Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A brief review of second-generation drugs, drugs that may be used to fight strains of HIV resistant to currently available drugs, is presented. The review describes amprenavir, ABT 378, AG 1776, and DPC 963. Clinical trials are currently being conducted on ABT 378, but human trials still have to be performed on many of these drugs.
STEP Perspect 1999
PMID:Second-generation drugs fight resistant virus. 1136 60

A presentation by Dr. Franco Lori at the 6th CROI suggested that early implementation of HAART and strategic treatment interruptions may control HIV by bolstering the immune system. The case study of the "Berlin patient" inspired clinical tests of this theory. Another researcher, Bruce Walker, noted that HAART therapy administered within three months after the onset of HIV can preserve a dynamic immune response. Unfortunately, interrupting HAART can result in surges of HIV levels and an increased risk of developing resistant strains of HIV, regardless of when HAART is begun. The concept behind intermittent breaks in HAART is that the immune system needs to be exposed to small amounts of HIV to continue building a response. Other means of stimulating CD4 cell activity are discussed.
STEP Perspect 1999
PMID:It's the immune system, stupid. 1136 62

T-20 is the first drug in a new class known as fusion inhibitors. Fusion inhibitors prevent HIV from adhering to CD4 (T-helper) cells. Human studies have shown good short-term results, but more studies are needed to judge T-20's long-term potential for suppressing HIV. If future studies show similar results, T-20 could be an alternative for those failing other anti-HIV therapies. T-20 is currently administered by injection under the skin, but a pump that can deliver the drug at a constant rate is in development.
STEP Perspect 1999
PMID:T-20: a new class of drugs. 1136 63

The first serious examination of the cause of lipodystrophy took place at the 12th World AIDS Conference. Lipodystrophy, or fat redistribution syndrome, is characterized by high levels of fat in the blood and fat deposits in the back of the neck, abdomen, or breasts. The disorder can also be accompanied by a loss of fat in the extremities, face and buttocks. Many cases of lipodystrophy in PWAs have been linked to therapy with PIs. Researchers have also found the syndrome in PWAs who have not taken PIs. Common treatments used for lipodystrophy include growth hormones, diet and exercise, anabolic steroids, and liposuction. Several studies presented at the conference examined how to effectively combat HIV, while managing lipodystrophy symptoms. The most common methods involved either switching to a non-PI regimen or adding a drug to treat the complication.
STEP Perspect 1999
PMID:Unsolved mystery of fat redistribution. 1136 64

Two clinical trials attempting to improve the immune system's response to HIV are briefly profiled. One trial interrupted HAART to determine whether HIV would remain undetectable. The other study attempted to revive resting HIV lodged in CD4 cells and purge the virus. Data gathered to date is preliminary and insufficient for judging long-term effectiveness of these methods. Each method carries risks which are outlined. Additional data showed that improvements in the immune system, which may help to fight opportunistic infections, are continuously occurring during HAART.
STEP Perspect 1999
PMID:A tale of two trials of HAART interruption. 1136 65

During the 6th Conference on Retroviruses and Opportunistic Infections (CROI), researchers at the University of Alabama reported that they have traced the origin of AIDS to a subspecies of chimpanzees (Pan troglodytes) found in Africa. Studies of simian immunodeficiency virus (SIV), which is harmless in chimpanzees, may facilitate understanding about HIV transmission and the immune system response. Unfortunately the chimpanzees are being eradicated by hunters and the logging trade. Scientists speculate that these practices may spread SIV and other viruses further to the human population. More research is needed before information useful to the epidemic in humans is found.
STEP Perspect 1999
PMID:Origin of AIDS discovered. 1136 66

Kaposi's Sarcoma (KS) is a type of cancer thought to be caused by the human herpesvirus-8 (HHV-8). KS causes cancerous lesions on or beneath the skin. The disease may overpower the immune system and, in some cases, cause death. Studies show that the transmission of HHV-8 is linked to sexual contact, either genital or oral, and that people cannot contract KS without first having HHV-8. The recent decrease in the number of KS cases has been attributed to the use of highly active antiretroviral therapy (HAART). However, the incidence of anal cancer among gay men with HIV is increasing. HAART may be prompting this trend by prolonging lives, and giving more time for the disease to develop. The progression of anal cancer is noted, along with information about available screening tests. Surgical and non-surgical treatments are listed. All men who engage in sex with men are urged to be screened for this type of cancer.
STEP Perspect 1999
PMID:The trouble with tumors. 1136 67

Participating in community wellness projects is one way occupational therapy students at Winston-Salem State University (WSSU), Occupational Therapy Program in North Carolina are learning to expand occupational therapy into the community. In a fieldwork experience, 13 juniors are assigned to a community HIV/AIDS project to increase community awareness and prevention of the spread of HIV/AIDS. The project is implemented in conjunction with HOPE (HIV Outreach Programs and Education), STEP ONE, and the Samaritan Ministries. The students' efforts culminate in an HIV/AIDS Rally. Student learning is grouped into categories of planning, implementation, and follow up. This experience resulted in students working as volunteers for HOPE; students collaborating together on a research project to determine the extent University students understand how to prevent the spread of HIV; and students considering a WSSU campus-based HIV/AIDS awareness activity during October 2001 AIDS Awareness Month.
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PMID:Occupational therapy students explore an area for future practice in HIV/AIDS community wellness. 1201 68

The first efficacy trials--named STEP--of a T cell vaccine against HIV/AIDS began in 2004. The unprecedented structure of these trials raised new modeling and statistical challenges. Is it plausible that memory T cells, as opposed to antibodies, can actually prevent infection? If they fail at prevention, to what extent can they ameliorate disease? And how do we estimate efficacy in a vaccine trial with two primary endpoints, one traditional, one entirely novel (viral load after infection), and where the latter may be influenced by selection bias due to the former? In preparation for the STEP trials, biostatisticians developed novel techniques for estimating a causal effect of a vaccine on viral load, while accounting for post-randomization selection bias. But these techniques have not been tested in biologically plausible scenarios. We introduce new stochastic models of T cell and HIV kinetics, making use of new estimates of the rate that cytotoxic T lymphocytes--CTLs; the so-called killer T cells--can kill HIV-infected cells. Based on these models, we make the surprising discovery that it is not entirely implausible that HIV-specific CTLs might prevent infection--as the designers explicitly acknowledged when they chose the endpoints of the STEP trials. By simulating thousands of trials, we demonstrate that the new statistical methods can correctly identify an efficacious vaccine, while protecting against a false conclusion that the vaccine exacerbates disease. In addition to uncovering a surprising immunological scenario, our results illustrate the utility of mechanistic modeling in biostatistics.
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PMID:On modeling HIV and T cells in vivo: assessing causal estimators in vaccine trials. 1678 16

A 'T-cell vaccine' aims at generating cytotoxic T-lymphocytes (CTLs; the so-called 'killer' T-cells) rather than antibodies (as for traditional vaccines). The first (phase IIb) trials of this concept against HIV/AIDS began in 2004. What can mechanistic modeling contribute to understanding the biological action of this class of vaccines, if any? Models are appropriate in any discussion of three potential vaccine effects: on acquisition of infection; on state of disease ('viral load', VL) after infection; and on preventing escape from immune control. Concerning the first two, P. Gilbert, S. Self and I introduced new stochastic models of early HIV infection and the CTL response, and, making use of recent estimates (derived in collaboration with O. Yang and L. Corey) of the rate that CTLs can kill HIV-infected cells, made the (surprising?) discovery that CTLs might prevent some infections--as the trial designers implicitly acknowledged when they chose the dual end points of the study. On sustaining control, we have derived a theoretical formula for the rate of escape by stepwise mutation and a new method of simulating HIV and CTL dynamics in vivo (permitting new mutant strains a stochastic evolution--essential, in our view). These quantitative models and simulation techniques can also prove useful to biostatisticians. For example, in preparation for the STEP trials, Gilbert, Bosch, and Hudgens developed a novel technique for estimating a causal effect of a vaccine on VL while accounting for post-randomization selection bias. By simulating thousands of trials, we demonstrated that GBH's method can correctly identify efficacy while protecting against falsely concluding that the vaccine exacerbates disease. When trial data becomes available, the models may also be exploited to make complementary analyses which, while not relevant to vaccine licensure, may suggest new biological hypotheses.
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PMID:On modeling the effects of T-cell vaccines on HIV acquisition and disease. 1826 25


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