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often--approximately 0.1% (1 infection per 1000 contacts) on average per genital sexual contact
with an HIV-infected person in the absence of factors that increase likelihood of transmission.
The greatest risk for transmission occurs soon after seroconversion when viremia is highest.
However, some persons have become HIV-infected after a single sexual contact, while other
persons have remained uninfected after hundreds of contacts.[129,130]
Estimates of HIV infectivity depend upon the nature of the sexual practice. For women
the risk is 0.1% to 10% per receptive vaginal intercourse. The risk ranges from 0.1 to 1% for
male insertive vaginal intercourse. For insertive anal intercourse, the risk varies from 0.1 to 1%,
but 1% to 30% for receptive anal intercourse. [131]
The rate of sexual transmission of HIV may depend upon the number of viral particles in
2
3
genital secretions. The number of CD4 cells per µL of seminal fluid ranges from 10 to 10 ,
6
while the number of virions can range from undetectable to over 10 . The numbers of virions in
the female genital tract is generally lower. Transmission can occur both cell-to-cell as well as
from cell-free fluid.[132,133] Thus, the transmission rate is two to three times higher from
infected males to females than from infected females to males, without other cofactors.[134]
The location of HIV in cells of the genital tract of infected persons varies between men
and women. In men, both the cells within seminal fluid, as well as the seminal fluid, harbor
virions of HIV, but spermatozoa are not a major source for HIV. Since most of the cell-free HIV
in the semen of men arises distal to the vas deferens, a vasectomy may have minimal impact on
the infectivity of seropositive males to sexual partners.[135] Seminal vesicles harbor
macrphages containing HIV.[136] In women, the greatest number of virions is present at the
squamocolumnar junction of the cervix, with far less HIV in vaginal epithelium. Langerhans
cells and macrophages in the lamina propria capable of harboring HIV can be found in a variety
of epithelia.[137]
The type of mucosa it contacts affects transmission of HIV. HIV can be sequestered
within squamous epithelium of the genital tract and can traverse epithelium via transcytosis,
endocytosis-exocytosis, and productive infection with release of virions, or via penetration of
gaps between epithelial cells. Though the thinnest epithelium (single cell layer) is in endocervix,
the surface area of stratified squamous epithelia of vagina and ectocervix is much greater. HIV
transmission can occur in the absence of cervix and uterus. In males, the poorly keratinized
foreskin is the most vulnerable to HIV infection, and though circumcision may reduce the risk
for transmission, HIV infection can occur in the absence of foreskin, most likely through penile
urethra. Transmission of HIV through gastrointestinal tract mucosa is a function or oral and anal
sexual practices. Gut-associated lymphoid tissue plays a role in this process. Additional cells
that can become infected or harbor HIV within the epithelium or submucosa include CD4
lymphocytes as well as Langerhans cells and macrophages.[130]
For persons who have regular intercourse with a single HIV infected (index) partner, risk
of transmission of HIV-1 depends upon the stage of HIV-1 infection. The risk is highest,
0.0082/coital act, within 2.5 months of seroconversion of the index partner. The risk drops to
0.0015/coital act within 6 to 15 months after index partner seroconversion and remains low
throughout the stage of clinical latency of HIV-1 infection. The risk rises again in the late stage
of clinical AIDS, at a rate of 0.0028 per coital act, within 6 to 25 months of death of the index
partner.[138]
The rate of HIV sexual transmission may also be due to the low infectivity of an
individual strain of virus, propensity for only selected individuals to transmit infective virus in
secretions, or presence of individual susceptibility factors.[104] Some HIV-1 subtypes may be