Today, December 1st is a World AIDS day. The acquired immune deficiency syndrome (AIDS) was first recognized in the early 1980s. AIDS is caused by the human immunodeficiency virus (HIV) and is spread through the exchange of body fluids (sexual encounters, sharing needles, blood transfusions).
Etiology
Recent research suggests the virus “jumped” to humans from a West African subspecies of chimpanzee (Pan troglodytes troglodytes) intermittently decades or even centuries ago. The World Health Organization (WHO) estimates that millions are infected with HIV worldwide and that it is the most devastating epidemic since the influenza pandemic of 1918. There are some predictions that HIV will not be controlled until the middle of the next century and that it may continue to devastate developing countries for the next 100 years.
Pathology
HIV is a unique human RNA virus, capable of infecting cells of the immune system. Specifically, HIV targets T helper cells (CD4 cells), leading to the eventual death of the cell. CD4 cells are vital players in the regulation of immune responses to invading microorganisms. In an untreated person, 10 billion to 100 billion new viruses are produced per day. This massive viral replication leads to a progressive loss of CD4 cells over a period of several years to as long as a decade. And destruction of CD4 cells renders a patient vulnerable to unusual opportunistic infections (OIs) that are rarely seen in healthy humans. Most patients who die from AIDS succumb to one or more OIs.
Diagnosis
Trend in seroconversion
HIV INFECTION begins with a sharp rise of virus in the blood (orange line) and a consequent drop in CD4 T cells (blue line). The immune system soon recovers somewhat, however, and keeps HIV levels fairly steady for several years. Eventually, though, the virus gains the upper hand. AIDS is diagnosed when the CD4 T cell level drops below 200 cells per cubic millimeter of blood or when opportunistic infections arise.
Treatment
Combinations of drugs such as nucleoside reverse transcriptase inhibitors and protease inhibitors can help control viral replication, restore immune function and maintain health. We have seen patients literally on their deathbed return to full-time employment. The bad news is that long-term toxicity to virtually all these drugs has increasingly been recognized as patients take these medications for longer periods of time. In addition, patients must take the combination (commonly called HAART, for highly active anti-retroviral therapy) exactly as prescribed.
If adherence to the regimen is not perfect, HIV can quickly become resistant to the medication. And once an initial combination fails, it is less likely a second, different combination will be effective. The good news is that newer drugs active against resistant viral strains and newer approaches to treatment are on the way. It is also important to note that HIV research may lead to advances in the treatment of other viral infections, as well as cancers, metabolic diseases (diabetes, high cholesterol) and other immune system disorders.
Updates
Researchers have designed a protein that can inhibit HIV infection by blocking the virus’s entry into cells. This protective protein, known as 5-Helix, binds to a vulnerable region of an HIV coat protein called gp41, thus preventing the virus from fusing with membrane of the cell it is attacking and infecting it. What’s more, 5-Helix appears to effectively thwart a wide range of HIV strains. As such, it may serve as the basis for developing a new class of anti-HIV drugs. Alternatively it could be used in prophylactic treatments (say, after an accidental needle prick in a hospital), or perhaps as a vaccine.
Laboratory tests used to justify therapies are often misleading and misinterpreted. And though some parents fervently believe their children have benefited, the Tribune found a trail of disappointing results from the few clinical trials to evaluate the treatments objectively.