A new protease inhibitor, currently in early clinical studies, is effective against HIV strains resistant to ritonavir (Norvir, Abbott).The drug, code named PNU-140690, is a third-generation non-peptidic derivative of coumarin. It is a sulfonamide-containing 5,6-dihydro-4-hydroxy-2-pyrone.
Reconstitution of HIV-ravaged immune systems is possible with effective antiretroviral therapy, mouse studies suggest. The studies provide in vivo evidence that people receiving highly active antiretroviral therapy (HAART) can regain most, but not all, lost immune function. They also suggest that stem-cell replacement, possibly incorporating anti-HIV gene therapies, could fully restore immune function.
A gene therapy already in Phase II clinical trials is intended to stimulate the same kind of cellular immune responses seen in people who remain healthy despite long-term HIV infection. The therapy calls for the genetic engineering of cytotoxicly mphocytes (CTLs) so that they express the universal T-cell receptor - the CD3 zeta chain - in combination with the CD4 receptor to which all strains of HIV bind.
HIV apparently hijacks the immune system's signalling system and uses it to its own ends. The culprit is the viral Vpr protein. Studies by University of Pennsylvania researchers Velpandi Ayyavoo, David B. Weiner, and colleagues show that the protein acts like a glucocorticoid (GC) hormone to inhibit immune responses, to induce the programmed cell death (apoptosis) of T cells, and to preserve antigen-stimulated T cells as long-lived "factories" for production of new virus.
Researchers have solved the atomic structure of a crucial portion of the HIV envelope. The finding is expected to lead to new small-molecule candidate AIDS therapies as well as to new targets for HIV vaccines.
New evidence offers hope of an immune therapy that could strengthen the ability of killer cells to fight HIV. As part of the immune system's extensive series of checks and balances, a minor subset of CD8(+) T cells expresses inhibitory natural-killer-cell receptors (NKRs) that bind human leukocyte antigen (HLA) class I molecules.
Anti-HIV chemokines could drive the virus to mutate to the form associated with disease progression. The finding has implications for the use of immunotherapies based on these chemokines.
There have been no new or recurrent Pneumocystis carinii pneumonia (PCP) infections - so far - in a group of HIV infected patients who stopped their PCP prophylaxis after responding to highly active antiretroviral therapy (HAART). The scientific debate continues over whether increased T-cell counts in HAART patients means that their immune systems have regained the ability to resist opportunistic infections.
Protease inhibitors get the headlines, but a more conventional combination therapy has saved more lives. Prophylactic treatment with trimethoprim and sulfamethoxazole (TMP/SMX) is highly effective in preventing new and recurrent Pneumocystis carinii pneumonia (PCP), the most common life-threatening opportunistic infection in AIDS.
Drugs and monoclonal antibodies in both the late and early stages of preclinical development could deny HIV access to the cellular co- receptors it needs to enter cells. Such agents would effectively mimic the genetic resistance to HIV seen in some infected patients with long-term nonprogression.
Switching to double-protease-inhibitor therapy with ritonavir (Norvir) and saquinavir (Invirase) does not provide long-term HIV suppression for patients who have failed indinavir (Crixivan) therapy. Data do not prove conclusively that switching to two new protease inhibitors cannot help patients who fail combination therapy that includes a protease inhibitor.
Slow but steady T-cell increases in people receiving effective anti-HIV therapy may mean that their immune systems eventually will recover. While it is too soon to know the extent to which competent immune function can be restored to people with HIV disease, available data are promising for those who begin highly active antiretroviral therapy (HAART) while their CD4 T-cell counts are still above 100 cells/(micro)L.
A new mucosal vaccine adjuvant designed for use with killed pathogens proved safe in humans. Tolerable dosages of the adjuvant, dubbed LT[R192G], were well within the range expected to be used in combination with vaccine immunogens.
Latent, replication-competent HIV persists in memory cells long after highly active antiretroviral therapy (HAART) has essentially ended virus production. Should drug treatment stop for any reason, the residual virus appears capable of restoring high-level HIV replication and progressive disease if HAART is not resumed.
The U.S. intends to build a centralized laboratory for AIDS vaccine development, announced Nobel laureate David Baltimore, chair of the U.S. AIDS Vaccine Research Committee (AVRC) The laboratory will be a joint project of the National Cancer Institute and the National Institute of Allergy and Infectious Diseases, Baltimore said. It will be built on the National Institutes of Health (NIH) campus in Bethesda, Maryland, by the year 2000.
Sometimes Peter Piot must think nobody is listening. His animated state-of-the-AIDS-epidemic lectures have been featured at every world AIDS conference and at the last several opening sessions of the American Society for Microbiology's Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC).
Patients who simply add a protease inhibitor to existing anti-HIV drug regimens risk treatment failure, new studies suggest. A report that more than half of real-world patients fail highly active antiretroviral therapy (HAART) was the most widely reported story from the American Society for Microbiology's 37th Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC), held September 28 to October 1, 1997, in Toronto, Ontario, Canada.
Increased use of zidovudine (AZT) plus routine HIV counseling and voluntary HIV testing for pregnant women has decreased mother-to-child HIV transmission dramatically. The finding comes from a study by the U.S. Centers for Disease Control and Prevention (CDC) that assessed implementation of U.S. Public Health Service (PHS) recommendations.
If anti-HIV therapy is effective, it buys one or more extra years of life for about $8000 per year. The figures come from an economic model developed by researchers at Glaxo-Wellcome Inc. to project lifetime treatment costs for people with HIV.
Enrollment has been halted in a clinical trial of passive immunoprophylaxis of mother-to-child HIV transmission. Early results from the trial showed that the study lacked power to detect whether addition of hyperimmune HIV immunoglobulin (HIVIG) improved this effect. Trial cessation was not due to any safety problems with HIVIG.
Vaccines that efficiently elicit T-cell mediated immune responses can be created via genetic, enzymatic, and/or chemical engineering. These various approaches create immunogenic chimeric molecules by combining T-cell antigens with self molecules.
A new group intends to focus and expedite vaccine research and development on a worldwide basis. "We expect to launch a longstanding organization that can sustain major efforts in this exciting field," said U.S. National Cancer Institute researcher Peter Nara, chair of the newly formed International Society for Vaccines (ISV). "We are jump-starting the vaccine era."
An experimental naked DNA HIV vaccine elicited anti-HIV antibodies in vastly higher quantities and of superior quality when administered with monophosphoryl lipid A (MPL) adjuvant.
A new vector greatly improves long-term intracellular immunization against HIV. Intracellular immunization against HIV - treatment of infection by genetically engineering antimicrobial resistance into a person's cells - is already being tested in preliminary clinical trials. But a major problem with the technique has been suboptimal expression of the antiviral genes.
Combinations of different anti-HIV monoclonal antibodies may both protect against the virus and prevent the emergence of viable escape mutants. The findings by a research team from Aaron Diamond AIDS Research Center (ADARC) and Scripps Research Institute are based on intensive studies of a single human MAb, IgG1b12.
An AIDS physicians' organization is organizing a clinical trial of a live HIV vaccine - and its leaders are the first to volunteer. The International Association of Physicians in AIDS Care (IAPAC) has established a subcommittee to organize and recruit subjects for a trial of a live, attenuated HIV vaccine. IAPAC hopes to begin the 1,000-person trial by the year 2000.
Glucocorticoids increased the nerve-cell toxicity of an HIV protein in laboratory studies, while estrogen decreased the effect. If the results are the same in humans with AIDS, the findings will have far-reaching clinical implications.
New data argue against the popular idea that HIV causes AIDS by directly killing off T cells. A study of tonsil biopsies from people at various stages of HIV disease show that depletion of CD4(+) T cells occurs when viral load reaches a threshold level in lymphoid tissue.
German researchers have created a retroviral vector able to deliver therapeutic genes to CD4(+) T cells. Such intracellular immunization of CD4 cells could be performed in vivo (by direct delivery to patients) or ex vivo (by removing CD4 cells from a patient, treating and expanding them in cell culture, and returning them to the patient).
The first HIV-1 subtype G infection in the United States - and the second U.S. HIV-1 group O infection - were identified in the state of Maryland, the U.S. Centers for Disease Control and Prevention (CDC) reported. Both viruses were reactive with normal HIV tests. The CDC warned, however, that this may not always be the case.
Understanding the immunology of the HIV-1 gp120 envelope glycoprotein is essential for the development of an AIDS vaccine, argues a team of leading AIDS researchers. The team, including David D. Ho, Martin Markowitz, and John P. Moore of the Aaron Diamond AIDS Research Center (ADARC), studied HIV antibody responses to HIV-1 Env and Gag antigens in several cohorts of HIV infected individuals.
HIV is unable to replicate in CD4(+) T cells made to express interleukin 16 (IL-16). While exogenous IL-16 inhibits HIV replication by 70 to 90 percent, constitutive expression of 1,000-fold smaller amounts of the cytokine by genetically engineered CD4(+) cells inhibited viral replication by as much as 99 percent.
HIV infection self-perpetuates by forcing quiescent T cells to become activated, infectable cells. A paradox of HIV disease is that productive infection requires replacements for the two billion susceptible T cells that are eliminated daily. The virus can complete its life cycle only in activated cells, but the vast majority of T cells are quiescent.
Interleukin 16 (IL-16) corrects some of the functional defects seen in HIV infected cells. The cytokine may thus have a therapeutic role in combination with IL-2, intermittent doses of which increase CD4(+) T-cell counts in people with HIV infection.
A year of highly active antiretroviral therapy (HAART) partially reverses - but does not fully restore - the delicate balance of the immune system. T cells normally maintain stable levels, expanding when needed to fight disease and contracting to original levels (by elimination of cells no longer needed) when the threat has passed: a phenomenon known as T-cell homeostasis.
Cord-blood CD34(+) cells from the children of HIV infected mothers are appropriate for ex vivo expansion. Should the children develop HIV infection, the cells could be used - either with or without gene therapy - for future engraftment.
Highly active antiretroviral therapy (HAART) can greatly reduce lymph-node HIV levels, but even a short interruption means starting all over again. This sobering new finding shows that there are strict limits to the even the most effective anti-HIV regimens.
Potent new therapies attack HIV in the blood and lymph nodes, but it remains unclear whether the virus lurks in other nooks of the body. Evaluating virus levels in such areas remains a challenge for the design of clinical trials.
An immune therapy being explored as a cancer treatment appears applicable to HIV disease. The therapy calls for dendritic cells, which are potent antigen-presenting cells (APCs), to be pulsed with tumor or HIV antigens and infused into patients to stimulate potent immune responses.
HIV can begin its replication process before entering cells, permitting it to infect quiescent cells previously thought to be virus resistant. "HIV virions can be able, in the correct extracellular milieu, to reverse transcribe its RNA to DNA," said Roger J. Pomerantz of the Center for Human Virology at Thomas Jefferson University, Philadelphia, Pennsylvania.
A peptide isolated from human chorionic gonadotropin (hCG) reduced HIV viral load by as much as 2 log[10] in a preliminary clinical study. The peptide, dubbed HIV associated factor C or HAF-C, is the most potent of several HIV inhibitory peptides isolated from hCG by Robert C. Gallo and co-workers at Gallo's Institute of Human Virology at the University of Maryland, Baltimore.
A novel approach to intracellular immunization against HIV would give cells three different weapons against the virus. The experimental treatment, still on the drawing board, calls for hematopoietic stem cells to be provided with three different genetic mechanisms for resisting HIV infection. The cells would then be grown ex vivo and infused into the patient.
Only three immunizations raised long-lasting neutralizing antibodies capable of protecting chimpanzees against challenge with infectious virus of the same type as that used for booster immunization. The animals were vaccinated using the prime/boost approach: they received intranasal priming immunization(s) with Wyeth-Ayerst's adenovirus-HIV-1[MN]gp160 followed by intravenous boosting with Chiron's HIV-1[SF2]gp120 in MF59 adjuvant.
Attenuation of HIV-1 by deletion of its nef gene retards but does not prevent CD4(+) T-cell loss in a mouse model of HIV infection. By far, the most effective AIDS vaccine prototype is a live simian immunodeficiency virus (SIV) vaccine attenuated by deletions in the nef, vpr, and LTR genes. The new findings may slow the growing support for human tests of a similarly attenuated live HIV vaccine.
A new approach to AIDS therapy would cause HIV infected cells to kill themselves. The approach is based on studies indicating that HIV causes infected cells to lose a surface molecule known as Fas ligand. Interaction of Fas with its ligand triggers cellular suicide, a phenomenon known as apoptosis or programmed cell death.
A new research tool has led to the discovery of seven new HIV epitopes likely to induce anti-HIV cytotoxic lymphocyte (CTL) responses. The finding is a first step in the development of a vaccine capable of inducing anti-HIV CTL responses to nearly all types of HIV-1 in nearly all types of people.
A naked DNA vaccine encoding attenuated versions of HIV-1 accessory genes elicits both humoral and cellular anti-HIV immune responses in animal studies. The findings suggest improvements for the naked DNA vaccine under development by Apollon Inc., Malvern,, Pennsylvania, in collaboration with researchers at the University of Pennsylvania, Philadelphia. This vaccine, which encodes the HIV-1 gp160 envelope precursor glycoprotein, entered a Phase I clinical trial in 1996.
A major U.S. pharmaceutical company has promised a full- scale effort to develop an HIV vaccine. The promise came from R. Gordon Douglas, president of Merck Vaccines, Merck & Co. Inc., in a briefing on AIDS vaccines delivered to the Congressional Task Force on International HIV/AIDS.
Several rhinovirus/HIV chimeric viruses induce high titers of neutralizing antibodies in animal studies. Two of these chimeras currently are being tested in chimpanzees, according to Gail Ferstandig Arnold and colleagues of Rutgers University, Piscataway, New Jersey.
Who, or what, are bob and bonzo? The answer is expected to provide insight into an as-yet unanswered question about HIV infection: how do macrophage- tropic viral strains - which are responsible for the vast majority of sexual transmissions - infect T cells?
Results of toxicity and pharmacokinetic studies of the antiviral phosphorothioate oligonucleotide ISIS 5320 conducted in cynomolgus monkeys were presented at the American Association for Cancer Research conference, held April 12-16, 1997, in San Diego, California.
Cellular immune responses to AIDS vaccines are effective against all of the many HIV subtypes. The good news comes from two different research groups reporting at the 9th Annual Meeting of the National Cooperative Vaccine Development Groups for AIDS (NCVDG), held May 4-7, 1997, in Bethesda, Maryland.
Humans infected with a harmless goat virus develop antibodies that neutralize HIV. The remarkable finding offers hope for a safe, attenuated AIDS vaccine using the goat virus or a genetically engineered variant carrying HIV genes. It is strikingly reminiscent of the earliest vaccine: Edward Jenner's discovery that a relatively harmless cow virus (cowpox or vaccinia) could protect humans against smallpox.
Prime/boost vaccination using a new HIV DNA vaccine protected monkeys from infection with a chimeric simian/human immunodeficiency virus (SHIV). The approach is now being tested in humans, reported Merck researcher Margaret A. Liu in a presentation to the 9th Annual Meeting of the National Cooperative Vaccine Development Groups for AIDS (NCVDG), held May 4-7, 1997, in Bethesda, Maryland.
A live HIV vaccine prototype not only protects against challenge after oral dosing but also reduces AIDS symptoms in animals already infected with SIV. The most effective AIDS vaccine prototype yet tested is a live simian immunodeficiency virus (SIV) from which the nef gene has been deleted.
A nef-deleted simian immunodeficiency virus (SIV) vaccine protected monkeys against disease after challenge with a different strain of pathogenic virus. Mark Lewis and colleagues of the H.M. Jackson Foundation, Rockville, Maryland, evaluated nef deletion in two SIV strains (SIVmac239-delta-nef and SIVsmPBj6.6-delta-nef) that cause AIDS in macaque monkeys.
A new vaccine strategy would force HIV to expose crucial epitopes normally hidden from the immune system. The strategy, still on the drawing board, is based on new insights into HIV gained from the identification of cellular chemokine receptors as necessary for HIV infectivity.
Nobel Laureate David Baltimore has a plan for AIDS vaccine development: back to the basics. Baltimore heads the National Institutes of Health AIDS Vaccine Research Committee, established in January 1997 to coordinate the agency's efforts to develop an HIV vaccine.
The use of suboptimal treatments in clinical trials is both wrong and dangerous, a leading AIDS researcher argues. In an extraordinary article in the journal Science, Joep M.A. Lange of the University of Amsterdam blasted the short- sightedness of clinical trial planners, the self-defeating requirements of regulatory agencies, and the greed of drug companies ("Current Problems and the Future of Antiretroviral Drug Trials," Science, 1997;276:548-50).
A new assay speeds and simplifies tests for HIV infectivity and drug susceptibility. The assay may even lead to a way to test patients' infectious viral burden, perhaps yielding previously unavailable prognostic data.
A genetically engineered vaccine against dental cavities induces T helper cells in the gut, stimulating the common mucosal immune system and resulting in circulating and mucosal antibodies. The vaccine targets the dental cavity-causing bacteria Streptococcus mutans, which sticks to teeth via an adhesin on its surface called AgI/II (also known as antigen B, P1, SpaP, and PAc). The saliva-binding region (SBR) of AgI/II is therefore an attractive vaccine antigen.
A new compound can block HIV replication by interfering with the RNA-binding activity of a viral regulatory protein known as Tat. Because this is the first report of an antiviral drug that specifically targets a protein/RNA interaction, the discovery represents a novel pharmaceutical approach to antimicrobial and antitumor agents.
Structural analysis of delavirdine may lead to improvements in this and other anti-HIV drugs. Delavirdine is a member of the broad class of drugs known as non-nucleoside reverse transcriptase (RT) inhibitors (NNRTIs or NNIs). Code named U-90152, it is a type of NNRTI known as the bis(heteroaryl)piperazines or BHAPs.
The rapid pace of AIDS research again has accelerated with the announcement that a modified (beta)-chemokine can block HIV infection. The naturally occurring (beta)-chemokines RANTES, MIP- 1(alpha), and MIP-1(beta) inhibit HIV infection by primary and macrophage-tropic HIV-1 isolates (Cocchi et al., Science, 1995;270:1811-5), but they cannot prevent infection of primary macrophage cultures. Moreover, their use as AIDS therapies is limited by their natural functions of leukocyte activation and chemotaxis signalling.
A leading AIDS researcher says that the molecules that permit HIV to enter cells appear to be the keys to HIV disease. These keys promise to unlock the doors to new drugs and vaccines and perhaps even to the long-sought animal model for AIDS.
It works, but until now no one knew why. Researchers at the Naval Medical Research Institute, Bethesda, Maryland, announced at the 1996 International Conference on AIDS that without drugs they could make cultures of CD4(+) T cells from people with HIV infection grow to huge numbers (see AIDS Weekly Plus, August 26/September 2, 1996). In an ongoing clinical trial, these expanded cell populations are being used to reconstitute patients' depleted T cells.
A pathogenic simian immunodeficiency virus (SIV) infects cells via the same coreceptor as macrophage-tropic strains of HIV-1. The finding suggests that HIV infectivity may depend on an extraordinarily well-conserved region of HIV. If so, the virus would likely be very limited in its ability to develop resistance to future drugs or vaccines exploiting this region.
How do people with a mutation in only one of HIV's two coreceptors resist infection? New studies suggest an answer, and provide a glimpse into the inner workings of the human immune system.
A UK/US research team has shown that the ability of cell- culture-adapted feline immunodeficiency virus (FIV) to infect and fuse with human cells is based on its use of the CXCR4 coreceptor. "We believe that this is the first evidence of shared chemokine receptor use between primate and non-primate lentiviruses," wrote University of Glasgow researchers Brian J. Willett and colleagues in a letter to the journal Nature ("Common Mechanism of Infection by Lentiviruses," Nature, 1997;385:587).
The "future of antiretroviral therapy" has arrived ahead of schedule. A new blood test permits physicians to rapidly determine whether a patient's HIV strain is susceptible to particular anti-HIV drugs. The genotypic assay, dubbed HIV-1 GenotypR Plus, is manufactured by Specialty Laboratories Inc., Santa Monica, California.
Strategies to inhibit HIV induced programmed cell death or apoptosis may backfire. New studies show that apoptosis may actually be a beneficial mechanism that limits the spread of HIV. Experimental inhibition of apoptosis actually enhanced in vitro and ex vivo HIV replication.
HIV vaccines containing cytotoxic lymphocyte (CTL) epitopes tailored to an individual's genetic makeup could prevent, or at least delay, AIDS, two new studies suggest. The studies define for the first time the nature of protective CTL responses against HIV - and also precisely show how the virus evades these responses.
Widely criticized for elitist and restrictive registration policies in the past, organizers of the Conference on Retroviruses and Opportunistic Infections appear to be ready to bow to pressure and expand next year's meeting. Details on just how big the conference will be, and who will be welcome, are yet to be worked out, but it seems certain that the conference, regarded the most important AIDS meeting held in the United States, still will not be open to everyone who wants to attend.
An inadequate supply of second-line antituberculosis drugs contributed to the spread of multidrug-resistant tuberculosis during a nosocomial outbreak in Buenos Aires, Argentina. The outbreak included more than 250 cases of multidrug- resistant tuberculosis occurring in HIV positive patients treated at a 500-bed infectious disease hospital.
HIV evades the human immune system by quickly evoking elimination of virus-specific T cell clones. This phenomenon does not occur during infection with Epstein-Barr virus (EBV), another chronic viral infection.
A mix of DNA vaccines encoding HIV structural, envelope, and regulatory genes could mimic a live attenuated vaccine, Swedish researchers suggest. A live attenuated SIV vaccine is the only HIV vaccine prototype to show complete protection in primates.
Common infectious diseases significantly increase HIV viral load, early data from a prospective study suggest. The infections also increased the exaggerated immune activation seen in people with HIV infection.
Increases in resting energy expenditure (REE) in people with HIV infection appear to be related to viral load. The determinants of high REE variability in the context of HIV disease have been a mystery since the first reports of the phenomenon.
Lymphoid tissues infected by AIDS-related opportunistic infections (OIs) are crawling with HIV. In many of the cells tested for HIV by in situ hybridization, the viral signal was so bright that the cell could not be seen.
The cytokines interleukin 13 (IL-13) and tumor necrosis factor alpha (TNF-(alpha)) synergistically inhibit HIV infection of macrophages. The in vitro findings suggest that IL-13 may represent a novel immunotherapy for patients with HIV infection, in whom high levels of TNF-(alpha) occur.
The principal component of antiviral immunity prematurely ages in most people infected with the virus, according to new data from the Multicenter AIDS Cohort Study (MACS). But early intervention with therapies including protease inhibitors may prevent this untimely aging.
Anti-HIV hyperimmune serum is safe and may be effective in preventing mother-to-child HIV transmission in Africa. Preliminary results from a Phase I/II trial show that a Ugandan HIV immunoglobulin (Ig) product had no serious toxicity after a single infusion given to mothers at 37-38 weeks' gestation and to infants within their first 16 hours of life.
Now that long-term suppression of HIV appears possible, the central question for treated patients is whether their full immune function can be restored. Longitudinal studies appear best suited to answer this question. A pilot study by a French research team provides intriguing baseline data and a glimpse into the future.
CD4 count - long used by AIDS clinicians to track HIV disease progression - is still the best surrogate marker for immune function. Sensitive new measures of HIV viral load provide a wealth of information on disease progression. These new tests may be the most sensitive measure of how well an individual is doing in his or her struggle with the AIDS virus.
Envelope-based candidate HIV vaccines are poorly immunogenic in people with HIV infection - even those with high T-cell counts. The findings apparently end hopes that the Genentech and Biocine recombinant gp120 envelope glycoprotein vaccines can strengthen the anti-HIV immune responses in people with existing infection.
A new protease inhibitor (PI) and a new nucleoside analog reverse transcriptase inhibitor (NARTI) packed a powerful anti-HIV combination punch in a clinical trial. Glaxo Wellcome is developing both drugs.
Influenza vaccination does not intensify HIV infection in children, a clinical study shows. Recent data suggest that immune activation temporarily increases HIV replication.
Why look for new anti-HIV drugs when media reports have declared that the advent of triple-drug combinations signals the end of AIDS? The answer, in a nutshell, is that the complex dosages, toxicities, and drug interactions of these treatments make them hard for patients to take and difficult for doctors to prescribe.
A naked-DNA HIV vaccine being tested in 15 human subjects with HIV infection appears safe. The vaccine is being developed by a research team led by David B. Weiner of the University of Pennsylvania in collaboration with Apollon Inc., Malvern, Pennsylvania.
CD4 counts and anti-HIV immune responses failed to improve in recipients of a therapeutic vaccine administered in combination with zidovudine (AZT). The vaccine, p24-VLP, contains the HIV p24 protein expressed by a genetically engineered yeast in the form of a virus-like particle.
Only a vaccine can stop the AIDS pandemic, said the head of the United Nations AIDS effort. Peter Piot, director of UNAIDS, the umbrella agency for United Nations AIDS programs, made his remarks in the plenary address to the Fourth Conference on Retroviruses and Opportunistic Infections, held January 22-26, 1997, in Washington, D.C.
HIV and its damaging effects are greatly reduced in mucosal lymphoid tissues during potent combination antiretroviral therapies. The findings are good news for people with access to the new treatments. They also provide new insights into the pathogenesis of HIV disease.
Even when HIV RNA vanishes from the lymph nodes after aggressive treatment, proviral DNA persists. Precisely how long the latent virus lurks is the question at the heart of whether HIV infection can ever be cured.
A person's genetic makeup determines the rate at which HIV disease progresses. Researchers I.P.M. Keet of the University of Alabama, Birmingham, and colleagues compared the human leukocyte antigen (HLA) types of three cohorts of homosexual men (MACS, n=139; DCG, n=102; and Amsterdam, n=140) who have been enrolled in prospective studies since they first seroconverted to HIV.
After aggressive antiretroviral therapy, a low level of HIV in the plasma is a bad sign. It means that the virus may be going wild in the lymph nodes, according to a study by University of California, San Diego researcher J.K. Wong and colleagues.
Researchers testing a promising HIV vaccine strategy say their approach is ready for efficacy trials. The approach employs priming immunizations with a recombinant canarypox virus (ALVAC, Virogenetics), dubbed vCP205, followed by boosting immunizations with recombinant HIV gp120 envelope glycoprotein (rgp120MN in MF59 adjuvant, Chiron/Biocine).
Responding to the concerns of the HIV community, as well as scientists, physicians, and other professionals engaged in AIDS research, major AIDS organizations, including AIDS Action Council, AIDS Project Los Angeles, AIDS Research Alliance, Gay Men's Health Crisis, Linda Grinberg Foundation, Project Inform, San Francisco AIDS Foundation, and Treatment & Data Committee, announced a campaign to persuade organizers of the Fourth Conference on Retroviruses and Opportunistic Infections to radically rethink the design of the conference and move the meeting to a larger venue in 1998.
Potent drugs given soon after infection completely change the course of HIV disease. There are indications that patients treated within 90 days of infection may clear the virus completely. Whether this is actually possible is the subject of intense investigation.
HIV dropped to undetectable levels in the majority of late-stage AIDS patients treated with three-drug combination therapy. The patients, who had a median CD4 count of 15 cells/(micro)L when the study began, had a median CD4 increase of 86 cells/(micro)L after 24 weeks of the three-drug treatment.
Charles W. Henderson, Publisher, and Daniel J. DeNoon, Senior Editor
The Centers for Disease Control and Prevention (CDC) and the U.S. National Institutes of Health (NIH) should be careful with whom they get into bed. The CDC/NIH collaborative relationship for a conference with the Infectious Diseases Society of America (IDSA) has damaged the reputation of these two federal agencies and has embroiled them in a major national catastrophe.
Repeal laws and regulations restricting the sale of sterile syringes and needles, medical ethicists recommend. Sterile syringes would greatly reduce the spread of blood- borne diseases such as AIDS, hepatitis, and malaria, argue authors Lawrence O. Gostin and Kathleen Flaherty of the Georgetown/Johns Hopkins Program in Law and Public Health, Washington, D.C., and Baltimore, Maryland; Zita Lazzarini of the Harvard School of Public Health, Boston, Massachusetts; and T. Stephen Jones of the U.S. Centers for Disease Control and Prevention (CDC), Atlanta, Georgia.
This information is designed to support, not replace, the relationship that exists between you and your doctor.