Anogenital Anatomy and Sexual HIV Spread

Anogenital anatomy and sexual HIV spread Fischer
Hypothesis: Anogenital anatomy and sexual HIV spread

Bastian Fischera
HIV/AIDS affects persons from Sub-Saharan Africa and men who have
sex with men (MSM) in a disproportionate way. This article analyzes
the evidence and the plausibility of anogenital anatomical factors which
may contribute to the HIV/AIDS pandemic in the key populations for
sexual transmission. The etiology of the pandemic is discussed. Direct
and indirect evidence for narrow anogenital anatomy is presented. Two
semi-theoretical arguments for anatomical factors are put forward.
Anogenital anatomy is analyzed in view of Hill's criteria for causation. I
describe how randomized controlled trials and other confirmatory
studies could be designed and discuss the consequences of the
hypothesis. While many contributing factors for the HIV/AIDS
pandemic are well established, direct and indirect empirical evidence,
as well as semi-theoretical arguments, militates for an additional role of
macroscopic anogenital anatomy in HIV key populations. This factor
fulfills Hill's criteria.
2015 Bastian Fischer
Keywords: MSM, African Americans, Sub-Saharan Africa,

anodyspareunia, dyspareunia, HIV prevention, anogenital
anatomy, epidemiology
_______________________________________________________________________________
a
Leipzig, independent scholar.

Correspondence to Bastian Fischer, MA, MD.
Arno-Nitzsche-Str. 28, 04277 Leipzig; e-mail: anlagezugross@gmx.net
Contents
1
1.1
4.3
4.4
5
Introduction
Disproportionate HIV spread in key
populations
Explanatory power of behavioral, socioeconomic,
and biological factors
The hypothesis
Evaluation
Direct evidence for anatomical differences
Indirect evidence for anatomical differences
Discussion
An argument from pathological principles and
eliminative induction
An argument from epidemiology and anatomy
against only micro-anatomical biological factors
Hill's criteria for causality
How to test and consequences
Conclusions
Introduction
1.1
Disproportionate HIV spread in key

populations
1.2
2
3
3.1
3.2
4
4.1
4.2
HIV/AIDS affects persons from Sub-Saharan Africa

and men who have sex with men (MSM) in a
disproportionate way: At the end of 2010, African
Americans made up the largest percentage (44 %) of
those diagnosed with HIV in the USA although they
make up only 12.6 % of the country's population
[1,2]. Similarly, Sub-Saharan Africa accounts for 69 %
of all people living with HIV while housing 12 % of
the world population [3]. Likewise, the rate of HIV
infection among MSM in capital cities is, on average,
13 times higher than in the general population [3].
This article analyzes the evidence and the theoretical
plausibility of anogenital anatomical factors which
may contribute to the pandemic in the key
populations for sexual transmission.
In the second part of this introduction, I will discuss
factors which have been considered as an explanation
of HIV's disproportionate spread. Then I will give the
direct and indirect evidence for narrow anogenital
anatomy (NAA) in the high-risk groups. I will evaluate
this evidence by considering two semi-theoretical
arguments for anatomical factors and by analyzing
whether these fulfill Hill's criteria of causality. I will
describe how randomized controlled trials and other

confirmatory studies could be designed in order to
test the hypothesis and will discuss its possible
consequences.
1.2
Explanatory power of behavioral,

socioeconomic, and biological factors
The exact etiology of the HIV/AIDS pandemic

remains poorly understood, especially in Sub-Saharan
Africa [4]. Multiple factors are held responsible for the
disproportionate HIV spread in each of the high-risk
groups. Elevated promiscuity, predominantly in the
form of concurrent relationships, is a contributing
factor [5,6] but its explanatory power for the
enormous pandemic in southern Africa continues to
be an issue of debate [7-9].
In the USA, sexual risk behavior fails to explain the
difference in HIV prevalence between white and black
MSM [10,11]. Instead, biological factors related to anal
intercourse play a central role in HIV transmission
among MSM worldwide as Beyrer et al. [12] showed in
a review of international data and by employing a
stochastic agent-based network simulation model: The
transmission and spread of the virus among MSM
seem heavily biologically determined rather than being
strongly related to promiscuity or other behavioral
factors studied so far.
Ethnicity is an independent risk factor, regardless of
sexual orientation: Being black remains the strongest
risk factor for HIV acquisition in South Africa after
controlling for various socioeconomic variables [1316]. The same holds true in the USA, where increasing
income protects all ethnic groups from sexually
transmitted infections (STI) but where ethnic identity
remains significantly associated with the diagnosis of
an STI after adjusting for socioeconomic covariates
[17] and behavioral factors [18].
Part of this disparity may still be explained by
differences in sexual behavior since concurrency itself
was found to be closely tied to ethnicity in a recent
review of six large sexual behavior surveys in South
Africa [19]: Concurrency in men was 7 to 16 times
higher in black than in white men while colored
men had intermediate rates of concurrency, reflecting
intermediate HIV prevalence (in women, concurrency
was significantly associated with being black in only
one survey). The mean number of men's sexual
partners within the last 12 months, however, was in
the range of 0.91 to 1.42 for all ethnic groups, with a
maximum difference between blacks and whites of no
2
more than 0.33. Even if a great proportion of HIV

transmissions are due to concurrent relationships, it
seems implausible that this non-monogamy alone,
directly, and precisely explains the South-African
epidemic given the low chance of per partner
transmission and the very low chance of per sexual
act transmission found in studies on serodiscordant
heterosexual couples with a mainly non-African ethnic
background [20,7].
Conclusive evidence for a causal role of intravaginal
practices for cleaning purposes or dry sex is still
lacking [21], and sexual violence seems low in
explanatory power as well: Although, for instance,
South Africa, Botswana, or Lesotho suffer a rape
epidemic, the number of police-reported rapes per
100,000 persons and year is similar for Zimbabwe,
Sweden, Belgium, and Australia [22]. In Kenya,
Uganda, or Cameroon, this rate is much lower than in
many European or South-American countries [22].
While police records on sexual violence may depend
on various social and political confounding factors, a
recent international review revealed only a moderately
significant association of intimate partner violence
with HIV infection among women [23]. Small sexual
networks in ethnic minorities might explain the
epidemic among African Americans but they fail in
African countries where black persons are in the
majority. Conversely, non-African ethnic or other
minorities are not affected by HIV so
disproportionately as are African ones.
Finally, biological factors have been put forward. They
were reviewed by Kaul et al. [24] with a focus on viral
clade, host genetics, and co-infections: Subtype C is
indeed the predominant clade of HIV-1 in SubSaharan Africa but the authors discard this factor
since people of Sub-Saharan African ethnic origin are
also unevenly affected in areas where a different clade
predominates, for example in North-America [25] (pp.
51-8). Conversely, India, where subtype C does
predominate [25], has a much lower prevalence (0.25
to 0.28 %) of HIV/AIDS than do most countries in
Sub-Saharan Africa [26,27].
Kaul et al. [24] mention the CCR5-32 mutation as a
protective mechanism against infection and disease
progression. This mutation of the CCR5 receptor
gene occurs frequently in Europe and Western Asia
but is uncommon in Sub-Saharan Africa [28]. The
allele was, however, found to be absent in most ethnic
populations in India [29], whose low HIV prevalence
has just been mentioned, and it was unable to prevent
infection rates in Caucasian urban MSM from being in
the same range as those of the general population in

various countries in Sub-Saharan Africa [27].
As far as non-sexually transmitted co-infections like
malaria, tuberculosis, schistosomiasis and other
parasitoses are concerned, Kaul et al. [24] discuss how
they increase the viral load of HIV, as well as the
number of activated CD4+ cells in anogenital sites,
and thus the likelihood of transmission. This
difference alone, however, fails to explain the ethnic
tropism of the virus in areas of the world where these
non-sexually transmitted co-infections are rare, as well
as the absence of high HIV rates in areas outside
Africa where they are not.
Sexually transmitted co-infections, as well as abnormal
vaginal flora and bacterial vaginosis, are, however, a
good candidate for a causal explanation of the HIV
pandemic because, in line with the findings already
mentioned, Kaul et al. [24] found these conditions to
prevail disproportionately in black persons around the
world. Peipert et al. [30] found the association of
bacterial vaginosis and incident STIs to be influenced
by African-American ethnicity even after adjusting for
sexual practices and other confounding variables.
Other STIs are indeed considered to be the most
important co-factor for HIV transmission [20,31].
Nevertheless,
the
reasons
for
both
the
disproportionate spread of STIs and the high
prevalence of bacterial vaginosis in black persons are
poorly understood [24,31]. One may wonder whether
this ethnic disparity is not a secondary phenomenon due
to some more fundamental biological factor, which
could, at the same time, be more intrinsically tied to
HIV transmission. Moreover, even for this good
candidate, causality has not been established and
seems questionable given the failure of most attempts
to reduce new HIV infections by more effectively
treating other STIs [32,33].
It may be speculated that, with the exception of
elevated concurrency and elevated prevalence of
STIs/vaginosis, most of the factors which have been
held responsibleincluding those not discussed here
(circumcision, condom use, education, testing,
migration or mobility, sex work, gender inequality
[16,27])are, in conjunction, comparable in many places
with low HIV rates so that even an essentially
multifactorial etiology of the pandemic seems
unpromising unless the list of contributing factors is
extended; India or South-American countries are
candidates for such places but more careful research
would be needed for such a claim to be validated.
Further factors, which may be more specific to SubSaharan Africa apart from high STI prevalence and
concurrency, especially the time of sexual debut or
age-disparate relationships [16], seem unlikely to play
an important role both for theoretical reasons and in
view of the evidence [19,34]. HIV stigma and
discrimination are real and harmful now [27] but this
factor cannot explain the initial spread of the virus in
the key populations because, due to the long clinical
latency stage of the infection, it probably happened at
a time when nothing about the disease, its causative
agent and transmission was yet known. The same
holds true for the current high prevalence of HIV in
key populations, which probably maintains the
disproportionate spread in them now but which
cannot explain why HIV disproportionately entered
these groups in the first place. Lastly, HIV seems well
able to leave the African continent given the similar
predicaments of MSM and black persons worldwide
(see above), which renders spaciotemporal
explanatory approaches implausible.
2
The hypothesis
Many behavioral, socioeconomic, or biological factors

are well established as contributing factors of the HIV
pandemic. Their plausibility as causal factors, however,
remains low for reasons of lacking consensus in the
scientific community or of lacking multivariate
significance, effect size, global coherence and
uniformity. This survey of risk factors suggests that
the pandemic also depends on further factors, which
are closely tied to ethnic and sexual identity. My
hypothesis is that the factors in question are macroanatomical in nature; more exactly, that the unfolded
circumference and/or distensibility of the anogenital
orifices are partly and causally responsible for HIV's
disproportionate spread in the key populations for
sexual transmission.
3
Evaluation
3.1
Direct evidence for anatomical differences
Pendergrass et al. [35] studied the vaginal shape in

[t]wenty-three [sic] African-American (7 nulliparous,
8 uniparous and 11 multiparous), 39 Caucasian (13
each nulliparous, uniparous, and multiparous) and 15
Hispanic women (1 nulliparous, 7 uniparous, and 7
multiparous) by taking vinyl polysiloxane casts in
lying, standing, and sitting positions. All women were
at least 18 years of age and had experienced sexual
intercourse. In 42 % of the African-American women,
a slim shape variant, the pumpkin seed, was
discovered. This was characterized as being very

wide from side to side but having little depth from
anterior to posterior walls and could not be found in
Caucasian or Hispanic women, whose vaginal casts
were conical, parallel, heart, or slug-shaped. No
correlation between shape and either age or parity was
found in the Caucasian group.
In addition to the molds, the maximally comfortable
introital caliber (MCIC) was measured by having the
subject insert a lubricated polypropylene Erlenmeyer
flask as far back in her vagina as possible without
causing discomfort. The circumference on the flask
was marked and measured, and the corresponding
caliber calculated. A statistically significant difference
was found: The average MCIC was 3.14 cm in African
Americans (this value is ambiguous in the study, the
other value: 3.73 cm) and 4.66 cm in Caucasians
(introital measurements could only be obtained from
5 Hispanic subjects, which forbade comparison with
this group). The average caliber of an erect penis, at
the base, in young men, and as measured by a health
professional, is 3.95 cm (standard deviation (SD): 0.38
cm, n = 111) [36].
For a study on a controlled way to perform lateral
sphincterotomies in patients with chronic anal fissure,
an ailment common among MSM [37] (p. 274), Cho
[38] measured the anal caliber in a way similar to
Pendergrass's measurement of the introital caliber:
Lubricated conical calibrators, scaled with 1-mm
diameter increments, were inserted into the anus until
the perianal skin was just about to be depressed in the
oral direction; at this point, the scale was read. This
objectification for measuring the distensibility of soft
tissue may seem even less precise than Pendergrass's
semi-subjective method but a high correlation (r =
0.958) was obtained for two independent examiners
and a group of 45 patients. This maximum
longitudinally tension-free anal caliber was determined
in an anorectally healthy group (n = 40) of patients
coming for arthroscopy or other procedures and in
anal fissure patients (n = 106) before sphincterotomy.
In both groups, measurement took place under spinal
anesthesia. The value was 34.6 1.4 mm (mean
SD) in the healthy group, confounding effects of age,
gender, weight, and height not being statistically
significant, and 29.0 2.7 mm in fissure patients.
From these direct measurements, it follows that
vaginal narrowness in African-American women is
significantly increased both in terms of vaginal shape
and in terms of introital caliber. The normal anal
caliber also seems narrow in relation to the penile one.
4
The validity of these results is limited by the different

methods of measurement and the small size of the
sample groups in the vaginal study, as well as by
missing standard deviations and other lapses such as
several ambiguous figures. In conclusion, direct
evidence for NAA seems scarce. Nevertheless, these
few direct data are curious and may serve as an
important piece of the puzzle.
3.2
Indirect evidence for anatomical

differences
In comparison with little direct evidence, there is

much indirect evidence for NAA in a large proportion
of HIV high-risk groups. These findings are evidence
in virtue of abductive reasoning, meaning that, if NAA
were true, then the following phenomena would be
expected and could be explained by NAA. They are
not conclusive evidence but they render the
hypothesis plausible.
Rosser et al. [39] and Damon and Rosser [40] found
relatively low rates of anodyspareunia in MSM (12 %
and 14 %, respectively), comparing them to rates of
colpodyspareunia in women. This form of
anodyspareunia was, however, already to the extent of
sex being too painful to continue or involving
severe pain, and of occurring life-long.
Participants rated a lack of lubrication, of feeling
relaxed, or of digitoproctic stimulation as the most
important factors. It was also associated with anxiety
or problems with gay identity and male sexual
partners.
In a large (n = 1752) recent study [41], however,
which used an anal adaptation of a validated female
sexual function index, 59 % of anoreceptive MSM
reported some degree of pain during or after
intercourse. Mild anodyspareunia, according to the
index, was present in 33 %, mild to moderate in 17 %,
moderate in 4 %, and severe in 2 %. Ten risk factors
were studied, including stimulation, lubrication, steady
relationship, number of previous partners, etc. Yet,
only age and the frequency of sex remained
significantly correlated with anodyspareunia on
multivariate logistic regression analysis, both higher
age and higher frequency being protective. In line with
the causal role that this result may imply for the
variable of frequency, already Lestar et al. [42]
clinically observed a temporary effect when the
anus was dilated to a circumference (12.8 cm, a caliber
of 4.07 cm) corresponding to that of the average
erect penis (see section 3.1). This effect lasted a few
days.
This suggests that, accelerated aging not being a

possible intervention, regular intercourse, or selfdilation, could causally prevent dyspareunia and
perhaps anogenital injury. Lestar et al. [42] also
measured the circumference of the anal sphincters in
dead human specimens and, extrapolating from
physiological knowledge on the distensibility of
muscle tissue, inferred that the anal sphincter complex
cannot be dilated with any lasting effect, and is
unlikely to suffer damage, if dilation is gentle and
limited to the circumference just mentioned. Given
the fast regeneration and great malleability of
epithelial in contrast to muscle tissue, these findings
and observations suggest that the unfolded
circumference and distensibility of the anoderm play a
more important role in the etiology of
anodyspareunia and anal fissures than do the muscle
tone and circumference.
Epithelial injury occurs in large proportions of HIV
high-risk groups: Anal bleeding during sex was found
to affect roughly a third of Mexican MSM at least
sometimes and was significantly associated with being
HIV-positive, even on multivariate analysis involving
behavioral, psychological, and other medical risk
factors [43]. In MSM in Mexico City (n = 2758), who
took an HIV test from June 1991 to December 1992,
9 % of all infections were statistically attributable to
anal bleeding and, among those affected by it at least
sometimes, 42.6 % of infections were attributable to
it. It may be objected that the cross-sectional character
of the study could mask the possible effect of anal
bleeding being caused by HIV infection but, even
among the men who tested negative, it occurred in
26.3 % sometimes and in 7.4 % from half the time to
always. Similarly strong associations between anorectal
trauma, or factors indicative of it, and HIV
seropositivity had been found previously in one other
cross-sectional [44] and two prospective studies
[45,46] while one longitudinal study [47] found a null
association, yet this one referred to a cohort where the
baseline analysis [44] had revealed a multivariate
relative odds of 7.72 for the highest level of trauma.
Nevertheless, except for the recommendation of
lubricants, this factor and its prevention never reached
the focus of HIV/AIDS education [43]. This
doubtlessly helpful remedy may have to be taken with
a grain of salt given the above hypothesis of a central
role of the anoderm and its maximum distended
circumference. Indeed, paradoxically, elevated
lubricant use for anal intercourse has been identified
as a risk factor for the acquisition of STIs in a non5
interventional analysis [48]. The necessity of much

lubricant may, however, indicate marked narrowness,
which, in turn, may increase the chance of STI
transmission via traumatic lesions. Physically,
lubricants decrease the friction between penis and
anoderm but they cannot increase the circumference
of the latter. Likewise, the association between the use
of relaxant sex drugs (e. g., inhaled nitrites) and HIV
infection, which led denialists to infer that the drugs
cause AIDS and which otherwise has been attributed
to disinhibition and carelessness of drug users [49,50],
could be due to anal narrowness as a common cause
for both variables. The drugs may, unconsciously or
deliberately, serve as a self-medication for
anodyspareunia with questionable effectiveness: they
relax the internal sphincter but they fail to widen the
anoderm.
NAA may partly explain maternal death rates. Similar

to its role in HIV spread, being black is a solid risk
factor for pregnancy-related mortality, independent of
various socioeconomic variables [58,59]. Significant
differences in the prevalence rates of preeclampsia,
eclampsia, Abruptio placentae, Placenta praevia, or
postpartum hemorrhage could not be found between
black and white women but the case-fatality rates of
all five conditions were significantly higher in black
women, with death from postpartum hemorrhage
being 3.3 times more likely [60]. It may be
hypothesized that hemorrhage is more severe due to
deeper lesions or more difficult to terminate because
of anatomy and the resulting surgical view.
The prevalence of vaginal bleeding in South-Africans

is comparable to that of anal bleeding in MSM: Coital
bleeding in the previous three months was reported
by roughly a fifth of both males and females in one
[51] and by roughly a third in two studies [52,53]. It
was associated with unprotected intercourse, multiple
partners, STI diagnosis, African ethnicity, and condom
breaks. Part of it was attributed to menstruation [51]
but some of these factors may imply traumatic causes.
A prospective cohort study [54] found a significant
association between coital genital bleeding and HIV
seroconversion. Few studies exist on the prevalence
of coital vaginal bleeding in other ethnicities. Yet, in a
large (n = 1513) British survey [55], the 12-month
cumulative incidence of postcoital bleeding in women
aged 18-54 years was merely 6 % (95 % CI 5 to 8 %).
Finally, Vansintejan et al.'s [41] result implying that

regular intercourse may ease dyspareunia, as well as
Lestar et al.'s [42] clinical observation of a
temporary dilation, whose effect lasts a few days,
suggests that NAA re-establishes itself rapidly. Given
this, NAA may explain the curious late seroconversion
of 11 Nairobi female sex workers who had previously
met criteria for HIV resistance [61]. Seroconversion
could be linked neither to anal sex, sex during menses,
intravenous drug use, sexual violence, medical
procedures, contraception method, nor other STIs.
The only risk factor shared by all but one of the
women was a reduction of sex work, where 9 of them
had stopped it altogether for at least two months
during the preceding year for social reasons, none of
them due to illness. Four of these 9 women were
abstinent from sex during the break, the other five
practiced monogamy or serial monogamy.
Concurrency, comparable to open relationships in

MSM [19,41], may itself be evidence for NAA, the
causal chain being: NAA causes anogenital health
problems, which, in turn, impede pleasant intercourse
in a monogamous setting. A similar explanation stands
to reason for rife secondary abstinence (no sex in last
12 months among those who ever had sex) in South
Africa [16], as well as for the low frequency of
intercourse found in various behavior surveys in SubSaharan Africa [7]. Bacterial vaginosis might be
explained by deeper or more numerous lacerations
from sex, which nurture commensal bacteria of the
vaginal microbiome whose growth would otherwise
be suppressed. Dry sex may be an epiphenomenon
of NAA: Marked virginity or tight vagina cults
[56,57] could be due to the high prevalence of a
natural narrow variant, leading to feelings of
insufficiency and desperate measures with drying
agents in women whose vaginas are loose.
It may be hypothesized that the sex workers' vaginas

narrowed during the periods of less regular
intercourse, possibly leading to more, more frequent,
or deeper lacerations and abrasions when sexual
activity was resumed, facilitating HIV infection. It was
hypothesized, instead, that ongoing exposure to HIV
may be necessary to maintain immunity [61], for
instance mediated by ongoing HIV-1-specific CD8+
lymphocytic responses. There is, however, a second
curious finding [62], which may refute this hypothesis:
Starting sex work in the 1980s, when the pandemic
merely began, or in the early 1990s, when its peak was
not yet reached, conferred immunity against HIV on
Nairobi's female sex workers. Each weighted year of
exposure resulted in a 12-fold reduction in
seroconversion risk. This could be explained neither
by risk behavior, STIs, seronegative HIV infection,
nor age. The effect of protection by starting sex work
in 1985-1993 as against 1994 was very large despite
6
the lack of continuous antigenic exposure when the

epidemic was mild or only developing.
Taken together, these two anomalies tend to refute
genetic mechanisms for HIV resistance of major
epidemiological significance, perhaps except for
genetic factors responsible for gross anatomy:
Mechanisms based on innate immunity or any
likely brought about by a lot of sexual intercourse and

reliably persists for a long time but also can vanish
quickly as soon as there is considerably less sex. Such
immunological mechanisms are not impossible but
seem implausible and have not been found.
For analogous reasons, Nairobi's sex workers tend to
refute immunological mechanisms for HIV spread
Why are genetic factors unlikely to play a major role in the SubSaharan African pandemic?
ANOMALY1: 11 Nairobi female sex workers highly exposed to the virus and meeting criteria for HIV
resistance did become HIV+; this could be linked neither to anal sex, sex during menses,
intravenous drug use, sexual violence, medical procedures, contraception method, nor other STIs;
the only risk factor shared by all but one of the women was a reduction of sex work: 9 had stopped
it altogether for at least 2 months for social reasons, none due to illness (4 were entirely
abstinent, 5 had monogamous relationships) continuous exposure to HIV needed to maintain
immunity? probably not:
ANOMALY2: Starting sex work in the 1980s (before pandemic) vs. 1994 (peak of pandemic)
conferred immunity on female sex workers in Nairobi; each year of exposure resulted in a 12-fold
reduction in HIV risk. Risk behavior, STIs, or age could not explain this. The effect of protection
against seroconversion by starting sex work in 1985-1993 vs. 1994 was very large despite the
lack of continuous exposure to HIV when the epidemic was mild or only developing.
Genetic mechanisms based on innate immunity or

biochemical entities unchanging in adulthood are
unlikely because they do not change in 10 years
(evolution is slow), let alone in a way that increases
susceptibility to a lethal virus, nor do they change
when somebody takes a break from sex work.
Mechanisms based on adaptive processes have not

been found and would have to be odd: They cannot
be constant once installed, due to ANOMALY1, yet
they cannot rely on ongoing HIV exposure either, due
to ANOMALY2. NAA is a simple, straightforward
explanation for both anomalies.
Fig. 1. Two anomalies in Kenyan female sex workers.
biochemical entity unchanging in adulthood are

almost ruled out because, due to the slow pace of
evolution, differences in them do not develop in ten
years, let alone in a way that increases, rather than
reduces, susceptibility to a lethal pathogen. Moreover,
such mechanisms are unlikely to change when a
person takes a break from sex work.
Mechanisms based on adaptive processes involving
the environment would have to be odd: They cannot
be constant once they are installed, due to the first
anomaly. Yet they cannot rely on ongoing antigenic
exposure, either, due to the second anomaly. They
would have to be mechanisms of a kind that is most
pertaining to genital microstructure or microbiology.

For example, a bacterium which confers immunity on
a large proportion of 1980s sex workers, who then
keep it, but that takes years of sex work to be
transmitted and at the same time is eliminated in
weeks with less sex would be a biological entity whose
existence is a priori improbable. A simple and
straightforward explanation for both anomalies is
NAA if it can be modified by frequent intercourse
and re-establishes itself rapidly as soon as abstinence
lasts more than a few days.
Discussion
Direct evidence for this anatomical factor is meager

and has various shortcomings such as a small size of
sample groups and the formal lapses mentioned. The
direct evidence that has been available so far allows no
conclusion about the validity or effect of this factor.
This does not, however, diminish the curiosity of
these few direct data on anogenital caliber. If there is
indeed a remarkable difference in anatomy specific to
HIV key populations, then it is likely to reveal itself in
studies of almost any size. Indirect evidence for NAA
is manifold, has unifying explanatory power even with
regard to puzzling and anomalous phenomena in HIV
epidemics but it has the obvious shortcoming of
being indirect. None of the studies I referred to
assessed HIV risk directly in light of NAA but all of
derived with necessity from the data which have been

gathered but will have to be evaluated more
thoroughly in future studies. Austin Bradford Hill was
motivated to formulate his criteria for a causal
correlation by the fact that, often, we do not know
what the exact links between harmful factors and
certain diseases are or which factors are harmful at all
[63]. Instead, in the scientific process, we have to rely
on indirect evidence and secondary, tertiary, etc.,
cross-links, which could guide us to causal factors in
the end. Hill's criteria are helpful in this quest,
especially in epidemiology, and this is why NAA and
the available evidence will be discussed in view of
them here. At first I will present a semi-theoretical
argument which analyzes the plausibility of NAA as a
further factor for HIV spread by employing
eliminative induction. I will present a second semi-
Eliminative Induction and Factors for Uneven HIV Spread
Socioeconomic and behavioral factors for HIV spread with weak or moderately significant evidence, globally
incoherent, or lacking explanatory power otherwise
Comparable initial spread in general population in Sub-Saharan Africa and MSM worldwide; comparable
prevalence rates in these key populations; but new infection numbers are stable or decreasing in Africa now
while they are on the rise in MSM
further, hidden factors are biological (evolutionary effect less immediate in MSM) unless there are
fundamental differences in the effect of prevention measures in Africa vs. MSM
Which biological factor?

Only 6 health-related biological
principles:
Neoplasm/Tumor
Circulation/Vascular system
both unlikely for
conceptual reasons
Infection/Inflammation
Non-STIs globally incoherent for key
populations, disproportionate STI spread in
them poorly understood, not established as
causal for HIV spread, most interventions to
reduce HIV infections by reducing other STIs
have failed
Genetics/Biochemistry/Microphysiology
unlikely because of anomalous infection
dynamics in Kenyan female sex workers
Anatomical variant
Trauma
only categories left;
traumatic factors likely
secondary because of
limited evidence for
trauma-inducing
intravaginal practices or
sexual violence as causal
Fig. 2. An argument from pathological principles and eliminative induction.
them concentrated on populations or groups which

do form specific high-risk groups for sexual HIV
spread and they did focus on factors which may
plausibly be linked to NAA. Any direct connection
between NAA and HIV spread cannot, however, be
theoretical argument against the plausibility of a high

impact of micro-anatomical factors for the
disproportionate sexual spread of HIV in at least one
of the key populations. I will finally discuss methods
to test the hypothesis, as well as possible
8
consequences.
4.1
An argument from pathological principles

and eliminative induction
Given the low explanatory power of various

behavioral and socioeconomic factors (see section
1.2), it seems rational to assume that an additional
factor of the pandemic is biological. Another hint for
the nature of such a new factor is given in section 4.3.
Let us further assume that health-related biological
mechanisms can exhaustively be described as
pertaining either to (a) neoplasm, (b) circulation or the
vascular system, (c) infection or inflammation, (d)
genetics, biochemistry, or microphysiology, (e)
anatomical variant, or (f) trauma, the classical
pathological principles. If these premises are granted,
the evidence available by now allows the following
eliminative induction:
The additional biological risk factor will hardly pertain
to (a) or (b) as they may be discarded as conceptually
implausible. (c) can be discarded because the factor of
non-sexually transmitted infections is globally
incoherent and because the higher prevalence of
STIs/vaginosis in the high-risk groups is itself a
mystery, which suggests that it is a secondary
phenomenon. Furthermore, causality has not been
established for STIs/vaginosis and seems implausible
because most interventions have failed (see section
1.2). (d) seems implausible because the infection
dynamics in Nairobi female sex workers tend to refute
immunological, genetic factors for the African
pandemic (see section 3.2). This claim is strong:
Strictly speaking, the infection dynamics in Nairobi
female sex workers are in a position to refute genetic
factors of major epidemiological significance only for
Nairobi. Yet, the studies on Kenyan sex workers had
been designed to catch major genetic factors if there
are any. Highly exposed but persistently seronegative
sex workers were presumably a good study focus for
tracking down any remarkable genetic influence. If
there is such influence, it should prima facie have been
revealed in this specific group. However, not only was
no major genetic factor discovered but anomalies
arose which tend to militate against its conceptual
possibility. Therefore, from an abductive standpoint, the
inference from the two anomalies in Nairobi female
sex workers to the ubiquitous absence of major
genetic factors may be considered as moderately
justified even though by no means conclusive.
The NAA hypothesis involves a combination of (e)
and (f), which are exactly the two options left.
Therefore, due to eliminative induction, an additional

etiological factor of the HIV/AIDS pandemic in SubSaharan Africa is likely to be tied to anatomy and/or
trauma.
4.2
An argument from epidemiology and

anatomy against only micro-anatomical
biological factors
Again, let us assume that behavioral and

socioeconomic factors are overestimated. Let us
further assume that there is arguably no primary
difference in the genital micro-structure or
microbiology between Sub-Saharan African women
and women with a different ethnic background, at
least none of major epidemiological significance. This
assumption seems rational because of the anomalies
in the infection dynamics of Nairobi female sex
workers (see section 3.2). Let us further assume that
the new biological factor for the pandemic is confined
to the anogenital organs (if it is not, different or
additional biological co-factors can, at least for the
sexual transmission through anal or vaginal
intercourse, hardly belong to the (e) or (f) categories
from 4.1, leaving only factors from (a)-(d), which,
arguably, are all implausible; therefore, the new
biological factor is probably confined to the
anogenital organs). If these premises are granted, the
following argument, taking the logical form of a
proof by contradiction, can be made.
If anal intercourse is, as is commonly assumed [12], a
much riskier practice than vaginal intercourse, it must
be so by virtue of some more fine-grained property or
properties of anus/rectum. Let x now stand for any
micro-anatomical property, or composite of such
properties, of anus/rectum (for instance, gutassociated lymphoid tissue, M-cells, rectal mucosa,
hemorrhoidal tissue, etc.). Due to the 13 times higher
prevalence of HIV among MSM in capital cities, as
compared with the general population [3],
epidemiology outside Africa implies that the
anus/rectum, by virtue of at least some x, is much more
susceptible to HIV transmission than female genitalia.
Yet, given the premises, Sub-Saharan African
epidemiology implies that the anus/rectum is just as
susceptible to HIV transmission as female genitalia,
or, for countries with the highest HIV rates, even less
susceptible. This is a contradiction.
Therefore, either no micro-anatomical property, or
composite of such properties, of anus/rectum is
biologically responsible for the MSM pandemic or
there are differences between the vaginas of African
9
women and those of women with a different ethnic

background other than micro-anatomical differences,
or both. Therefore, micro-anatomical differences
alone cannot explain the HIV spread in each and
every high-risk group for sexual transmission. If the
4.1 argument is valid and if traumatic factors are only
secondary to anatomical factors (which seems rational
because of little evidence for major effects of
intravaginal practices or intimate partner violence on
HIV spread; see section 1.2), it follows from 4.1 and
this argument here that a non-microscopic anatomical
property may constitute a hidden factor in at least one
4.3
Hill's criteria for causality
I will now analyze whether NAA fulfills Hill's criteria

for a causal factor [63], i. e., whether NAA is a good
candidate for a cause of HIV's disproportionate
spread in the key populations, over and above a mere
correlation or contributing factor:
Strength: The association is strong in the sense that,
according to both direct and indirect evidence
(pumpkin seed variant, anodyspareunia, mucosal
injuries), roughly a third of those in HIV key
Some unknown biological factors also central for HIV pandemic

Probably no primary difference in genital micro-structure or microbiology
between Sub-Saharan African women and women of different ethnic
background (because of infection dynamics in Kenyan female sex workers)
A further biological factor probably confined to anogenital organs (if it were
something beyond anogenital organs, then anatomical and traumatic factors
would seem implausible candidates yet they are the most likely ones
according to eliminative induction)
Let x now stand for any

microscopic anorectal
property/ies (GALT, M-cells,
rectal mucosa, hemorrhoids,
etc.)
13 times higher prevalence of
HIV in gay/bisexual men than
in general population outside
Africa seems to imply:
Anus/rectum, by virtue of some x, much more

susceptible to HIV than vagina
Sub-Saharan African epidemiology:
comparable HIV rates as in gay/bisexual men
Vagina just as susceptible to HIV as
anus/rectum or even more so (Swaziland,
e.g.) CONTRADICTION.
Therefore, either no microscopic anorectal

property responsible in gay/bisexual men or nonmicroscopic differences in vaginas exist or both
MICRO-ANATOMY NO UNIVERSAL FACTOR
Fig. 3. An argument from epidemiology and anatomy against only micro-anatomical biological factors.
key population for the sexual spread. NAA now is a

macro-anatomical property, which empirically seems
to be similar in MSM and people of recent SubSaharan African ethnic origin. By virtue of Occam's
law of parsimony, this common and simple factor
seems likely to be intrinsically tied to HIV spread and
might be preferred to more complex theories if it
sufficiently explains many HIV transmission and
spread phenomena in future investigations.
populations seem to be affected by clinically

significant NAA. Consistency: The data presented were
gathered in various countries, on various continents,
by different researchers, and have yielded results
pointing to NAA through the previous decades until
now. Specificity: Given that MSM are the only group
who, due to the male anatomy, use predominantly the
anus for sexual intercourse and given that a vaginal
shape variant, high rates of vaginal bleeding, and
elevated rates of maternal death could be found
10
specifically in persons of recent Sub-Saharan African

descent, (sexually relevant) NAA seems to occur
almost exclusively in HIV key populations, at least in
such high proportion and extent.
Temporality: There is little doubt that NAA or sexual
intercourse precedes sexual HIV transmission in time.
Biological gradient: If sex drugs, elevated lubricant use,
and anogenital bleeding are indicative of more marked
NAA, the dose-response relationship suggests a causal
role for NAA as these factors were associated with
HIV or STI acquisition. Plausible mechanism: A narrow
orifice is physically more likely to suffer more, deeper,
or more frequent lacerations, abrasions, or
microscopic cracks when it is penetrated than a wide
orifice. These lesions, which may occur with or
without evident bleeding, may facilitate HIV
transmission.
Coherence: Surveying HIV mucosal transmission studies
tissue or in vitro cellular models, not complete

mammalian organisms. They do not show that
seroconversion and systemic infection are possible
despite mucosal integrity, let alone the usual case. The
experiments on rectal HIV transmission in humanized
mice are in line with NAA: Either systemic infection
was not possible (despite adding seminal plasma and
inducing colitis) [68], or it was but a grinding stone bit
for rotary tools had to be employed in order to cause
abrasion in the anorectum [69,70]. In one experiment
where systemic infection and seroconversion were
possible without causing anorectal trauma [71], the
mouse model can hardly be adequate for the human
case since X4 tropic HIV-1 infection was easier
vaginally than rectally.
High variations in HIV rates within Sub-Saharan
Africa (an objection put forward by James Blanchard;
personal communication) do not refute NAA. Vaginal
narrowness may vary across Sub-Saharan African
Narrow anogenital anatomy and HIV spread: Bradford Hill criteria for a causal
association
STRENGTH: roughly a third of gay and
bisexual men and of Black women
have narrow anogenital anatomy
TEMPORALITY: cause before

effect hardly doubtable; no
sexual HIV transmission before
sex
CONSISTENCY: results from different

continents, by different researchers,
and from three decades until recently
point to the factor of narrow anatomy
BIOLOGICAL GRADIENT: factors

indicative of more marked
narrowness are correlated with
higher HIV transmission risk
SPECIFICITY: anus due to male

anatomy main copulation orifice for
gay and bisexual men; vaginal
shape variant, higher rate of coital
bleeding, higher maternal death
rates specifically in Black women
PLAUSIBLE MECHANISM: a
narrow orifice is physically
more likely to suffer more,
more frequent, or deeper
lacerations than a wide orifice
during penetration
COHERENCE: experiments on rectal

HIV transmission in humanized mice
either failed or were only possible
after causing anorectal trauma with
rotary tool bit or easier vaginally than
rectally; prevalence variations in
Africa are closely tied to ethnicity
EXPERIMENT: semi-experimental
evidence from 11 Kenyan sex workers
thought to be immune; infection
occurred after less regular sexual
intercourse
ANALOGY: disproportionate spread of
other STIs in HIV key populations, NAA
explains concurrent relationships,
little sex and secondary abstinence,
bacterial vaginosis, dry sex, and tight
vagina cults
Fig. 4. Hill's criteria.
from the last three decades revealed no laboratory or

other finding directly contradicting an important role
of NAA. The studies showing that HIV crosses intact
epithelium in the rectum/vagina and reaches
lymphoid tissue (e. g. [64-67]) involved only ex vivo
ethnicities. In Nigeria, for instance, the highprevalence states and the low-prevalence states reflect
geographic boundaries of ethnolinguistic groups [72]
(p. 181), with the Tiv being hit hardest by HIV and
the Yoruba, e. g., being almost spared [73] (pp. 30-1).
11
Zamani et al. [74] show that high ethnic diversity is

consistently associated with low HIV rates but low
ethnic diversity is not necessarily associated with high
HIV rates: Rwanda and Burundi, being low in both
variables, were strong anomalies of this negative
correlation, which diminishes the likelihood that low
ethnic diversity or HLA variability per se is the culprit
and an alloimmune vaccine the key. Indeed,
contrary to earlier conjectures on some protective
effect of mucosal alloimmunizations from sexual
Factors lacking global

coherence:
Non-STIs, CCR5-32
mutation, HIV clade C, small
sexual networks in minorities,
circumcision, gender
inequality, testing, mobility
however, did not clearly distinguish resistant sex

workers from those who did seroconvert. Yet it may
have offered additional protection: Wide vaginal
anatomy, even if it should turn out as important, may
not offer absolute protection as this is unlikely a priori.
Moreover, this genetic association hardly explains
away the anomalous correlation in question. This
negative correlation of the frequency of unprotected
intercourse and the amount of alloimune responses
seems even more remarkable given the moderate
Factors with weak or

Factors with strong evidence, Unable to explain
moderately significant globally coherent, specific: initial uneven
evidence:
spread:
Concurrent relationships
Socioeconomic factors,
HIV stigma and
(mechanism unclear)
sexual violence,
discrimination
STIs (interventions failed)
intravaginal practices, Biological factors of anal

Prevalence/Force
early sexual debut, etc.
of infection
intercourse in MSM
NAA
3.46 0.14
cm
Longitudinally
tension-free
anal caliber
SD
Direct evidence
3.14 or 3.73
cm
MCIC in
AfricanAmerican
women (data
ambiguous)
3.95 0.38
cm
4.66 cm
Mean erect
penile caliber
SD
Indirect (abductive) evidence
Anodyspareunia in MSM and its risk factors

Epithelial injuries in MSM and South-Africans
Lubricant and sex drugs anomalies
Concurrency, 2ndary abstinence/little sex,
bacterial vaginosis, dry sex, tight vagina cults
Maternal death rates in Black women
Two anomalies in Nairobi female sex workers
MCIC in
Caucasian
women
Theoretical plausibility
Disproportionate
HIV spread in key
populations for
sexual
transmission
(MSM and
Black persons)
Anatomy a
novel factor
NAA prevention
methods:
conceivable
Eliminative induction:
unknown factors likely tied
to anatomy and/or trauma
Cultural
Micro-anatomy unlikely to
explain pandemic in all key acceptability:
problematic
populations
Bradford Hill criteria fulfilled
Fig. 5. Summary.
intercourse [75], the amount of alloimmune responses

in Abidjan highly exposed but persistently
seronegative female sex workers was found to be
negatively correlated with the frequency of unprotected
sexual intercourse [76], a result which could also be
explained by a persistently wide vaginal anatomy and,
hence, fewer mucosal lesions, which would otherwise
enable local or systemic exchange of foreign cellular
material. A genetic factor, inhibitory killer-cell
immunoglobulin-like receptors in the absence of their
HLA ligands, was found to have had a moderately
significant protective effect in this cohort [77]. This,
significance of this genetic factor, which, furthermore,

could not be established as having major impact in
HIV epidemiology.
Evolutionarily speaking, if narrow vaginal anatomy
increased the chance of acquiring STIs, it should be
expected to have been selected against when
populations mixed and proper medical treatment was
unavailable. This might be the reason why this marked
form of vaginal narrowness is presumably absent in
most ethnicities derived from prehistoric migrations
from Africa. Even more disconcertingly, evolution
12
may partly explain why HIV infection numbers now

are stable or decrease among high-risk heterosexual
populations but continue to be on the rise, and
virtually out of control, in MSM despite prevention
and better treatment in both groups [78,12]: narrow
vaginal anatomy might be dying out. In MSM,
however, evolution operates less immediately and less
quickly. In view of similar initial infection dynamics in
MSM worldwide and in various Sub-Saharan
countries, as well as in view of comparable HIV
prevalence rates in these key populations [27], this
discrepancy promotes the hypothesis that the
pandemic is heavily biologically determined not only in
MSM [12] but also in Sub-Saharan Africa (and thus
the first premises in arguments 4.1 and 4.2)unless
there are fundamental differences in the effect that
prevention, including treatment, may exert on MSM
vs. on people from southern Africa.
(Semi-)experimental evidence: There is a dearth of
experimental studies on copulation in relation to NAA
and mucosal lesions but the late seroconversion of the
11 Nairobi sex workers is good semi-experimental
evidence in favor of the NAA hypothesis. If NAA is
an important causal factor and re-establishes itself
rapidly, these seroconversions should have been
expected. Analogy: There are various analogous effects
that NAA may cause, for example the
disproportionate spread of other STIs among MSM
[79,80] and Africans/African Americans (see section
1.2). The explanatory power of NAA may also extend
to concurrent partnerships, secondary abstinence and
a low frequency of intercourse, to bacterial vaginosis,
and to dry sex and tight vagina cults as has been
expounded in section 3.2.
4.4
How to test and consequences
The infection dynamics in Nairobi's sex workers and

the finding that frequent sex may prevent dyspareunia
imply a way to test the hypothesis: Randomized
controlled trials could be designed where intervention
groups have intercourse or self-dilate regularly and
where control groups continue as before. New HIV
infections would be primary endpoints. Known
protective measures must unconditionally be allowed
for ethical reasons.
It may be objected that, unlike other sex-positive
prevention methods, any intervention which explicitly
involves more sex may indeed dilate anogenital
orifices but also lead to more viral exposures, which
could dampen or counteract a protective effect. In
case of counteraction, this is a danger but the
evidence that HIV spread is biologically, rather than

behaviorally, determined in MSM [12] and perhaps
also in black persons (at least for behavioral factors
considered so far) diminishes its likelihood. Various
behavioral data in Sub-Saharan Africa indicate low
frequencies of intercourse [7] and rife secondary
abstinence [16]. Solitary sexual activity is also
significantly more frequent in MSM than in
heterosexual men both with and without steady
relationships [81]. Kenyan female sex workers,
however, acquired over 100-fold protection against
seroconversion by starting sex work before the
outbreak of the pandemic in comparison with sex
workers starting at its peak [62] despite regular sexual
intercourse with multiple partners. In spite of minute
inquiries into the total number of partners, various
high-risk behaviors, sexual roles, or detailed practices,
the study of the exact frequency and/or regularity of
sexual contacts, especially in direct connection with
HIV incidence, has been neglected in HIV key
populations in the same way as has the study of
anatomical variables. Furthermore, interventions may
leave the number of contacts unchanged while test
groups use self-dilation in greater intervals between
events of actual intercourse.
Alternatively, a non-interventional test of the
hypothesis would be to study the vaginal caliber in
high-prevalence regions in the way described by Cho
[38] or Pendergrass et al. [35] and compare it with that
in low-prevalence regions. Studying the anogenital
caliber in HIV-positive vs. HIV-negative individuals
highly exposed to the virus, as well as their
frequencies and intervals of intercourse, may clarify
the role of gross anatomy retrospectively. If these
alternative studies are positive, ethical concerns about
interventions may be minimized.
As for the consequences of the hypothesis in case of
empirical confirmation, its theoretical analysis in view
of Hill's criteria suggests that measures directly
addressing anatomy might be effective in HIV
prevention since they may modify an important causal
factor. Adverse effects and cultural acceptability of
these measures will have to be evaluated carefully
because human taboos are involved and traditional
ethical beliefs challenged, and because data on health
benefits and risks of frequent anal or vaginal
intercourse and self-dilation are few.
It is acknowledged that various safe, effective, and
sex-positive prevention methods against HIV spread
are already available: Condoms, pre-exposure
prophylaxis, either with antiretroviral oral medication
13
or topical microbicides, or male circumcision. None

of them, however, immediately addresses anatomical
factors. These methods are also, in themselves, not
ideal and could possibly be augmented by ones which
do affect NAA. Despite the high protective effect of
condoms, condom failure seems responsible for a
considerable proportion of infections among MSM,
probably for more transmissions than are due to
entirely unprotected intercourse [82], which
nonetheless accounts for another large proportion.
Consistent condom use and other behavioral
interventions would, even in combination, reduce but
a minor proportion of new infections [12]. Behavioral
approaches are also limited for pragmatic reasons [83].
Human passion and weakness are major obstacles.
Oral and topical antiretrovirals face adherence and
acceptability problems and may come short of their
maximum theoretical effectiveness for this reason [8487]. To date, microbicides were able to reduce only a
medium-sized proportion of HIV transmissions in
clinical trials in Sub-Saharan Africa [88]. Conceptually,
sexual intercourse or dilating anogenital orifices
represent more natural, ordinary activities for HIV key
populations and human adults in general than taking
medication, inserting microbicides, or carrying drugeluting vaginal rings. Therefore, acceptability of
methods directly addressing anatomy could, a priori, be
higher than that of other helpful means of
prevention, especially if they might at the same time
reduce dyspareunia, a possibility which needs further
study and evaluation at first.
Circumcision reduces the chance of HIV transmission
by approximately 60 % [89-92] and seems not to be
effective in MSM [93,94]. In heterosexuals,
circumcision is effective presumably because there is
less delicate tissue for viral entry after it, primarily
preventing infection in men. Circumcision is thus
moderately effective in heterosexuals but MSM, a
majority of whom are versatile in their sexual roles
[95], keep all biological anal risk factors as soon as
they are receptive.
Ubiquitous, regular, or home-based testing and
treatment as prevention are promising but face
socioeconomic and psychological obstacles. In global
terms, more than half of HIV-positive people do not
know that they are [96]. Identifying and linking
enough infected people into medical care meets
logistic and cultural difficulties. Violating human
rights and restricting personal freedom for that end is

not an option. Treatment as prevention may also fail
as a long-term solution if HIV is not completely
eradicated while possibly causal anatomical factors for
its spread persist.
These shortcomings of the safe and effective means
of HIV prevention may justify their augmentation by
innovative measures after careful evaluation of their
own safety and effectiveness.
5
Conclusions
Many non-biological and biological factors for the

HIV/AIDS pandemic play an important role as
contributing factors but lack either high plausibility,
convincing evidence, or global coherence in causal
terms. Direct and indirect empirical evidence militates
for an important role of NAA in HIV key
populations. Semi-theoretical arguments are in favor
of NAA factors, which fulfill Hill's criteria. The
hypothesis can be tested in non-interventional studies
and randomized controlled trials. It may reduce HIV
spread. Adverse effects and acceptability of measures
addressing this additional factor will have to be
evaluated carefully.
Acknowledgments
The work has received no funding whatsoever. The
author is a medical and philosophical graduate of two
German universities but proposes this hypothesis as
an independent scholar. I thank numerous MSM for
discussion and comments and an anonymous
epidemiologist for encouraging me to write this
article.
Authors contributions
BF conceived, wrote, and revised the article. He has
read and approved the final manuscript.
Conflicts of interest
There are no financial competing interests for the
author to declare. I declare that I derive no personal
or sexual pleasure from this hypothesis. The author is
a feminist, gay, and wishes to reduce HIV spread
through causal prevention.
14
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Anogenital anatomy and sexual HIV spread Fischer

Hypothesis: Anogenital anatomy and sexual HIV spread

Keywords: MSM, African Americans, Sub-Saharan Africa,

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