A Quantitative History of the First Two Decades of the AIDS Epidemic:

Trends, Treatment, and Mortality

By @fakeaarontweets
 Abstract
HIV now is a chronic illness for patients, with medication-compliant patients having
lifespans similar to their uninfected counterparts. This was not always the case. Before the
introduction of modern antiretroviral drugs, effective to the point of being distinguished from
their predecessors with the acronym HAART, meaning highly active antiretroviral therapy, the
progression of HIV to AIDS was inevitable for all but a small minority, and death from AIDS a
certainty. This paper uses data from the CDC WONDER program to chart trends in AIDS
diagnoses over the first two decades of the epidemic, from the first clusters of strange and lethal
immune dysfunctions diagnosed in 1981, through 2002, the last year of this data source, by
which time a number of effective treatments had been developed. Blood donation policy is
examined, as is the effect of novel treatment availability on patient outcomes, with significant
findings for the effects of each. In the course of analyzing WONDER’s data, we see significant
effects of age, sex, ethnicity, sexual orientation, and of course the time (in months or years since
the outbreak started) of diagnosis on mortality.

Introduction
The first trace of AIDS (Acquired Immune Deficiency Syndrome) in the public eye came
with the publication in July of 1981 on page A20 of the New York Times with the article “Rare
Cancer seen in 41 Homosexuals” by Lawrence Altman. It would not make its front page debut at
that paper until May of 1983, by which time more than 500 were dead. (Dunlap, 2014) What had
started out as an unexpected set of Kaposi’s Sarcoma patients would kill an estimated 35 million
people globally to present. (UNAIDS 2017) HIV, the Human Immunodeficiency Virus, the virus
which causes AIDS, was not identified until 1983, and effective treatments would take far longer
to discover.
As it would turn out, HIV not only existed but was becoming epidemic long before it was
known to exist. HIV is a member of the lentivirus family, a family of viruses known for having
exceptionally long periods of clinical latency, the time between infection and display of
symptoms. In the case of HIV, this latency is composed of a long period of only gradually if at
all eroding levels of CD4+ T lymphocytes, cells preferentially targeted by HIV, which are
important for activating immune responses. (McCune, 1995)
Public health concerns include treatment as well as prevention of HIV. HIV is not
destroyed by treatments. Antiretroviral therapy simply aims to stop the virus from reproducing,
causing it to stay inert in infected cells.

Methods

Data comes from CDC WONDER, which provides a series of demographic data about
859,000 people diagnosed with AIDS between 1981 and 2002. This surveillance data comes from
the electronic transmission of case reports from state and local health officials through a CDC
developed program – WONDER – which also monitors a number of other health and safety issues.
AIDS data is available only through 2002, as many of the monitored health and safety issues have
data only for a limited period. In this report, data used include exposure category (that is, how
health officials determine someone most likely contracted AIDS based on personal risk factors,)
age at diagnosis, the month or year diagnosed, vital status at the end of 2001 (the last date of
collection for this information,) ethnicity, sex, and sexual orientation. Still more demographic
information is available from WONDER.
Programming is performed in Matlab. Regressions make extensive use of this
programming language’s hac (heteroskedasticity and autocorrelation robust regression) and fitglm
(fit generalized linear regression model) built-in functions. In attempting to ascertain causality and
measure effects, a combination of discontinuity testing and trend analysis over specific periods is
employed. Probit models are also used, and tables of projected survival probabilities are included
using an analysis of the marginal effects to create an intuitive sense of their implications.
Results
First considering the relative frequency of AIDS cases by exposure category, we regress
the proportion of AIDS diagnoses by exposure category on a function of the month diagnosed.
Exposure categories include homosexual sexual contact (shortened to MSM, a public health
acronym standing for “men who have sex with men,”) heterosexual sexual contact, IV drug use,
both being an MSM and using IV drugs, having a mother with HIV, being a hemophiliac, being a
blood transfusion recipient, and unknown cause, with these last three categories being separated
into adult and pediatric cases. In order to test for autocorrelation in the trend analysis, for each
equation given by 𝑃𝑟𝑜𝑝𝑜𝑟𝑡𝑖𝑜𝑛𝑖,𝑗 = 𝛽0 + 𝛽1 ∗ 𝑀𝑜𝑛𝑡ℎ + ⋯ + 𝛽𝑛 ∗ 𝑀𝑜𝑛𝑡ℎ𝑛 + Ɛ𝑖 where j
signifies the previously described exposure categories, the residual r𝑖+1 was regressed on r𝑖 . The
following table indicates F-statistic with its p-value for this regression in each exposure category,
with all figures reported to five digits:
Table 1

Exposure Category F p
MSM 137.14 <.00001
Heterosexual Contact 21.00877602 <.00001
IV Drug Use 9.4992 0.00229
MSM & IV Drug Risk 0.00167 0.9674
Hemophiliac 6.58722 0.01085
HIV+ Mother 2.45965 0.11807
Pediatric Hemophiliac 4.77087 0.02987
Pediatric Blood
Recipient 4.22005 0.04099
Pediatric Unknown 40.18475 <.00001
Adult Blood Recipient 26.38552 <.00001
Risk Unknown 24.10609 <.00001
 A lack of autocorrelation is rejected for all exposure categories for which p < .05. Of the
ten categories, all but two indicate autocorrelation. Given this and the lack of a justification for
assuming heteroskedasticity, in testing for trends in the proportion of new AIDS diagnoses each
category, a Newey-West estimator will be used to estimate the covariance matrix for the
regressions on all exposure categories. Since the data is annual, a maximum lag time of twelve
periods (months) is employed arbitrarily.
Trends were estimated by regressing the proportion of all new AIDS diagnoses on the
highest degree polynomial of the number of months into the data set (with one being all 1982
diagnoses, two being January of 1982, three being February of 1982, so on until December of
2002, enumerated as 253) for which all coefficients were statistically significant at the p = .05
level – all parameters given as non-zero, therefore, are statistically significant at this level. The
figure below indicates the results of this trend testing. Note that no statistically significant trends
were found by this method for diagnoses of an unknown exposure source among pediatric
patients, and so that population is not shown below. The greatest number of diagnoses for AIDS
among pediatric patients with an unknown exposure source in a single month was 5; the
maximum proportion these patients comprised in a single month was .015385, and they account
for only 174 of 859,000 diagnoses included in the dataset, less than any other category. P
<.00001 for all F tests.
Table 2
Exposure Month Month2 Month3
Category Intercept (SE) (SE) (SE) R2 F
-0.00151
MSM 0.66968 (0.00009) 0 0 0.93268 3477.6
Heterosexual -0.00071500 0.000014803 -0.000000037136
Contact 0.0232 (0.00012484) (0.0000012349) (0.0000000033688) 0.98776 6698.6
0.00041311 0.0000086657 -0.000000042663
IV Drug Use 0.157624 (0.00024657) (0.0000023822) (0.0000000062873) 0.87289 569.97
MSM & IV -0.00027423
Drug Risk 0.10316 (0.000011388) 0 0 0.77662 872.64
0.00020194 -0.0000018435 0.0000000040307
Hemophiliac 0.0038309 (0.015099) (0.00012562) (0.000000309735) 0.65923 160.57
HIV+ -0.000073092
Mother 0.020248 (0.0000045579) 0 0 0.50143 252.44
Pediatric -0.0000061234
Hemophiliac 0.001246 (0.00084674) 0 0 0.18049 55.279
Pediatric
Blood -0.000047968 0.00000012508
Recipient 0.00446895 (0.0000050193) (0.0000163308) 0 0.42957 94.135
Adult Blood 0.00053458 -0.0000056128 0.000000014125
Recipient 0.0074611 (0.000090893) (0.00000082171) (0.0000000020798) 0.70196 195.49
Risk -0.0013438 0.0000090365
Unknown 0.077595 (0.000086877) (0.00000037224) 0 0.97573 502.57
 The monthly new AIDS diagnoses by exposure category are shown below by exposure
category. Note that in order to allow for consideration of both relative frequency trends and
relevance to the total population of AIDS diagnoses, the trends and monthly proportions are
displayed against a maximum y-axis value of 1, .5, .25, or .1.

Figures 1-10
 To highlight key changes among notable exposure categories, the following figure
depicts monthly new diagnoses of men who have sex with men, heterosexual contact, IV drug
use, and unknown risk.
 Figure 11

The greatest upwards trend was seen among diagnoses of an unknown risk factor, while
there was a marked decline in the proportion of new AIDS diagnoses attributed to MSM.
Transfusions
A pair of exposure categories of interest of interest was the recipients of blood, adult and
pediatric. Due to concerns about the safety of blood transfusions as the AIDS epidemic became
increasingly demanding of attention, in March of 1983 the FDA set out its first series of
recommendations with regards to AIDS which included deferral for members of at risk groups,
including MSM and IV drug users, and strict adherence to medical guidelines on blood
transfusion. (FDA, 1983) These would be coupled with testing for hepatitis B antibodies as a
proxy for the then-untestable HIV by some institutions. (Institute of Medicine, 1995)
As such, it was of interest to test whether there existed a discontinuity in the number of
total diagnoses of AIDS in patients whose primary exposure category was being a recipient of
blood. As mentioned previously, HIV has a long period of chronic infection before AIDS
symptoms develop. Estimates for the mean length of this period are given as 117 months
(Longini and Clark 1989,). Testing for a discontinuity at that point would almost certainly
inevitably lead to a slope change as the number of new diagnoses of AIDS cannot increase
indefinitely: the number of diagnoses for this exposure category begins at zero, if the change in
policy had no effect we might expect to see the number of new diagnoses tend towards a value
asymptotically which reflects the probability of a blood recipient contracting AIDS multiplied by
the number of blood recipients. A better examination would be to test whether there was a
tendency towards a decreasing number of diagnoses in the period succeeding this estimated
mean. If so, this would indicate that diagnoses from exposure via blood transfusion prior to the
policy change were not being maintained by new diagnoses from this mechanism at an
equilibrium rate. Allowing a delay of full policy implementation through April of 1983, this 117
month change should occur in January of 1992.
The following model is implemented:
𝑌 = 𝛽0 + 𝛽1 ∗ 𝑀𝑜𝑛𝑡ℎ𝑠 + Ɛ
Where Y is the total number of new AIDS diagnoses in the exposure categories of adult or
pediatric recipient of blood, restricted to data entries during and following January of 1992 and
Months is the number of months since December of 1991. The following reflects a
heteroskedasticity and autocorrelation (lag time: 12 months) robust regression of the model:
Table 3

Variable Coefficient Standard Error 95% Confidence Interval P

Intercept 62.0786 3.5671 55.0871 69.0702 <.00001
Months -0.4415 0.0451 -0.3531 -0.5299 <.00001
2
R = 0.8297 F = 633 (p<.00001)

Separate testing was not performed on pediatric and adult cases due to the low number of
pediatric cases (385 over 253 months, with a maximum of 8, as compared to 9152 and 88
respectively for adults).
The regression suggests a statistically significant impact of the FDA policy change on the
number of new AIDS diagnoses due to blood transfusions. The estimator of -.4415 reflects a
decrease in new AIDS diagnoses occurring after the mean time from HIV exposure to diagnoses
following the policy change.
Figure 12
 Changes in Mortality with Time
The fraction of those diagnosed with AIDS within a specific month who survived until
the end of 2001 (the vitality status provided by CDC WONDER) is displayed below for dates
through the end of 2001.
Figure 13

February of 1995 represents the first month for which more than half of newly diagnosed
patients survived.
The first drug approved by the FDA to prolong the lives of those with AIDS was AZT,
approved in March of 1987. It was followed by a number of drugs of the same class, nucleoside
reverse transcriptase inhibitors, compounds which interfere with the ability of a retrovirus to
translate its RNA into DNA. Didanosine was approved in 1991, and Stavudine in 1994. (Fischer
& Robin, 2006) These early drugs showed the same problem – limited effective time and severe
toxicity. (Caliendo & Hirsch, 1994)
Highly Active Antiretroviral Therapy (or HAART) refers to the practice of combining
multiple antiretroviral agents, often of different treatment mechanism categories, and including
more effective agents than were previously used. Mechanisms of action include entry inhibitors,
which interfere with the process by which a virus binds to and penetrates a cell, nucleoside
reverse transcriptase inhibitors as were discussed previously (they have a non-nucleoside
counterpart with a similar method of action,) and integrase inhibitors which interfere with the
process of viral DNA particles being integrated into a host cell’s DNA. July of 1995 represents
the introduction of potent antiretroviral therapy, therapy defined as patients receiving two or
more protease inhibitors, a far more effective treatment than any of the previous treatment plan.
(Detels et al., 1998)
The stochastic nature of the progression of AIDS to death, the presence of prior (though
less effective) AIDS treatments, as well as the fact that HAART was not implemented as the
universal treatment for HIV/AIDS immediately upon its discovery – the Detels cohort, for
instance, has 49% of patients receiving what they termed ‘potent antiretroviral therapy’ between
July of 1995 and the data’s end in July of 1997 – makes it difficult to consider an exact point to
consider for a structural break in survival rates. It could be true that some AIDS patients
diagnosed in 1981 who survived until the end of 2000 would not have done so were it not for the
introduction of HAART – the same might be said for any period in the data set. However, for
simplicity, a structural break analysis is done on the probability of a patient surviving AIDS as a
function of the log of the months into the data a patient was diagnosed, modeled as such:
𝐿𝑜𝑔(𝐹𝑟𝑎𝑐𝑡𝑖𝑜𝑛 𝑆𝑢𝑟𝑣𝑖𝑣𝑖𝑛𝑔) = 𝛽0 + 𝛽1 ∗ 𝑀𝑜𝑛𝑡ℎ𝑠 + 𝛽2 ∗ 𝑓(𝑡) + Ɛ
𝑓(𝑡) = 0 𝑓𝑜𝑟 𝑀𝑜𝑛𝑡ℎ𝑠 𝑝𝑟𝑖𝑜𝑟 𝑡𝑜 𝐽𝑢𝑙𝑦 1995
𝑓(𝑡) = 1 𝑓𝑜𝑟 𝑀𝑜𝑛𝑡ℎ𝑠 𝑖𝑛𝑐𝑙𝑢𝑑𝑖𝑛𝑔 𝑎𝑛𝑑 𝑓𝑜𝑙𝑙𝑜𝑤𝑖𝑛𝑔 𝐽𝑢𝑙𝑦 1995
Where Months begins as 1 for patients diagnosed in 1981, and ends at 253 for patients
diagnosed in December of 2002. The following data and figure represent the outcome of this
regression:
Figure 14

Table 4
 Variable Coefficient Standard Error 95% Confidence Interval P
Intercept -3.229 0.1016 -3.428 -3.030 <.00001
Months .01159 0.001147 0.009339 0.01383 <.00001
f(t) 0.6153 0.1487 0.3237 0.9068 0.00004
2
R = .9647 F = 325 (p<.00001)

Standard Errors are heteroskedasticity and autocorrelation robust (lag time: 12 months).
Unsurprisingly, there exists a statistically significant structural break in the log fraction of
survivors, representing an estimated 𝑒 0.6153 − 1 = 85.02% greater probability of survival if
diagnosed with AIDS during or after July of 1995 compared to being diagnosed prior had the
discontinuity not occurred.
Considering Mortality as a Function of Age
In pursuit of further examining how demographics affected mortality among those
diagnosed with AIDS, CDC WONDER data on vitality at the end of 2001 was considered. The
following shows the relationship between age at diagnosis and the fraction of those within an age
range.
Figure 15

No obvious linear or logistic relationship exists. To test for the significance of difference,
Chi-Square testing was done using the following table, with the null hypothesis being that age
was independent of the probability of surviving:
 Table 5

Age Group Survived Perished Total

Less than 1 Year 1091 2280 3371
1 - 12 Years 2812 3037 5849
13 - 19 Years 3009 1810 4819
20 - 24 Years 14887 15356 30243
25 - 29 Years 46296 62521 108817
30 - 34 Years 81311 104605 185916
35 - 39 Years 86881 105266 192147
40 - 44 Years 66508 77979 144487
45 - 49 Years 40145 45820 85965
50 - 54 Years 20838 25333 46171
55 - 59 Years 10150 14885 25035
60 - 64 Years 5054 8760 13814
65+ Years 4028 8338 12366
Total 383010 475990 859000
Percent in Category 44.5878929 55.412107

This yields a test statistic of 232.67 for the Chi-Squared statistic, the sum of the squared
differences between the observed and expected number of fatalities supposing independence
between age group and mortality divided by the expected values. For a Chi-Squared test having
12 degrees of freedom, the critical value for p = .05 is 21.03 so we can certainly reject the
hypothesis that age is independent of mortality status as of the end of 2001.
Given the lack of a clear relationship between age and mortality (the bar graph shows no
obvious continuous trend) it was investigated whether or not there may have been trends in age
at diagnosis over time – if there were, it would be possible that later or earlier diagnosis for an
age group is creating a bias in considering mortality as a function of age.
A heteroskedasticity and autocorrelation robust regression was used to fit a first degree
polynomial to the fraction of diagnoses which were from each of the above thirteen age groups in
a given month as a function of time entry (by month) in the data set – the first time period being
1, the last being 253. At the p = .05 level (that is, an absolute critical z-statistic of 1.96 or greater
for the coefficient on the month variable divided by its standard deviation,) all groups but the 13-
19 group showed a statistically significant trend over time. The table on the following page,
Table 6, lists the age groups, the coefficients on month from the above mentioned regression for
each respectively, and the z-statistic.
 Table 6

Age Group Coefficient*103 Z-Statistic

Less than 1
Year -0.02724379 -4.324229443
1 - 12 Years -0.014503749 -1.552031663
13 - 19 Years 0.021773265 5.84885039
20 - 24 Years -0.069552386 -4.930920226
25 - 29 Years -0.429310561 -23.36338927
30 - 34 Years -0.385205419 -11.5254893
35 - 39 Years 0.089359076 3.241348967
40 - 44 Years 0.312446671 19.96647662
45 - 49 Years 0.257869949 10.04833852
50 - 54 Years 0.115040983 4.822386788
55 - 59 Years 0.044976994 3.831175701
60 - 64 Years 0.039762072 5.093732695
65+ Years 0.044586895 5.048281084

The only group for which there was not a statistically significant effect trend in the first
degree polynomial of months into the data set was in the 1-12 years group. Therefore, it is
possible that age and months would confound each other. To test the against the null hypothesis
that only one or the other influenced mortality prior to the end of 2001, the following Probit
model was estimated:
12

𝑌𝑖∗ = 𝐵0 + 𝐵1 ∗ 𝑋1𝑖 + ∑ 𝑍𝑗𝑖 ∗ 𝐵𝑗 + 𝜀𝑖

𝑗=1

𝑌𝑖 = 1 𝑖𝑓 𝑌𝑖∗ > 𝑐
= 0 𝑖𝑓 𝑌𝑖∗ ≤ 𝑐
Where X1 is the number of months since the end of 1981 and Zji is a binary variable
which taken on the value of 1 if an individual i is in age group j and 0 otherwise, Yi* is
unobserved, and Yi is whether or not an individual survived until the end of 2001. >65 is being
used as the baseline group.
The following reflects the results of the probit model estimation:
Table 7

Variable Coefficient 95% Confidence Interval Z-Statistic

Less than 1 Year 0.8808 0.8231 0.9385 29.91486378
1 - 12 Years 1.2313 1.185 1.2777 52.0035048
13 - 19 Years 1.1459 1.094 1.1979 43.18717941
20 - 24 Years 0.9957 0.9629 1.0284 59.60093464
 25 - 29 Years 0.8305 0.8012 0.8598 55.56812118
30 - 34 Years 0.7502 0.7215 0.7789 51.24716693
35 - 39 0.6684 0.6398 0.6971 45.74255005
40 - 44 Years 0.5904 0.5615 0.6192 40.08773199
45 - 49 Years 0.5136 0.484 0.5431 34.07196217
50 - 54 Years 0.4371 0.4061 0.4681 27.62805029
55 - 59 Years 0.3363 0.3027 0.37 19.60586343
60 - 64 Years 0.2025 0.1647 0.2404 10.48223423
Months 0.021 0.02093 0.0211 506.8907976
Constant -3.9616 -3.993 -3.9304 -248.518884

All variables are statistically significant at the p = .05 level, suggesting that age group
and the month diagnosed (between 1981 and 2001) are both contributors to mortality.
This regression clarifies what we had seen in the bar graph of the fraction of each group
surviving AIDS diagnoses prior: changes in trends of age at diagnosis have skewed the actual
effect of age on mortality in those diagnosed with AIDS. The following shows the estimators for
the coefficients on each age group, that of >65 years being zero by default:
Figure 16

The trend seen here is clearer: a tendency for greater mortality as age at diagnosis
increases, with an exception for infants, among whom there is higher mortality than seen in
immediately older age groups.
 In order to get an intuitive understanding of the meaning of these figures, we estimate
marginal effect of belonging to each category we calculate that the average month for diagnosis
was 148 months into the dataset, corresponding to March of 1993. The following represents the
calculated marginal effects of being in each age group at this point in time, derived as
𝑃(𝑆𝑢𝑟𝑣𝑖𝑣𝑎𝑙 𝑖𝑛 𝑔𝑟𝑜𝑢𝑝 𝑗) = 𝛷(-3.9616+148*0.021+∑12 𝑗=1 𝑍𝑗𝑖 ∗ 𝐵𝑗 )

Wherein again, Zij is a dummy variable which equals 1 if individual i is in age group j
and 0 otherwise, with Bj being the corresponding coefficient. The following represents the
estimated probabilities of survival at this time point for the following age groups:
Table 8

Age Group Probability of Survival

Less than 1 Year 0.4985
1 - 12 Years 0.7365
13 - 19 Years 0.6821
20 - 24 Years 0.5839
25 - 29 Years 0.4754
30 - 34 Years 0.4216
35 - 39 0.3672
40 - 44 Years 0.318
45 - 49 Years 0.2707
50 - 54 Years 0.227
55 - 59 Years 0.1764
60 - 64 Years 0.1234
>65 Years 0.0646

Mortality as a Function of Ethnicity, Age, Sex, Sexual Orientation, and Year Diagnosed
Previous analyses of mortality among AIDS patients have found a number of predictive
variables, such as age, race, and education. (Coehlo et al., 2016) Given the large population
presented by the CDC WONDER data (859,000 patients total, with 475,990 having died prior to
the end of 2002) it is of interest to test for the predictive nature of demographic data on this
population. Due to the impracticality (CDC WONDER refuses to return such a large file) of
using months as our time variable to analyze AIDS mortality tendencies, years are used instead.
CDC WONDER includes only male sexual orientation
The following represents the model used:
12 2 5

𝑌𝑖∗ = 𝐵0 + 𝐵1 ∗ 𝑋1𝑖 + ∑ 𝑍𝑗𝑖 ∗ 𝐵𝑗 + ∑ 𝐺𝑘𝑖 ∗ 𝐵𝑘 + ∑ 𝐸𝑚𝑖 ∗ 𝐵𝑚 + 𝜀𝑖

𝑗=1 𝑘=1 𝑚=1

𝑌𝑖 = 1 𝑖𝑓 𝑌𝑖∗ > 𝑐
= 0 𝑖𝑓 𝑌𝑖∗ ≤ 𝑐
 Table 9

Variable Coefficient 95% Confidence Interval Z-Statistic

Constant -3.699 -3.821 -3.577 -59.35
Year 0.2544 0.2534 0.2554 500
Sex and Sexual Orientation
Female 0.03223 0.02294 0.04151 6.802
Sexual Minority Male 0.05858 0.05079 0.06637 14.7
Age Group
Less than 1 Year 0.8974 0.8395 0.9553 30.37
1 - 12 Years 1.243 1.196 1.289 52.32
13 - 19 Years 1.133 1.082 1.186 42.68
20 - 24 Years 0.9647 0.932 0.9975 57.67
25 - 29 Years 0.791 0.7617 0.8204 52.85
30 - 34 Years 0.7103 0.6816 0.7391 48.48
35 - 39 Years or age is missing 0.6346 0.606 0.6633 43.41
40 - 44 Years 0.5613 0.5324 0.5901 38.12
45 - 49 Years 0.4841 0.4546 0.5137 32.12
50 - 54 Years 0.4062 0.3752 0.4372 25.68
55 - 59 Years 0.3069 0.2733 0.3405 17.9
60 - 64 Years 0.1754 0.1375 0.2132 9.082
Ethnic Group
American Indian /Alaskan Native -0.6928 -0.823 -0.5627 -10.43
Asian / Pacific Islander -0.5319 -0.6554 -0.4085 -8.444
Black -0.7077 -0.826 -0.5895 -11.73
Hispanic -0.612 -0.7304 -0.4937 -10.14
White -0.6018 -0.72 -0.4836 -9.978

Looking at sex and sexual orientation, all other explanatory variables held constant,
females and sexual minority males were significantly more likely to survive until the end of 2001
than heterosexual males. Trends in mortality as a function of age followed the same pattern
mentioned in the previous probit estimation – the highest mortality rates among those aged 65
and older, with a trend towards less mortality at younger ages with the sole exception of infants,
who have greater mortality than those in several categories senior to them. Those of unknown
ethnic origin had surprisingly the lowest mortality rates, followed by Asian/Pacific Islanders,
whites, Hispanics, American Indians/Alaskan Natives, and the highest were among blacks.
The attached table following the works cited uses an analogous method to that mentioned
in the Probit model to suggest probabilities for surviving given specific sex and sexual
orientation, age, and ethnic background, calculated in percentages for convenience. 12.87 reflects
the mean value of the year of infection, 1 having been the first year of collection (1981) and 22
the last (2002,) considering the number of diagnoses of AIDS in each year. The probability of
survival for a demographic group is done as formulated below
𝑃(𝑆𝑢𝑟𝑣𝑖𝑣𝑎𝑙 𝑖𝑛 𝑔𝑟𝑜𝑢𝑝 𝑗, 𝑘, 𝑚) =
𝛷(-3.699+12.87*0.2544+ ∑12 2 5
𝑗=1 𝑍𝑗𝑖 ∗ 𝐵𝑗 + ∑𝑘=1 𝐺𝑘𝑖 ∗ 𝐵𝑘 + ∑𝑚=1 𝐸𝑚𝑖 ∗ 𝐵𝑚 )

With variables and coefficients being as described in the introduction of this Probit
model. From this, a more intuitive impact of the scale of effect from being in different
demographics groups can be ascertained.

Discussion

All but one exposure category in the CDC WONDER data saw fluctuations in proportion
of new AIDS diagnoses as a function of time. Declines among hemophiliacs and blood
transfusion recipients can be considered as a function of changing policies with regards to blood
donation – and, in the case of hemophiliacs, a degree of exhaustion of the vulnerable community.
In a United Kingdom study of hemophiliacs from 1977-1998, just over 17% contracted HIV, of
whom around 64% died, compared to just 14% of those who did not contract HIV. (UK
Haemophilia Centre Doctors' Organisation, 2004) What can be ascertained as a whole from the
relative frequencies of different exposure mechanisms is that infectious diseases are dynamic and
risks change. Infection of unknown exposure category appeared set to overtake homosexual male
sex as the most frequent infection source towards the end of data collection. Infection from
heterosexual intercourse made up around four times the frequency of AIDS exposure category
towards the end of 2002 as it did in 1981.
Analyzing the decline in new diagnoses of AIDS among recipients of blood transfusions
as a function of the change in FDA policy is somewhat challenging. The progression from HIV
exposure to AIDS is stochastic – there exist both rapid progressors and total non-progressors,
and the total number of people receiving blood transfusions may not be constant. These make
precise estimation of effect size more difficult, but as the discontinuity in Figure 12 shows, there
is a rather profound decline. Issues of measuring the effect precisely aside, the case for a
meaningful association between the change in FDA policy and the decline in new AIDS
diagnoses from blood transfusion seems strong.
The same sorts of stochastic issues are at play in estimating the effect size of the
discontinuity in AIDS mortality rates as a function of time, as was done in the analysis of figure
13. It is inevitable that there be some reflection of treatment in the mortality rates – Nakagawa et
al. write that while AIDS diagnosis once carried a 20-month median lifespan, “With timely
diagnosis, access to a variety of current drugs and good lifelong adherence, people with recently
acquired infections can expect to have a life expectancy which is nearly the same as that of HIV-
negative individuals.” The profound effect of HAART on those with AIDS led to the dubbing of
starting on these treatments causing a “Lazarus syndrome,” (Sowell et al., 1998) as patients
returned to healthy from near-death. However, for a better estimation of this effect in the
population, it would be preferable to have more data on percentages of patients receiving these
treatments at different points in time, as well as to use a more stochastically-rooted model.
Considering the results of the first Probit model, focusing solely on age and time of
diagnosis as factors in mortality before 2002, we see that greater age is associated with a higher
risk of mortality, as is having been diagnosed earlier – for age, however, there is an exception,
with infants having a higher mortality risk than those of greater age in the age groups
immediately senior to them. This helped clarify the role of age in mortality – the trends in age at
diagnosis over time obfuscated this relationship in the raw fraction from each group surviving
through the end of 2001 as depicted in figure 15.
In the second Probit model, we see race and ethnicity having a meaningful impact on
mortality. No information on income was reported in CDC WONDER, so it may well be that
these variables are serving as proxies for other socioeconomic factors – income, but also
education and other factors associated with accessing medical care that could not be examined.
Regardless of exact cause, this is concerning. Black men, regardless of sexual orientation, are
more likely to contract HIV than their white or Hispanic counterparts, as holds for black women
– not just on a per capita basis, but even in terms of absolute diagnoses. (CDC, 2017) The
combination of these facts is worrying – while AIDS may no longer be a death sentence, do the
same factors that made mortality worse among the black population continue to impact health
disparities in HIV treatment? For the most effected group to perhaps have the worst outcomes is
an unfortunate combination.
With regards to sex, sexual orientation, and mortality, it was somewhat surprising to see
heterosexual men as having the worst survival probabilities: as a rule of thumb it would seem
reasonable to expect the worst outcomes in minority groups. There are is one confounder that
needs to be considered and one plausible explanation as to why this might be the case. The
confounder is exposure method. The risk of acquiring HIV for a male during heterosexual sex is
quite small, smaller than it is for females or for either partner in homosexual male sex. (Wilton,
2012). As such, it might be considered that this group is might up quite disproportionately of IV
drug users. There is research (Hendriks, 1999) indicating a faster progression from HIV infection
to mortality among IV drug users than MSM.
However, there exist plausible reasons to suspect that the protective effect of being a
male sexual minority seen in the Probit model represent a genuine, non-endogenous impact. Due
to its disproportionate impact on this community, many resources related to AIDS bear an
attachment to male sexual minorities. The first AIDS activism group was the Gay Men’s Health
Crisis, founded in January of 1982. (Graham, 2006) The CDC its first report on what would later
be identified as AIDS in the form of its defining illnesses only months prior in June of 1981
(CDC, 1981) – simply stating unusual clusters of Pneumocystis pneumonia and Pneumocystis
carinii among gay men. Larry Kramer, having been a founder of that group, would also help
found ACT UP in 1987, after AIDS had been identified along with its its causal agent, HIV.
ACT UP would not only organize protests against slow drug approval processes, but became
intimately involved in the oversight of these processes through its Treatment Action Group.
(Kolota, 1994) Dr. Anthony Fauci, director of the National Institute of Allergy and Infectious
Diseases since 1984 commented in 1990: “Did Act-Up play a significant role in the whole idea
of expanded access to experimental drugs? The answer is yes.” (DeParle, 1990) With the male
sexual minority community having these ties to treatment advocacy, it may well be that exposure
to better information and treatment resulted in lessened mortality among sexual minorities.

Conclusion

Between 1981 and 2002, the CDC recorded 859,000 diagnoses of AIDS – not simply
HIV, but the actual immunocompromising syndrome it causes. Of these, only 383,100, or about
44.6%, would survive until the end of 2001. Even the highly active antiretrovirals of HAART do
not destroy HIV, they simply interfere with its reproduction methods. The high statistical power
that this dataset offers is predicated on an epidemic number of diagnoses – and hundreds of
thousands of deaths.
CDC WONDER provides a fantastic quantity of information, and for this reason a far
more extensive probing of it would be valuable. With its 20 years of data and 859,000 patients,
high power testing is easy. Besides what demographic data was reported here, WONDER
contains regional data, country of birth, multiple modes of exposure, a set of toggles with regards
to having a risk factor of exposure from a heterosexual partner, and different diagnostic criteria.
Interactions between all of the above and the demographics reported here might be of interest.
Time at diagnosis, in particular, was shown to be of the utmost importance in survival (see
Figure 13,) and many demographic traits of those diagnosed with AIDS varied in time.
The analysis in this paper is not close to an exhaustive take on CDC WONDER – that
would be an extensive undertaking. Rather, it provides some understanding into the history of
AIDS from a demographic perspective, both in diagnosis and outcomes. The availability of large
public datasets of health information is invaluable. Statistics that would be impossibly laborious
for a single researcher to attempt to collect can be part of the daily workings of a large public
organization.

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