[Expansion of the jaws under the effect of flexible activators].
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Biomedical subjects
Publications and source records attributed to P Roques.
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We developed an animal model for the male-to-female transmission of human immunodeficiency virus, consisting of an atraumatic vaginal application of simian immunodeficiency virus onto the intact vaginal mucosa of cynomolgus macaques. Different doses of a pathogenic isolate of SIVmac251, with or without seminal plasma, were infused into the vaginas of female macaques. Infection of macaques could be achieved after a single exposure to the virus. Two patterns of infection were underscored with no relation to the virus dose inoculated: in 50% of the monkeys, SIV was persistently recovered and a strong antibody response to SIV was evidenced in blood and vaginal secretions. In the other infected animals, SIV infection was only transiently evidenced and a weak systemic antibody response was detected. It appeared that the presence of seminal plasma may be implicated in this variability only when low doses of virus are inoculated. Sequence analysis of the env gene of SIV revealed that most of the persistently viraemic animals were infected with a viral variant different from that of transiently viraemic macaques.
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HIV human infections therapy requires at least two different approaches: antiretroviral therapy, and immune system modulation (stimulation or suppression depending on the clinical and biological stage, and upon the pathogenesis of the disease). Because no animal model is today available, little is known about the pathogenic mechanisms of HIV infections in humans. Therefore, only antiviral drugs might be involved in standardized middle or short term clinical trials, because virologic parameters are easily measurable, thought immunomodulators may require more than two or three years before getting informations on their efficiency. AZT is of benefit for treated patients within the first 6 or 8 months of therapy, and, after one year, survival of treated patients seems to be identical to survival of control groups. This might be related to the pharmacokinetic of the drug, which has to be phosphorylated before being active on HIV, and all the susceptible cells to HIV are not able to perform this phosphorylation (macrophages for example). Other therapeutic agents are today either in the early in vitro development (antisens, glycosylation inhibitors), or in phase II clinical trial, and when administered to patients, they do not exhibit any antiviral effect (soluble CD4), suggesting that new pharmacologic administration forms are required.