A Manhattan judge has ordered the city to obey the law and provide "medically appropriate" housing to homeless AIDS patients who reportedly have been living in deplorable, life-threatening conditions. State Supreme Court Justice Eileen Bransten issued the order after seven homeless people with AIDS complained in November 2001 that the city was sending them to virtually uninhabitable single-room occupancy hotels. Bransten's ruling said the "petitioners' statements establish that their housing is not suitable for healthy individuals, much less for persons with severely compromised immune systems."
The seven said the hotels were infested with rats and roaches; had filthy bathrooms; lacked heat, hot water, electricity, clean mattresses and bed linens; and had no elevators for disabled clients on upper floors. One petitioner whose complaints were typical was a 33-year-old woman who has cancer and asthma in addition to AIDS. The judge said she was put in a filthy rodent-infested room on the fourth floor of a hotel with no elevator. The woman took numerous life-sustaining medications but had no refrigeration for them, the judge said, and when she complained, a hotel employee told her in rude terms to leave if she was unhappy.
The judge directed the HIV/AIDS Service Administration to provide: housing with "suitable and appropriate furnishings"; accessible rooms when buildings without elevators are used; "usable" bathrooms that are maintained and cleaned; placements free of vermin; and operating utility services such as electricity and hot water.
City law requires that homeless people with AIDS be provided housing. Armen H. Merjian, lawyer at Housing Works Inc., which sued on behalf of the petitioners, called the ruling a "tremendous victory." Meanwhile, David Neustadt, spokesperson for the city's Housing Resource Administration, said that four of the seven petitioners have been placed in "more permanent type housing," and the other three are being housed in compliance with Bransten's orders. (Associated Press, 09.13.02, Samuel Maull)
HIV-positive infants can be treated with multiple antiretroviral agents although the therapy has limited effectiveness, researchers report in a study published in the Pediatric Infectious Disease Journal (2002;21(6):518-525). Albert Faye and colleagues at Robert Debre Hospital in Paris and other institutions in France conducted a study to "assess tolerance and efficacy of early multitherapy including a protease inhibitor for infants perinatally infected with HIV."
Antiretroviral multitherapy slowed or reversed disease progression in infants, but was hampered by rapid viral resistance, Faye and coauthors found. The researchers evaluated protease inhibitor-based multitherapy in a group of 31 HIV-positive infants. Clinical progression and CD4 cell loss were halted in all of the treated children, without severe drug toxicity, they said. HIV RNA levels dropped by a median of 2.7 logs after 3 months, and more than half of the treated infants showed viral loads lower than 500 copies/mL after 6 months, study data showed. Two years after the initiation of multitherapy, however, the median viral load reduction had fallen to 1.7 logs, with only 18 percent of the study group showing viral loads below 500 copies/mL.
Most children with consistently high HIV RNA levels after 6 months carried viral populations with protease and/or reverse transcriptase resistance mutations. "Despite the absence of clinical or immunologic progression, the high frequency of virologic failure associated with genotypic resistance reveals the difficulties associated with implementing antiretroviral multitherapy in infants," Faye and colleagues concluded. "Suboptimal doses of protease inhibitor could be a factor contributing to treatment failure." (AIDS Weekly, 08.26.02, Michael Greer)
Scientists, public health advocates, gay rights groups and some women's organizations are launching a public awareness campaign next month to attack the popular spermicide Nonoxynol-9. "In the interest of public health, the safest thing to do is eliminate N-9 condoms and lubricants from the market," said campaign organizer Lori Heise of the Program for Appropriate Technology in Health.
Originally developed as a detergent, N-9 has been used for nearly 50 years as a vaginal cream that rapidly kills sperm cells. Cautions issued on N-9 for at least two years were reinforced over the summer, when the World Health Organization and the CDC issued warnings that N-9 has been found to be ineffective in stopping HIV and other STDs.
The campaigners intend to recommend that N-9 not be used during anal intercourse, by prostitutes, by anyone engaged in multiple acts of intercourse in one day, or to prevent STDs. The groups believe that N-9, which is present in many spermicides used with diaphragms and cervical caps, can be safely used by women not at risk for HIV. Researchers say that N-9 can break up or irritate the cell lining, or epithelium, of the rectum and vagina, making it easier for infecting organisms to invade. The danger with anal sex is especially significant, because the rectum only has a single-cell wall, while the vagina has a wall about 40 cells thick.
A study to be published in this week's Lancet reports that prostitutes using N-9 with multiple sex partners had more genital lesions and higher HIV rates than others using a placebo. And a small study by David Phillips of the Population Council of New York found that even low doses of N-9 caused heavy sloughing of the rectal epithelium. The epithelium regenerated itself in eight to 10 hours.
A Johnson & Johnson spokesperson said the company ceased production of its KY Plus with N-9 in July and will phase out N-9-treated condoms, which are manufactured for sale in Brazil and Colombia, early next year. Also stopping sales of N-9 products are Planned Parenthood and fourth-largest U.S. condom maker Mayer Laboratories Inc. But a spokesperson for the Advanced Medical Technology Association, which represents medical device makers, said the top three condom makers have no plans to pull their N-9 products. According to one person familiar with ongoing talks, the maker of No. 1-selling Trojan condoms is developing a new label that will say something like "for vaginal use only." (Wall Street Journal, 09.25.02, Rachel Zimmerman)
Despite hopes that taking regularly scheduled breaks from combination therapy would train the immune system to keep HIV under control, a new study published online in the Proceedings of the National Academy of Sciences Early Edition (2002;10.1073/pnas.202372199) fails to detect any benefit of such drug holidays. Interest in drug holidays is high because, although combination therapy has been life-extending for many people, the drugs are expensive and can have serious side effects. In addition, some people have a hard time sticking to the complicated daily regimen of pills.
A few reports have suggested that structured, physician-supervised breaks from combination therapy may improve the ability of the immune system to fend off HIV. The hope was that repeatedly exposing the immune system to HIV during short drug vacations might lower the set-point viral load.
In a study of 97 patients with chronic HIV infection, however, that did not turn out to be the case. Dr. Annette Oxenius, of the Eidgenossische Technische Hochschule in Zurich, Switzerland, found that viral load was slightly lower after drug vacations, but the difference was very small.
Taking a break from combination therapy did not affect CD8 T cells that specifically target HIV. Only those patients who had vigorous CD8 responses to HIV before taking a break continued to do so afterwards. The researchers concluded that structured treatment interruption is "generally unable" to alter how a person's immune system responds to HIV. The authors point out, however, that the study included patients who were chronically infected with HIV. Research has shown that structured treatment interruptions for newly infected patients can alter the immune response to HIV. (Reuters Health, 09.23.02)
At the 2002 Ryan White Comprehensive AIDS Resources Emergency conference, some of the latest research into the differences between minority and white HIV patients and access to HIV treatment indicated that there were not huge disparities within HIV programs. However, "When you sum it up across states and programs, you get disparities," says Stephen F. Morin, Ph.D., professor of medicine at the University of California-San Francisco, AIDS Research Institute.
"So it's a complicated picture, and there's a huge difference in how people receive care through Medicaid and the AIDS Drug Assistance Program," Morin said. "African-Americans are far more likely to receive access to antiretrovirals through Medicaid, and people on Medicaid are less likely to be on optimum therapy than people in ADAP."
Research at the conference, which was sponsored by the Health Resources Services Administration of Rockville, Md., indicated that differences in household income and disability status led to proportionately more African-Americans in Medicaid programs than whites and Latinos. Studies also showed a greater proportion of Latinos in ADAP programs than in Medicaid, a difference that investigators attributed partly to the fact that Medicaid programs require a residency test for enrollees and ADAPs do not.
Perhaps the biggest problem with the current Medicaid/ADAP safety net for uninsured and poverty-level people infected with HIV is that their access to care is largely dependent upon their state of residence and whether they were tested for HIV soon after becoming infected, research shows. Some states have stringent Medicaid requirements in which enrollees must have an AIDS-defining illness or a disability before they qualify for HIV medications and services. And in some states and communities, minorities are less likely to learn of their HIV status until after they begin to experience symptoms, said T. Anne Richards, M.A., a research specialist with the UCSF Department of Medicine.
U.S. Rep. Nancy Pelosi (D-Calif.) and others in Congress have sponsored a bill called the Early Treatment for HIV Act of 2001, which would enable more HIV-infected poor people to receive antiretrovirals and HIV treatment before their disease progressed to illness, said Scott Brawley, M.S.W., director of public policy for AIDS Action, an advocacy group in Washington, D.C. However, the bill has been stalled in the House subcommittee on health since shortly after it was introduced in June 2001. Also, 2002 has not been a good year for a bill that would cost states more money, he noted. (AIDS Alert, 11.01.02)
Highly active antiretroviral therapy (HAART) has been associated with the development of lipodystrophy syndromes. Lipodystrophy, a clinical condition characterized by poor or uneven distribution of fat cells, can lead to lower belly obesity and a hump on the upper back. Lipodystrophy side effects also include diabetes and high levels of cholesterol and triglycerides.
In a test-tube study published in Mitochondrion (September 2002), researchers from the National Cancer Institute, the National Institute of Standards and Technology, and Purdue University report that protease inhibitors, a component of HAART, can lead to mitochondrial toxicity. The clinical features of HAART-associated lipodystrophy are similar to those seen in people with mitochondrial dysfunction. The powerhouse of the cell, the mitochondrion processes proteins and produces energy. Interference with its normal activity can lead to distortion or dysfunction of other cellular processes.
Researchers have long known that the nucleoside-analogue reverse transcriptase inhibitors (NRTIs) in HAART cocktail regimens can cause mitochondrial toxicity by inhibiting a mitochondrial enzyme called DNA polymerase gamma. The current study shows that protease inhibitors can directly affect the enzyme mitochondrial processing protease (MPP), thus leading to mitochondrial dysfunction that might contribute to the development of lipodystrophy.
While protease inhibitors alone do not necessarily cause lipodystrophy, the combined direct effects on mitochondria of protease inhibitors and NRTIs can possibly lead to the condition. In addition, protease inhibitors are highly hydrophobic (water insoluble), and may concentrate in fatty tissues. The drugs would have a greater impact on mitochondria in tissues with chronic exposure. "This finding that protease inhibitors affect MPP could be useful if one wants to develop inhibitors of MPP for other conditions, such as cancer," said Henry Weiner, Ph.D., of Purdue University.
The authors do not know to what degree MPP inhibition correlates with mitochondrial disruption, nor if their results with isolated mitochondria in the test tube study actually occur in patients. However, scientists have found that both NRTIs and protease inhibitors have direct effects on fat cells, and mitochondrial abnormalities in fat tissue have been found in patients with lipodystrophy. The researchers call for further study of MPPs and recommend that scientists designing new HIV/AIDS drugs attempt to minimize the drugs' adverse effects on mitochondria. (AIDS Weekly, 10.28.02)
The chances of eventually developing cirrhosis or another serious liver disease from hepatitis C virus (HCV) may be lower than many experts believe, according to a computer simulation based on U.S. liver disease statistics. "The news would be better if we could reliably predict which patients will and which will not progress quickly, which is not possible at this time," said study coauthor Dr. Joshua A. Salomon of the World Health Organization. As such, doctors must still face the difficult decision of when to put which patients on potentially toxic medications to slow the infection's damage to the liver, Salomon said.
Salomon added that many previous estimates of when HCV patients can expect to develop liver disease have been based on patients who have already been diagnosed with liver disease. Patients who come to doctors because they are sick will most likely progress more quickly, the researcher noted, while those who are healthy enough to remain in the general population may stay disease-free for longer periods.
In the current study, "Empirically Calibrated Model of Hepatitis C Virus Infection in the United States," published in the Oct. 15 American Journal of Epidemiology (2002;156:761-773), Salomon and colleagues designed a computer simulation of the U.S. population that could predict when different HCV patients would develop liver disease, then tweaked it until its results matched current data registries and national surveys. The investigators discovered that the model that best matched what is seen in real HCV patients was one in which they had a relatively low rate of developing liver disease.
"Because the disease progresses so slowly in some people, they are likely to reach an old age and die from something else before their hepatitis C infections ever progress to serious liver disease such as cirrhosis or cancer," Salomon explained. For example, past studies have suggested that people infected with the virus in their 20s might develop cirrhosis anywhere from 20 to 38 years later. The new calculation suggested that half of men infected at age 25 would develop cirrhosis within the next 46 years and that fewer than 30 percent of women infected at this age "would ever develop cirrhosis," according to the report.
However, each individual is different, Salomon noted. "The fact that many infected people will not progress to cirrhosis should be one of several important considerations in individual decisions about whether or not to start treatment, along with the costs, potential side effects, and limited effectiveness of available therapies," said Salomon. (Reuters Health, 10.25.02, Alison McCook)
New unpublished and published research shows that gay and bisexual men who use methamphetamine have a greater HIV prevalence than men who have sex with men (MSM) who do not use the drug, leading some researchers to speculate that methamphetamine use could result in a resurgence of the virus among MSM. The research highlights the need for targeted substance abuse programs directed toward MSM who use methamphetamine. "I see HIV in my community, and it's in drug users and drug-using gay men," said Steve Shoptaw, Ph.D., principal investigator with Friends Research Institute in Los Angeles.
"If 62 percent of the guys are infected by the time they show up for [substance abuse] treatment, then that tells me there's a high concentration of the virus where these guys interact," Shoptaw said. Drug treatment significantly reduces HIV-related sexual risk behaviors immediately, and those reductions are observed at a one-year follow-up, according to Shoptaw's most recent research.
"We see, on average, men ... reporting three or four instances of unprotected anal receptive intercourse with someone other than their primary partner at baseline in 30 days prior to their first visit," said Shoptaw. "After treatment, at one-year follow-up, it's [less than] one instance." "At baseline, there were nine to 10 average days out of 30 of meth use, and [after treatment] at a 52-week follow-up, there were three to 3.5 days." One of the first HIV prevention strategies for some MSM populations may be to encourage men to enter substance abuse treatment.
"Clinicians need to be aware of symptoms of substance abuse," said Perry N. Halkitis, Ph.D., assistant professor of psychology at New York University and co-director of the Center for HIV Educational Studies & Training in New York City. Clinicians working with MSM patients need to deal with substance abuse early, as methamphetamine typically begins as weekend party behavior, but eventually spreads to everyday use and addiction, said Halkitis. He recommends substance abuse treatment with cognitive therapy programs that use motivational interviewing to motivate people to think about and change their behavior. He advocates abstinence from the drug because "eventually dependence is not going to be eliminated with a harm reduction approach."
While not every expert on methamphetamine use among MSM would agree that total drug abstinence is the only solution, there is some agreement that some substance abuse treatment is necessary as part of an HIV prevention program. "Current [substance abuse] treatment models don't have good efficacy and come at a big expense at a clinical level," said Michael Clatts, Ph.D., medical anthropologist and associate professor of public health at Columbia University. "They break down people and try to rebuild them." For this reason, Clatts said he would recommend putting a public health emphasis on harm reduction education. (AIDS Alert, 11.01.02, Vol. 17, No. 11, P. 137)
One reason AIDS may progress is that HIV mutates so rapidly within the human body that it confounds the already-weakened immune system's ability to defend against it, researchers report. In addition, conventional tests used to determine how well a person with HIV can mount an immune defense can be misleading, researchers from Harvard Medical School's Center for Blood Research have found.
"The immune system needs to evolve along with the virus, and this evolution becomes difficult because it is in a milieu of immune deficiency," researcher Premlata Shankar told UPI. While the immune system's memory-based component might continue to resist the strain of HIV it first encountered -- or strains used in laboratory tests -- subsequent viral mutations weaken its ability to mount an effective defense. The researchers reported their findings in the article "The Functional CD8 T-Cell Response to HIV Becomes Type-Specific in Progressive Disease" in the November issue of the Journal of Clinical Investigation (2002;110:1339-1347).
HIV's ability to mutate is well-documented, but the effects of those mutations on an infected individual have not been thoroughly studied. In examining the immune system's killer cell responses to mutated forms of HIV taken from people at different stages of HIV infection, the researchers found that killer cells from patients with more advanced infections could not destroy the mutated virus, even though they could still neutralize common laboratory strains. But killer cells from people with less-advanced HIV could destroy both the lab strains and their own mutated forms.
According to immunologist Beth Jamieson of the University of California-Los Angeles' David Geffen School of Medicine, "The side-by-side comparison of cellular responses to laboratory strains and autologous [mutated after infection] strains at different stages is new. This shows that the response to virus is lost later in infection. Now we need to know why."
When a person is first infected with HIV, the immune system produces CD8-T killer and CD4-T helper cells. The system remembers the type of molecules on the surface of the attacking virus, so the next time the system encounters the virus, it produces, from memory, many cells to attack it again. But when the virus mutates, the immune system is no longer able to identify and kill the mutations. The researchers also found that much of the deficiency occurs because HIV destroys the helper cells, stopping the efficient production of new killer cells and helping weaken those that are produced. Because of this finding, Jamieson recommended further research "looking at the epitopes [surface proteins] on the virus over time in individuals."
"While there are no direct implications for diagnosis or treatment, an important motivation for this sort of study is the development of knowledge that could lead to successful HIV vaccines, both to prevent and to treat HIV infection," infectious disease specialist Stuart Ray, of the Johns Hopkins University School of Medicine in Baltimore, told UPI. (United Press International, 11.05.02, Joe Grossman)
Veterans in New York have an alarmingly high rate of hepatitis C virus (HCV) and HIV infection, according to a study published in American Journal of Gastroenterology ("Prevalence of Hepatitis C and Coinfection With HIV Among United States Veterans in the New York City Metropolitan Area," 2002;97(8):2071-2078).
Norbert Brau and colleagues at Veterans Affairs Medical Centers in the Bronx, New York City and Brooklyn, and Veterans Affairs Healthcare Systems in Hudson Valley, Montrose, and Castle Point, N.Y., and East Orange and Lyons, N.J., examined "the prevalence of coinfection with HIV and its risk factors, among patients with confirmed HCV infection." HIV/HCV coinfection was common enough -- almost a quarter of patients with HCV antibodies were coinfected with HIV -- to warrant routine testing in HCV-infected patients, Brau and coauthors found.
The researchers surveyed nearly 2,000 patients undergoing phlebotomies at six Veterans Affairs Medical Centers in the New York City metropolitan area. Just over half of these patients agreed to be tested for HCV and to provide demographic and risk factor data. More than 10 percent of the patients who agreed to be screened tested positive for HCV antibodies, and active HCV viremia was found in more than 8 percent of tested patients, data showed. Most infected patients carried HCV type one, with this genotype seen in almost 90 percent of viremic patients. Injection drug use was a strong independent risk factor for HCV infection, researchers noted, as were alcohol abuse and Vietnam-era service. (AIDS Weekly, 11.04.02, Michael Greer)
This article was provided by Body Positive. It is a part of the publication Body Positive.