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Matthew G Law, Philip S Rosenberg, Ann McDonald and John M Kaldor
MJA 1996; 164: 715-718.
This article has been published in the Medical Journal of Australia. Readers may print a single copy for personal use. No further reproduction or distribution of the articles in whole or in part should proceed without the permission of the publisher. For copyright permission, contact the Australasian Medical Publishing Company
Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Author's Details - Table - Figure 1 - Figure 2
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About 85% of both AIDS cases and diagnosed HIV infections in Australia
have been in men who have had homosexual contact.4 Over the period of the current AIDS
epidemic, it could be expected that a new generation of homosexual men
has become sexually active and at risk of HIV infection. An important
question, therefore, is whether and how HIV incidence among younger
homosexually active men has changed over time. The method of
back-projection has become the preferred method for estimating past
HIV incidence, and for projecting future AIDS incidence, in most
developed countries.5-7
Here, using an extension of the back-projection method,8 we estimate the age at HIV infection
among homosexually active men in Australia.
Methods
Our analyses were based on AIDS cases diagnosed by 30 June 1994 and
reported to the National AIDS Registry (NAR) at the National Centre in
HIV Epidemiology and Clinical Research by 31 March 1995 in men with a
history of homosexual contact, including those who were intravenous
drug users. These AIDS incidence data were adjusted for the reporting
delay between the time of diagnosis to the time of entry of the case on
the NAR.9 All estimates of HIV
incidence were adjusted for underreporting of AIDS cases to the NAR,
which is currently estimated to be about 10%.3
Age-specific HIV incidence was estimated using the back-projection
method suggested by Rosenberg,8 in which the rate of progression to
AIDS is assumed to be associated with age.10
To reflect the uncertainty in the rate of progression to AIDS,
particularly beyond 10 years following HIV infection, we used two
different progression-rate distributions derived from a
large-cohort study of HIV-infected homosexual men.11 A faster progression-rate
distribution was based on a median "time-to-AIDS" of nine years for
people aged 30 at diagnosis of HIV infection, and the rate of
progression to AIDS was taken to increase by 1.042 for each year the age
at HIV infection was above 30, and to decrease by 1/1.042 for each year
the age was below 30. A slower progression rate was based on a median
"time-to-AIDS" of 9.8 years and an age-effect of 1.037. As the effect
of age on modifying the progression rate to AIDS is uncertain and the
assumption of an age-effect would lower the back-projection
estimate of median age at HIV infection, we also analysed the
progression rates with the age-effects at both zero and half of the
above values.
The extended definition of AIDS adopted in Australia in January 1988
was assumed to result in a 10% increase in the rate of progression to
AIDS.12 The effect of
antiretroviral and prophylactic treatments on the progression rate
was incorporated into the analysis by assuming that 20% of
HIV-infected people were first diagnosed as HIV positive at
diagnosis of AIDS and so would not have received treatment before the
diagnosis of AIDS,13 and
that zidovudine became available in Australia from mid-1987 and was
accepted and tolerated by up to 90% of people with diagnosed HIV
infection. The effect of treatment was assumed to be a modest 20%
reduction in the rate of progression to AIDS and to gradually diminish
during ex- tended use, consistent with randomised clinical trials of
zidovudine.14-16 We also
did further analyses assuming a stronger treatment effect which
corresponded to a 50% reduction in the progression rate.
Back-projections were conducted for five time periods (early 1977 to
mid-1981, mid-1981 to mid-1984, mid-1984 to mid-1986, mid-1986 to
mid-1989 and mid-1989 to mid-1994) and for five age groups (17 to 20, 21
to 24, 25 to 29, 30 to 39 and 40 to 59 years). To allow direct comparison of
estimates of HIV incidence in different age groups and time periods,
estimates of HIV incidence in a given age group and time period were
standardised by dividing the estimated total number of new HIV
infections by the product of the number of age-years and
calendar-years.
Results
There were 4661 cases of AIDS diagnosed by 30 June 1994 and reported to
the NAR by 31 March 1995 among homosexually active men. After
adjusting for reporting delays, analyses were based on 4769 cases of
AIDS. We did not analyse other exposure categories as there were too
few AIDS cases in these categories.
The patterns of HIV incidence were similar for both the faster and the
slower progression-rate distributions, with a rapid increase in the
annual number of HIV infections in the early 1980s to a peak of between
2600 and 3100 per year in the mid-1980s, followed by a steep decline.
The faster progression rate gave a smaller estimate of the cumulative
HIV incidence to 30 June 1994 than the slower progression rate: 11 800
HIV infections, compared with 14 700, respectively. Both the pattern
of HIV incidence and the cumulative HIV incidence estimated by the
age-specific analysis are consistent with the non-age-specific
back-projections for homosexually active men shown in the Box.
The median age at HIV infection was similar for both the faster and
slower progression-rate distributions (Figures 1a and 1b). As the
epidemic developed, there was a decline in the median age at HIV
infection, from 31 years in 1982 to 1984, to 23 and 25 years for both the
faster and slower progression-rate distributions, respectively,
in 1987 to 1989, and to 25 and 27 years in 1990 to 1994. The age-effect of
zero on the progression rate to AIDS gave similar results, showing a
decline in median age at HIV infection from 34 and 33 years for both the
faster and slower progression-rate distributions, respectively,
in 1982 to 1984, to 24 and 26 years, respectively, in 1987 to 1989, and to
27 and 28 years, respectively, in 1990 to 1994. Analyses which assumed
half the age-effect also gave similar results.
Although the median age at HIV infection has declined during the
epidemic, HIV incidence has declined in all age groups from a peak in
the mid-1980s (Figures 2a and 2b). However,
this decline has been more pronounced in the older age groups; most HIV
infections in recent years appear to have been in men under 30 years.
HIV incidence was similar in the age groups 21 to 24, 25 to 29 and 30 to 35
years in 1982 to 1984, but by 1990 to 1994 HIV incidence was
substantially higher in the 21 to 24 years age group.
Sensitivity analyses which assumed a stronger treatment effect (a
50% reduction in the progression rate to AIDS) gave similar results
and are not shown.
Discussion
The decrease in the estimated median age at HIV infection among
homosexually active men, as shown by our age-specific
back-projection analysis, has previously been reported using
similar methods in the United States,17 and has also been observed in open
cohorts of homosexual men attending genitourinary medicine clinics
in London between 1988 and 1994.18
Since 1991, another Australian source of information about new HIV
infections has been reported cases to the NAR of newly acquired HIV
infection. Diagnosed HIV infections are considered to be newly
acquired if the person had a negative HIV test within a year of their
positive HIV test or if a HIV seroconversion illness was diagnosed.
About 200 newly acquired HIV infections are reported each
year,4 and the median age of
these people has been around 30 to 31 years since 1991 (more than the
median age of between 25 and 27 years estimated by the age-specific
back-projection analyses in our study). However, HIV incidence
since 1991 has been estimated to be around 500 cases per year,3 so only about 40% of these cases are
diagnosed each year as newly acquired. It is possible that this 40% is a
biased sample of all new HIV infections and, in particular, slightly
older than new HIV infections which are not diagnosed as newly
acquired.
Back-projection analyses are based on assumptions that are
subject to uncertainty, in particular the assumed progression-rate
distributions. The available Australian data were part of a large-
cohort study of HIV-infected homosexual men,11 and indicate that the overall
progression rate in homosexually active men in Australia is broadly
consistent with both the faster and slower progression-rate
distributions that were assumed in the age-specific
back-projections. Other major sources of uncertainty are in the
modifying effect of age at HIV infection and the effect of
antiretroviral and prophylactic treatments on the progression rate
to AIDS. The general trend of decreasing age at HIV infection was,
however, a robust feature of sensitivity analyses which
investigated these uncertainties, suggesting that this trend is at
least qualitatively correct.
Examining the history of the HIV epidemic among homosexually active
men in Australia lends further support for a decreasing age at HIV
infection. When the HIV epidemic began in Australia around 1980,
homosexually active men of all ages were at risk of infection. As the
epidemic progressed, new homosexual men were at risk of HIV infection
as they became sexually active, generally at a younger age. Thus, the
age distribution of homosexually active men at risk of HIV infection
(and hence of those already infected) would be expected to have
decreased as the epidemic progressed.
The estimates of HIV incidence were standardised for the number of
calendar-years and age-years in each time period and age group. This
allows direct comparison of HIV incidence if the number of
homosexually active men can be assumed to be constant across
different age groups over the time period of the epidemic. Based on the
1991 census,19 the resident
male population in Australia was fairly uniformly distributed
across the age range 15 to 44 years (at about 140 000 men per age-year)
but there were fewer men in older age groups. In the age range 17 to 39
years, however, direct comparison of the standardised estimates of
HIV incidence appears valid, provided that the proportion of
homosexual men is constant over the age range.
One feature of our analyses which requires cautious interpretation
is the apparent small increase in HIV infection in some age groups
between 1987 to 1989 and 1990 to 1994. As few people infected with HIV in
the most recent period would be expected to have progressed to AIDS,
these figures are uncertain. The most appropriate interpretation is
that the number of new HIV infections has been reasonably stable in all
age groups between 1987 and 1994.
In conclusion, age-specific back-projections suggest that the
median age at HIV infection among homosexually active men has
decreased over the period 1982 to 1994, and that most HIV infections in
more recent years have occurred in men aged under 30. These results
suggest that education programs aimed at preventing HIV infections
in homosexually active men should be targeted towards younger age
groups, in particular homosexually active men in their early
twenties.
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Acknowledgements
The National Centre in HIV Epidemiology and Clinical Research is
funded by the Australian National Council on AIDS through the
Commonwealth AIDS Research Grants Committee. The authors thank the
National HIV Surveillance Committee and the doctors who reported
AIDS cases under national surveillance procedures.
References
(Received 13 Nov 1995, accepted 2 April 1996)
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Figure 1: Estimated median age at HIV infection by calendar year (a) faster progression-rate distribution, (b) slower progression-rate ditribution (see text)
Figure 2: Estimated HIV incidence by age group at HIV infection and by calendar year (a) faster progression-rate distribution, (b) slower progression-rate ditribution (see text)
Authors' details
National Centre in HIV Epidemiology and Clinical Research, The
University of New South Wales, Sydney, NSW.
Matthew G Law, MSc, Statistician. Ann McDonald, MPH,
Senior Research Assistant. John M Kaldor, PhD, Professor of
Epidemiology.
National Cancer Institute, Rockville, USA.
Philip S Rosenberg, PhD, Biostatistician.
No reprints will be available. Correspondence: Mr M G Law,
National Centre in HIV Epidemiology and Clinical Research, The
University of New South Wales, 376 Victoria Street, NSW 2010.
E-mail: mlaw@nchecr.unsw.edu.au
Readers may print a single copy for personal use. No further
reproduction or distribution of the articles
should proceed without the permission of the publisher. For
permission, contact the
Australasian Medical Publishing Company
Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>".
<URL: http://www.mja.com.au/>
© 1996 Medical Journal of Australia.
