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langerin expression as well as function. Continuous HSV-2 shedding from mucosal tissues
maintains the presence of HSV-2 that blocks langerin function and induces the activation of
Langerhans cells that aid in capture of HIV.[149]
Chancroid ulcer size is increased with presence of HIV, and there is increased viral
shedding via ulcer exudation or bleeding. The pyogenic lymphadenitis (bubo) of chancroid often
ulcerates as well. The H ducreyi infection increases CCR5 chemokine coreceptor expression by
macrophages. HIV infection increases the incubation period for H ducreyi and increases the
number of genital ulcers. There is slower healing with therapy for chancroid when HIV is
present.[150]
Though treatment of these STDs may help to reduce the number of new HIV-1 cases, this
is not always possible, since it has been shown that treatment with acyclovir to suppress herpes
simplex virus does not reduce the incidence of infection with HIV-1.[151] The cofactor effect of
genital ulcer disease is approximately five times higher for female-to-male than for male-to-
female transmission. A higher prevalence of STD’s in the population will equalize HIV
transmission between the sexes.[134]
Intravaginal practices during sexual intercourse that introduce a variety of fluids or
introduce objects that reduce vaginal lubrication (“dry sex”) may increase the risk for
transmission of HIV. This may occur through damage to the vaginal epithelium, increased
inflammation, and greater prevalence of bacterial vaginosis.[152]
The use of crack cocaine can increase the transmission rate for HIV. This increase in
infectivity can be due either to the greater numbers of oral sores with inflammatory cells
containing HIV in the infected person or to the increased numbers of inflammatory cells with
CD4 receptors in the contact person waiting to become infected, from the loss of an intact
epithelial barrier.[153]
The use of methamphetamine may enhance transmission of HIV infection.
Methamphetamine upregulates the expression of CCR5 receptors on macrophages.
Methamphetamine also suppresses intracellular IFN-/STAT1 expression to promote HIV
infection of macrophages.[154]
Genital ulcers with inflammation also provide a more direct route to lymphatics draining
to lymph nodes containing many CD4 lymphocytes, macrophages, and follicular dendritic
cells.[150] Tissue trauma during intercourse does not appear to play a role in HIV
transmission.[129] HIV-1 can be demonstrated in semen even in the first few weeks following
acute infection, with a peak viral load at 30 days, then declining to reach a nadir at 10
weeks.[155] The transmission of HIV can occur with the act of sexual intercourse in any style or
position, though a greater relative risk exists with anal receptive intercourse.[129]
Once HIV is introduced into a promiscuous population, seroprevalence increases with
time. Increasing the number of sexual partners increases the likelihood of contacting a
seropositive individual.[156,157] If the number of infected individuals in a population is high,
then even one sexual encounter carries a significant probability of contacting an infected
individual. This was demonstrated in one high risk group over a three year period (1978-1981)
early in the AIDS epidemic in which the HIV infection rate was 44%.[158] Overall, the most
important factor for both the spread and the risk of infection from HIV is the degree of sexual
activity with multiple sexual partners.[130]
HIV has another important secondary means of spread through blood or blood products
(Table 2). Parenteral exposure to blood and blood products is the most highly efficient method
of HIV transmission—from 67% to over 90%.[131,159] There are many more peripheral blood