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The lining of the rectum in particular is extremely thin and overlies tissues rich in activated T cells the immune system cells that HIV targetsso unprotected anal intercourse carries a high risk of HIV infection. Anal intercourse is common among men who have sex with men but is also more common in heterosexual populations than is generally thought.
Tenofovir an antiretroviral drug that counteracts HIV after it has entered human cells given by mouth partly protects macaques against rectal infection with simian immunodeficiency virus SIV; a virus that induces AIDS in monkeys and apes so the researchers wanted to know whether this drug might be effective against rectal SIV infection if applied at the site where the virus enters the body.
What Did the Researchers Do and Find? To answer this question, the researchers rectally infected several macaques with SIV up to 2 h after rectal application of a gel containing tenofovir, after rectal application of a gel not containing the drug, or after no treatment.
In addition, a few animals were treated with the tenofovir gel after the viral challenge. Most of the animals given the tenofovir gel before the viral challenge were partly or totally protected from SIV infection, whereas all the untreated animals and most of those treated with the placebo gel or with the drug-containing gel after the viral challenge became infected with SIV. High blood levels of tenofovir 15 min after its rectal application correlated with protection from viral infection.
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The researchers also collected rectal and small intestine samples from tenofovir-treated macaques that had not been exposed to SIV and asked which samples were resistant to SIV infection in laboratory dishes. They found that only the rectal samples were resistant to infection and only rectal cells contained tenofovir.
Finally, activated T cells that recognized an SIV protein were present in the blood of some of the animals that were protected from SIV infection by the tenofovir gel.
What Do These Findings Mean? These findings, although based on experiments in only a few animals, suggest that rectal treatment with antiretroviral drugs before rectal exposure to HIV might prevent rectal HIV transmission in people. However, results from animal experiments do not always reflect what happens in people. Indeed, clinical trials of a potential vaginal microbicide that worked well in macaques were halted recently because women using the microbicide had higher rates of HIV infection than those using a control preparation.
However, because HIV targets activated T cells, viral rechallenge experiments must be done to check that the activated T cells induced by the virus in the presence of tenofovir do not increase the likelihood of infection upon re-exposure to HIV before this potential microbicide is tried in people. The relative ease by which HIV is transmitted rectally [ 1 — 4 ] makes this a particularly important, although relatively neglected, route to target with prevention strategies.
Unlike the vagina, the rectal canal has only a single layer of columnar epithelium overlying tissue rich in activated lymphoid cells [ 56 ] and therefore for reasons of both anatomy and immunological status presents a particular challenge for preventative modalities. It is difficult to estimate the prevalence of anal intercourse AI in the heterosexual population, but recent studies have indicated that it may be far more common than had been thought.
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In a population-based study of 2, Northern Californian women aged 18—29 y, AI was reported in Higher rates of AI have been described in women at particular risk of HIV infection through drug use, forced intercourse, and prostitution [ 8 — 11 ].
These figures alone demonstrate the need for the development of rectal microbicides, a focus catalyzed by the more visible need of the population of men who have sex with men, which still accounts for the majority of new infections in North America, South America, and Europe.
Moreover, many of these men who have sex with men are having unprotected AI irrespective of their HIV status [ 14 ].KP Vlog #2 - About me
To date preclinical studies of tenofovir in the macaque rectal challenge model using either simian immunodeficiency virus SIV or recombinant chimeric simian HIV SHIV have focussed on the use of the orally bio-available prodrug tenofovir disoproxil fumarate TDF [ 1516 ].
Although partial protection was observed against multiple low dose mucosal virus challenge, it appeared that the dose of available drug may have been suboptimal.
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We have taken a different approach, reasoning that the optimal route to protect cells of the rectum and possibly beyond may be through local application of tenofovir given, in effect, as a rectal microbicide.
As well as testing this hypothesis, we sought to determine if protective efficacy correlated with drug uptake and whether exposure to virus in the absence of overt infection stimulated virus-specific T cell responses.
Purpose-bred male rhesus macaques Macaca mulatta of Indian origin aged 4—6 y were obtained from a UK breeding colony. Animals were killed humanely by an overdose of anaesthetic. None of the animals had been used previously for experimental procedures and all animals were shown to be SIV negative by virus isolation [VI], PCR, and serology before entering the experiment.
The process was atraumatic with no obvious leakage.
Assignment of macaques to different treatment groups is shown in Table 1. Virus inoculum was diluted aseptically shortly before challenge and administered in 3-ml volumes with a 6 FG soft catheter 8 cm into the rectum.
At 1, 2, 6, 12, 16, and 20 wk postchallenge macaques were bled to provide 15 ml of heparinised blood for VI and proviral DNA assay, 2 ml of EDTA blood for plasma vRNA load determination, and 2 ml of clotted blood for serum antibody analysis. Animals were observed for adverse effects immediately after injection of test substance, followed by daily observation for the duration of study. At each time of sedation the following clinical data were taken for each animal: At necropsy, the animals were assessed for gross pathology and the following specimens collected for analysis: Cultures were examined at the time of feeding every 3—4 d for cytopathic effect cpe.
Cultures where cpe was not seen were kept for at least 28 d. Virus growth was confirmed by immunofluorescent staining of acetone-methanol fixed cells for the detection of SIV antigens using a polyclonal antiserum from an SIV infected macaque.
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A similar procedure was used for back titration of the challenge stock virus, where fold dilutions were added to four replicate flasks of C cells for each dilution tested. Where a final work has been obtained through the compilation or processing of a source file or multiple source files, all underlying source data should be available alongside the work itself under the same conditions.
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