited statistical power, we conclude that most lifestyle variables appear to act as exposure factors in HIV infection but not as cofactors in the development of AIDS.     

AIDS-associated malignancies: research perspectives

The appearance in 1981 of a usually rare malignancy, Kaposi’s sarcoma, in homosexual men [1] was one of the first harbingers of an epidemic caused by a retrovirus, human immunodeficiency virus (HIV), which causes the acquired immunodeficiency syndrome (AIDS). Lymphoid and other malignancies were also increased, most strikingly non-Hodgkin’s lymphoma and primary central nervous system (CNS) lymphoma. Advances in molecular biology, immunology, virology, and anti-viral therapy have combined to create unique research opportunities. One developing theme is the role of viral co-infection and malignancy. Human herpes virus 8 (HHV8), Epstein-Barr virus (EBV) and papilloma virus each may have a causal role in the development of HIV-associated malignancy. New antiretroviral therapies are able to substantially reverse or delay the profound immunosuppression of HIV infection. The changes in the epidemiology of malignancies, and understanding the mechanism of action of these new therapeutics provide research opportunities to understand the pathogenesis of these malignancies. The opportunities to discover the consequences of T-cell based immunodeficiency and the interactions with specific viral pathogens will likely lead to progress in HIV treatment and new strategies for other malignancies.     

The Progress on the Studies of HIV/AIDS Vaccine

人类控制HIV感染长远的目标是发展安全、有效、廉价的HIV AIDS疫苗。但经 2 0多年的努力 ,人类探索HIV AIDS疫苗之路仍在继续。分析了疫苗研究的复杂性和发展HIV AIDS疫苗过程中所面临的挑战 ,并对发展HIV AIDS疫苗的可能性从实验和临床方面进行了阐述。同时结合HIV感染的免疫应答原理对现有的各种HIV AIDS疫苗研究策略作一综述 ,并根据以往HIV AIDS疫苗研究的经验和教训提出未来疫苗的发展思路及展望。     

Statistical modelling of the AIDS epidemic for forecasting health care needs

The objective of this paper is to develop statistical methods for estimating current and future numbers of individuals in different stages of the natural history of the human immunodeficiency (AIDS) virus infection and to evaluate the impact of therapeutic advances on these numbers. The approach is to extend the method of back-calculation to allow for a multistage model of natural history and to permit the hazard functions of progression from one stage to the next to depend on calendar time. Quasi-likelihood estimates of key quantities for evaluating health care needs can be obtained through iteratively reweighted least squares under weakly parametric models for the infection rate. An approach is proposed for incorporating into the analysis independent estimates of human immunodeficiency virus (HIV) prevalence obtained from epidemiologic surveys. The methods are applied to the AIDS epidemic in the United States. Short-term projections are given of both AIDS incidence and the numbers of HIV-infected AIDS-free individuals with CD4 cell depletion. The impact of therapeutic advances on these numbers is evaluated using a change-point hazard model. A number of important sources of uncertainty must be considered when interpreting the results, including uncertainties in the specified hazard functions of disease progression, in the parametric model for the infection rate, in the AIDS incidence data, in the efficacy of treatment, and in the proportions of HIV-infected individuals receiving treatment.     

Risk for AIDS in multiethnic neighborhoods in San Francisco,California. The population-based AMEN Study.

To examine the actual and potential spread of human immunodeficiency virus (HIV) from an acquired immunodeficiency syndrome (AIDS) epicenter to surrounding neighborhoods, we studied the prevalence of the viral infection and AIDS risk behaviors from 1988 to 1989 in a representative sample of unmarried whites, African Americans, and Hispanics living in San Francisco. We surveyed 1,770 single men and women aged 20 to 44 years (a 64% response rate) in a random household sample drawn from 3 neighborhoods of varying geographic and cultural proximity to the Castro District where the San Francisco epidemic began. Of 1,369 with blood tests, 69 (5%) had HIV antibodies; all but 5 of these reported either homosexual activity (32% HIV-positive; 95% confidence interval [CI] = 23%, 41%), injection drug use (5% HIV-positive; CI = 1%, 14%), or both (59% HIV-positive; CI 42%, 74%). Homosexual activity was more common among white men than among African-American or Hispanic men, but the proportion of those infected was similar in the 3 races. Both the prevalence of homosexually active men and the proportion infected were much lower in the 2 more outlying neighborhoods. Risk behaviors in the past year for acquiring HIV heterosexually--sex with an HIV-infected person or homosexually active man or injection drug user, unprotected sexual intercourse with more than 4 partners, and (as a proxy) having a sexually transmitted disease--were assessed in 1,573 neighborhood residents who were themselves neither homosexually active men nor injection drug users. The prevalence of reporting at least 1 of these risk behaviors was 12% overall, and race-gender estimates ranged from 5% among Hispanic women to 21% among white women. We conclude that in San Francisco, infection with HIV is rare among people who are neither homosexually active nor injection drug users, but the potential for the use spread of infection is substantial, as 12% of this group reported important risk behaviors for acquiring the virus heterosexually.     

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.     

Neuromuscular diseases of AIDS

Neuromuscular diseases are common in acquired immune deficiency syndrome (AIDS). Although the clinical incidence of peripheral neuropathy has not been systematically studied, various reports suggest that up to 40% of AIDS patients have clinical symptoms. Biopsy and autopsy studies have shown an inflammatory neuropathy with a variable component of demyelination and axonal loss. Evidence of direct involvement by the human immunodeficiency virus (HIV) is scant. Immunosuppression followed by cytomegalovirus (CMV) infection appears to be a direct cause of polyradiculoneuropathy and perhaps other forms of peripheral neuropathy in AIDS. The clinical incidence of myopathy in AIDS is less clear, and clinically less appreciated than the neuropathy. Scattered reports have identified an inflammatory myopathy that does not appear to be due to direct HIV infection, but could be mediated by another human retrovirus. HIV seropositive patients being treated with antiviral drugs develop a unique set of neuromuscular diseases that must be distinguished from the non-drug-related conditions.