HIV–positive people are unaware that they are infected with the virus. For example, less than 1% of the sexually active urban population in Africa have been tested and this proportion is even lower in rural populations. Furthermore, only 0.5% of pregnant women attending urban health facilities are counselled, tested or receive their test results. Again, this proportion is even lower in rural health facilities. Since donors may therefore be unaware of their infection, donor blood and blood products used in medicine and medical research are routinely screened for HIV.Many
HIV–1 testing consists of initial screening with an enzyme–linked immunosorbent assay (ELISA) to detect antibodies to HIV–1. Specimens with a nonreactive result from the initial ELISA are considered HIV–negative unless new exposure to an infected partner or partner of unknown HIV status has occurred. Specimens with a reactive ELISA result are retested in duplicate. If the result of either duplicate test is reactive, the specimen is reported as repeatedly reactive and undergoes confirmatory testing with a more specific supplemental test (e.g., Western blot or, less commonly, an immunofluorescence assay (IFA). Only specimens that are repeatedly reactive by ELISA and positive by IFA or reactive by Western blot are considered HIV–positive and indicative of HIV infection. Specimens that are repeatedly ELISA–reactive occasionally provide an indeterminate Western blot result, which may be either an incomplete antibody response to HIV in an infected person, or nonspecific reactions in an uninfected person. Although IFA can be used to confirm infection in these ambiguous cases, this assay is not widely used. Generally, a second specimen should be collected more than a month later and retested for persons with indeterminate Western blot results. Although much less commonly available, nucleic acid testing (e.g., viral RNA or proviral DNA amplification method) can also help diagnosis in certain situations. In addition, a few tested specimens might provide inconclusive results because of a low quantity specimen. In these situations, a second specimen is collected and tested for HIV infection.
Treatment for HIV
There is currently no vaccine or cure for HIV or AIDS. The only known method of prevention is avoiding exposure to the virus. However, a course of antiretroviral treatment administered immediately after exposure, referred to as post–exposure prophylaxis, is believed to reduce the risk of infection if begun as quickly as possible. Current treatment for HIV infection consists of highly active antiretroviral therapy, or HAART. This has been highly beneficial to many HIV–infected individuals since its introduction in 1996, when the protease inhibitor–based HAART initially became available. Current HAART options are combinations (or “Cocktails”) consisting of at least three drugs belonging to at least two types, or “Classes,” of antiretroviral agents. Typically, these classes are two nucleoside analogue reverse transcriptase inhibitors (NARTIs or NRTIs) plus either a protease inhibitor or a non–nucleoside reverse transcriptase inhibitor (NNRTI). New classes of drugs such as Entry Inhibitors provide treatment options for patients who are infected with viruses already resistant to common therapies, although they are not widely available and not typically accessible in resource–limited settings. Because AIDS progression in children is more rapid and less predictable than in adults, particularly in young infants, more aggressive treatment is recommended for children than adults. In developed countries where HAART is available, doctors assess their patients thoroughly: measuring the viral load, how fast CD4 declines, and patient readiness. They then decide when to recommend starting treatment.
HAART neither cures the patient nor does it uniformly remove all symptoms; high levels of HIV–1, often HAART resistant, return if treatment is stopped. Moreover, it would take more than a lifetime for HIV infection to be cleared using HAART. Despite this, many HIV–infected individuals have experienced remarkable improvements in their general health and quality of life, which has led to a large reduction in HIV–associated morbidity and mortality in the developed world. One study suggests the average life expectancy of an HIV infected individual is 32 years from the time of infection if treatment is started when the CD4 count is 350/µL. In the absence of HAART, progression from HIV infection to AIDS has been observed to occur at a median of between nine to ten years and the median survival time after developing AIDS is only 9.2 months. However, HAART sometimes achieves far less than optimal results, in some circumstances being effective in less than fifty percent of patients. This is due to a variety of reasons such as medication intolerance/side effects, prior ineffective antiretroviral therapy and infection with a drug–resistant strain of HIV. However, non–adherence and non–persistence with antiretroviral therapy is the major reason most individuals fail to benefit from HAART. The reasons for non–adherence and non–persistence with HAART are varied and overlapping. Major psychosocial issues, such as poor access to medical care, inadequate social supports, psychiatric disease and drug abuse contribute to non–adherence. The complexity of these HAART regimens, whether due to pill number, dosing frequency, meal restrictions or other issues along with side effects that create intentional non–adherence also contribute to this problem. The side effects include lipodystrophy, dyslipidemia, insulin resistance, an increase in cardiovascular risks and birth defects.
The timing for starting HIV treatment is still debated. There is no question that treatment should be started before the patient’s CD4 count falls below 200, and most national guidelines say to start treatment once the CD4 count falls below 350, but there is some evidence from cohort studies that treatment should be started before the CD4 count falls below 350. In those countries where CD4 counts are not available, patients with WHO stage III or IV disease should be offered treatment.
Anti–retroviral drugs are expensive, and the majority of the world’s infected individuals do not have access to medications and treatments for HIV and AIDS. Research to improve current treatments includes decreasing side effects of current drugs, further simplifying drug regimens to improve adherence, and determining the best sequence of regimens to manage drug resistance. Unfortunately, only a vaccine is thought to be able to halt the pandemic. This is because a vaccine would cost less, thus being affordable for developing countries, and would not require daily treatment. However, after over 20 years of research, HIV–1 remains a difficult target for a vaccine.
Treatments in development
Promising new treatments include Cre recombinase and the enzyme Tre recombinase, both of which are able to remove HIV from an infected cell. These enzymes promise a treatment in which a patient’s stem cells are extracted, cured, and reinjected to promulgate the enzyme into the body. The carried enzyme then finds and removes the virus.
In 2008, Dr. Gero Hütter announced that an HIV–positive leukemia patient had been “Functionally cured“ following a bone marrow transplant from a compatible donor who possessed the CCR5–Δ32 mutation (which confers resistance to HIV). After 600 days without antiretroviral drug treatment, no HIV was detectable in the patient's blood or tissues. The mortality risk associated with bone marrow transplants may contraindicate the use of this treatment for HIV–positive individuals without leukemia or lymphoma.
Sunday, Mar 26th
Last update:05:44:44 AM IST