HIV AIDS (HIVP-AIDS) (HIV Potentiated AIDS)
Acquired immune deficiency syndrome (aka acquired immunodeficiency syndrome) (AIDS or Aids) is a set of symptoms and infections considered to be the result of damage to the human immune system caused by the human immunodeficiency virus (HIV), while many investigators believe a multitude of other factors contribute to the syndrome. AIDS was a well-defined medical illness long before anyone heard of HIV. Therefore, in this article, I will refer to HIVP-AIDS (HIV Potentiated AIDS).
This condition, whatever the complex of causes, progressively reduces the effectiveness of the immune system and leaves individuals susceptible to opportunistic infections and also tumors. HIV is transmitted through direct contact of mucous membrane or the bloodstream with bodily fluid containing HIV, such as blood, semen, vaginal fluid, pre-seminal fluid, and breast milk. This transmission can involve blood transfusion, anal, vaginal or oral sex, contaminated hypodermic needles, exchange between mother and baby via blood contact in the placenta during pregnancy, childbirth, or breast feeding, or other exposure to one of the above bodily fluids.
AIDS is now considered a “pandemic,” i.e. an epidemic (a sudden outbreak) that becomes widespread and affects a whole region, a continent, or the world. In 2007, an estimated 33.2 million people lived with the disease worldwide, and it killed an estimated 2.1 million people (6.33%), including 330,000 children. Over 3/4 of these deaths occurred in sub-Saharan Africa where malnutrition and starvation contributes to the syndrome and to the death rate. (Most researchers believe that HIV originated in sub-Saharan Africa during the twentieth century.)
The disease itself was first identified by the U.S. Centers for Disease Control and Prevention in 1981. The HIV virus was identified by American and French scientists in the late 1980s.
Although treatments for HIV-AIDS can slow the course of the disease and perhaps arrest it, there is currently no vaccine or cure. Anti-retroviral treatment reduces both the mortality and the morbidity of HIV-AIDS infection, but these drugs are expensive and routine access to anti-retroviral medication is not available in all countries. Due to the difficulty in treating HIV infection, preventing infection is a key aim in controlling the HIV-AIDS epidemic, with health organizations promoting safe sex and needle-exchange programs in attempts to slow the spread of the virus.
HIV-AIDS was first reported June 5, 1981, when the U.S. Centers for Disease Control and Prevention recorded a cluster of Pneumocystis carinii pneumonia (now still classified as PCP but known to be caused by Pneumocystis jirovecii) in five homosexual men in Los Angeles. In the beginning, the Centers for Disease Control and Prevention (CDC) did not have an official name for the disease, referring to it by way of the diseases that were associated with it, for example, lymphadenopathy, the disease after which the discoverers of HIV originally named the virus. They also used Kaposi’s Sarcoma and Opportunistic Infections. In the general press, the term GRID, which stood for Gay-related Immune Deficiency, was coined. The CDC, in search of a name, and looking at the infected communities coined “the 4H disease,” as it seemed to single out Haitians, homosexuals, hemophiliacs, and heroin users. After determining that HIV-AIDS was not isolated to the homosexual community, the term GRID became misleading and HIV-AIDS was introduced at a meeting in July, 1982. By September, 1982 the CDC started using the name HIV-AIDS, and properly defined the illness.
A more controversial theory known as the OPV HIV-AIDS hypothesis suggests that the HIV-AIDS epidemic was inadvertently started in the late 1950s in the Belgian Congo by Hilary Koprowski’s research into a poliomyelitis vaccine. According to scientific consensus, this scenario is not supported by the available evidence.
A recent study states that HIV probably moved from Africa to Haiti and then entered the United States around 1969.
The symptoms of HIV-AIDS are primarily the result of conditions that do not normally develop in individuals with healthy immune systems. Most of these conditions are infections caused by bacteria, viruses, fungi and parasites that are normally controlled by the immune system that HIV damages. Opportunistic infections are common in people with HIV-AIDS. HIV affects nearly every organ system. People with HIV-AIDS also have an increased risk of developing various cancers, e.g. Kaposi’s sarcoma, cervical cancer and cancers of the immune system known as lymphomas. Additionally, people with HIV-AIDS often have systemic symptoms of infection like fevers, sweats (particularly at night), swollen glands, chills, weakness, and weight loss. The specific opportunistic infections that HIV-AIDS patients develop depend in part on the prevalence of these infections in the geographic area in which the patient lives.
Pneumocystis pneumonia (originally known as Pneumocystis carinii pneumonia, and still abbreviated as PCP, which now stands for Pneumocystis pneumonia) is rare in immunocompetent people, but common among HIV-infected individuals. It is caused by Pneumocystis jirovecii. Before the advent of effective diagnosis, treatment and routine prophylaxis in Western countries, it was a common and immediate cause of death. In developing countries, it is still one of the first indications of HIV-AIDS in untested individuals, although it does not generally occur unless the CD4 count is less than 200.
Tuberculosis (TB) is unique among infections associated with HIV because it is transmissible to immunocompetent people via the respiratory route, easily treatable once identified, may occur in early-stage HIV disease, and is preventable with drug therapy. However, multi-drug resistance is a potentially serious problem. Even though the incidence of TB has declined due to the use of effective antibiotics and other improved practices in Western countries, this is not the case in developing countries where HIV is most prevalent. In early-stage HIV infection (CD4 count greater than 300), TB typically presents as a pulmonary disease. In advanced HIV infection, TB often presents atypically with systemic manifestations a common feature. Symptoms are not localized to one particular site, often affecting bone marrow, bone, urinary and gastrointestinal tracts, liver, regional lymph nodes, and the central nervous system or combinations thereof.
Esophagitis is inflammation of the esophagus (usually the lining of the lower end). In HIV infected individuals this is normally due to fungal (candidiasis) or viral (herpes simplex-1 or cytomegalovirus) infections. In rare cases, it can be due to mycobacteria.
Unexplained chronic diarrhea in HIV infection is due to many possible causes, including common bacterial (Listeria, Campylobacter, Salmonella, Shigella,) and parasitic infections; also uncommon opportunistic infections such as cryptosporidiosis, microsporidiosis, astrovirus, adenovirus, rotavirus, Mycobacterium avium complex (MAC) and cytomegalovirus, Diarrhea may be a side effect of several drugs used to treat HIV, or it may simply accompany HIV infection, particularly during primary HIV infection. It may also be a side effect of antibiotics used to treat bacterial causes of diarrhea (common for Clostridium difficile). In the later stages of HIV infection, diarrhea is thought to be a reflection of changes in the way the intestinal tract absorbs nutrients, and may be an important component of HIV-related wasting.
Neurological and Psychiatric Symptoms
HIV infection may lead to a variety of neuropsychiatric sequelae, either by infection of the now susceptible nervous system by organisms, or as a direct consequence of the illness itself.
Toxoplasmosis is a disease caused by the single-celled parasite Toxoplasma gondii. It usually infects the brain causing toxoplasma encephalitis but it can infect and cause disease in the lungs and eyes as well.
Cryptococcal meningitis is an infection of the meninges (the membranes enclosing the brain and spinal cord) by the fungus Cryptococcus neoformans. It can cause fevers, headache, fatigue, nausea, and vomiting. Patients may also develop seizures and confusion. Untreated, it can be fatal.
Progressive multifocal leukoencephalopathy (PML) is a demyelinating disease, in which the gradual destruction of the myelin sheath covering the axons of nerve cells impairs the transmission of nerve impulses. It is caused by a virus which occurs in 70% of the population in latent form, causing disease only when the immune system has been severely weakened, as is the case for HIV-AIDS patients. It progresses rapidly, usually causing death within months of diagnosis.
HIV-AIDS dementia complex (ADC) is a metabolic encephalopathy induced by HIV infection and fueled by immune activation of HIV infected brain macrophages and microglia which secrete neurotoxins of both host and viral origin. Specific neurological impairments are manifested by cognitive, behavioral, and motor abnormalities that occur after years of HIV infection, associated with low CD4+ T cell levels and high plasma viral loads. Prevalence is 10–20% in Western countries but only 1–2% of HIV infections in India. This difference is possibly due to the HIV subtype in India.
HIV-AIDS related mania is sometimes seen in patients with advanced HIV illness; it presents with more irritability and cognitive impairment and less euphoria than a manic episode associated with true bipolar disorder. Unlike the latter condition, it may have a more chronic course. This syndrome is less common with the advent of multi-drug therapy.
Tumors and Malignancies
Patients with HIV infection have substantially increased incidence of several malignant cancers. This is primarily due to co-infection with an oncogenic DNA virus, especially Epstein-Barr virus (EBV), Kaposi’s sarcoma-associated herpesvirus (KSHV), and human papillomavirus (HPV).
Kaposi’s sarcoma (KS) is the most common tumor in HIV-infected patients. The appearance of this tumor in young homosexual men in 1981 was one of the first hints of the coming HIV-AIDS epidemic. Caused by a gamma herpes virus called Kaposi’s sarcoma-associated herpes virus (KSHV), it often appears as purplish nodules on the skin, but can affect other organs, especially the mouth, GI tract, and lungs.
High-grade B cell lymphomas such as Burkitt’s lymphoma, Burkitt’s-like lymphoma, diffuse large B-cell lymphoma (DLBCL), and primary central nervous system lymphoma present more often in HIV-infected patients. These particular cancers often foreshadow a poor prognosis.
Cervical cancer in HIV-infected women is rhought of as associated with HIV-AIDS. It is caused by human papillomavirus (HPV).
In addition to the HIV-AIDS-defining tumors listed above, HIV-infected patients are at increased risk of certain other tumors, such as Hodgkin’s disease and anal and rectal cancers. However, the incidence of many common tumors, such as breast cancer or colon cancer, does not increase in HIV-infected patients. In areas where HAART (highly active anti-retroviral treatment) is used to treat HIV-AIDS, the incidence of many HIV-AIDS-related malignancies has decreased, but at the same time malignant cancers overall have become the most common cause of death of HIV-infected patients.
Other Opportunistic Infections
HIV-AIDS patients often develop infections that present with non-specific symptoms, especially wight loss and low-grade fever. These include infection with Mycobacterium avium-intracellulare and cytomegalovirus (CMV). CMV can cause colitis and CMV retinitis which can cause blindness. Penicilliosis due to Penicillium marneffei is another common opportunistic infection (along with extrapulmonary tuberculosis and cryptococcosis) in HIV-positive individuals. This is especially true in Southeast Asia.
Progression of Disease
In the absence of anti-retroviral therapy, the median time of progression from HIV infection to HIV-AIDS is nine to ten years, and the median survival time after developing HIV-AIDS is only 9.2 months. However, the rate of clinical disease progression varies widely between individuals, from two weeks up to 20 years. Factors which influence the body’s ability to defend against HIV include the general immune function. Older people have weaker immune systems, and therefore have a greater risk of rapid disease progression. Poor access to health care and the existence of coexisting infections such as tuberculosis also may predispose people to faster disease progression. Genetic inheritance plays an important role and some people are resistant to certain strains of HIV.
Sexual transmission occurs with contact between sexual secretions of one person with the rectal, genital or oral mucous membranes of another. Unprotected receptive sexual acts are riskier than unprotected insertive sexual acts, and the risk for transmitting HIV through unprotected anal intercourse is greater than the risk from vaginal intercourse or oral sex. However, oral sex is not entirely safe, and HIV can be transmitted through both insertive and receptive oral sex. The risk of HIV transmission from exposure to saliva is much smaller than the risk from exposure to semen. It is believed that one would have to swallow liters of saliva from a carrier to run a significant risk of becoming infected. Sexual assault greatly increases the risk of HIV transmission as protection is rarely employed and physical trauma to the vagina frequently occurs.
Other sexually transmitted infections (STIs) increase the risk of HIV transmission and infection, as they cause the disruption of normal epithelial barrier integrity by genital ulceration and by accumulation of pools of HIV-susceptible or HIV-infected cells (lymphocytes and macrophages) in semen and vaginal secretions. Genital ulcers, such as those caused by syphilis and/or chancroid, increase the risk of becoming infected with HIV by about four-fold. There is also a significant although lesser increase in risk from STIs such as gonorrhea, Chlamydial infection and trichomoniasis, which all cause local accumulations of lymphocytes and macrophages.
Transmission of HIV depends on the infectiousness of the infected partner and the susceptibility of the uninfected partner. Infectivity seems to vary during the course of illness and is not constant between individuals. An undetectable plasma viral load does not necessarily indicate a low viral load in the seminal liquid or genital secretions. However, each 10-fold increase in the level of HIV in the blood is associated with an 81% increased rate of HIV transmission. Women are more susceptible to HIV-1 infection due to hormonal changes, vaginal microbial ecology and physiology, and a higher prevalence of sexually transmitted diseases. People who have been infected with one strain of HIV can still be infected later on in their lives by other, more virulent strains.
Exposure to Blood-borne Pathogens
This transmission route is particularly relevant to intravenous drug users, hemophiliacs and recipients of blood transfusions and blood products. Sharing and reusing syringes contaminated with HIV-infected blood represents a major risk for infection with HIV. Needle sharing is the cause of one third of all new HIV-infections in North America, China, and Eastern Europe.
The risk of transmitting HIV to blood transfusion recipients is extremely low in developed countries where improved donor selection and HIV screening is performed. However, the overwhelming majority of the world’s population does not have access to safe blood and between 5% and 10% of the world’s HIV infections come from transfusion of infected blood and blood products.
Transmission of the virus from mother to child can occur in utero during the last weeks of pregnancy and at childbirth. In the absence of treatment, the transmission rate between a mother and her child during pregnancy, labor and delivery is around 25%. However, when the mother takes anti-retroviral therapy and gives birth by caesarean section, the rate of transmission is just 1%. The risk of infection is influenced by the viral load of the mother at birth, with the higher the viral load, the higher the risk. Breast feeding also increases the risk of transmission by about 4 %.
Many misconceptions have arisen surrounding HIV/HIV-AIDS. Three of the most common are that HIV-AIDS can spread through casual contact, that sexual intercourse with a virgin will cure HIV-AIDS, and that HIV can infect only homosexual men and drug users. Other misconceptions are that any act of anal intercourse between gay men can lead to HIV-AIDS infection.
The pathophysiology of HIV-AIDS is complex. HIV is believed to trigger HIV-AIDS by depleting CD4+ T helper lymphocytes which weakens the immune system and allows opportunistic infections. T lymphocytes are essential to immune response and without them, the body cannot fight infections or kill cancerous cells.
During the acute phase, HIV-induced cell lysis and killing of infected cells by cytotoxic T cells accounts for CD4+ T cell depletion. Apoptosis (A form of cell death in which a programmed sequence of events leads to the elimination of cells without releasing harmful substances into the surrounding area) may also be a factor.
During the chronic phase, the consequences of generalized immune activation coupled with the gradual loss of the ability of the immune system to generate new T cells appear to account for the slow decline in CD4+ T cell numbers.
Although the symptoms of immune deficiency characteristic of HIV-AIDS do not appear for years after a person is infected, the bulk of CD4+ T cell loss occurs during the first weeks of infection, especially in the intestinal mucosa, which harbors the majority of the lymphocytes found in the body. A vigorous immune response eventually controls the infection and initiates the latent phase. However, CD4+ T cells in mucosal tissues remain depleted throughout the infection, although enough remain to initially ward off life-threatening infections.
Continuous HIV replication results in a state of generalized immune activation which persists throughout the chronic phase. Immune activation results in the release of inflammatory cytokines. There is also a breakdown of the immune surveillance system of the mucosal barrier caused by the depletion of mucosal CD4+ T cells during the acute phase of disease which results in the body-wide exposure of the immune system to microbial components of the gut’s normal flora. In a healthy person this is kept in check by the mucosal immune system. The activation and proliferation of T cells that results from immune activation provides fresh targets for HIV infection.
Direct killing of CD$+ T cells by HIV alone cannot account for the observed depletion of these cells since only 0.01-0.10% of CD4+ T cells in the blood are infected. A major cause of CD4+ T cell loss appears to result from their heightened susceptibility to apoptosis when the immune system remains activated. In other words, they kill themselves. Although new T cells are continuously produced by the thymus to replace the ones lost, the regenerative capacity of the thymus is slowly destroyed by direct infection of its thymocytes by HIV. Eventually, the minimal number of CD4+ T cells necessary to maintain a sufficient immune response is lost, leading to HIV-AIDS
The virus, entering through which ever route, acts on the following cells:
- Lymphoreticular system:
- CD4+ T-Helper cells
- CD4+ Monocytes
- CD4+ Macrophages
- Certain endothelial cells
- Central nervous system:
- Microglia of the nervous system
- Astrocytes of the nervous system
- Oligodendrocytes of the nervous system
- Neurons of the nervous system (indirectly by the action of cytokines)
The Effect of HIV
How the virus weakens these cells is still not clear. It can remain inactive in these cells for long periods. The most prominent effect of the HIV virus is its T-helper cell suppression and destruction. The cell is simply killed off or deranged to the point of being useless (not responding to foreign antigens). The infected B-cells can not produce enough antibodies either. Thus the immune system collapses leading to the familiar HIV-AIDS complications, for example infections and neoplasms. The effect is to weaken resistance to other viruses, e.g. Cytomegalovirus, Hepatitis virus, Herpes simplex virus, etc. These viruses lead to further cell damage.
Here are the stages of HIV-AIDS:
- Stage I: HIV infection is asymptomatic and not categorized as HIV-AIDS
- Stage II: includes minor mucocutaneous manifestations and recurrent upper respiratory tract infections
- Stage III: includes unexplained chronic diarrhea for longer than a month, severe bacterial infections and pulmonary tuberculosis
- Stage IV: includes toxoplasmosis of the brain, candidiasis of the esophagus, trachea, bronchi or lungs and Kaposi’s sarcoma; these diseases are indicators of HIV-AIDS.
Many people are unaware that they are infected with HIV, especially in Africa. Less than 1% of the sexually active urban population in Africa has been tested, and this proportion is even lower in rural populations. Furthermore, only 0.5% of pregnant women attending urban health facilities are counseled, tested or receive their test results.
HIV tests are usually performed on venous blood. Many laboratories use fourth generation screening tests which detect anti-HIV antibody (IgG and IgM) and the HIV p24 antigen. The detection of HIV antibody or antigen in a patient previously known to be negative is evidence of HIV infection. Individuals whose first specimen indicates evidence of HIV infection will have a repeat test on a second blood sample to confirm the results.
The window period (time between initial infection and the development of detectable antibodies) can vary, taking 3–6 months to seroconvert and test positive. Detection of the virus using polymerase chain reaction (PCR) during the window period is possible, and evidence suggests that an infection may often be detected earlier with a fourth generation EIA screening test. Positive results obtained by PCR are confirmed by antibody tests. HIV tests for infection in neonates born to HIV-positive mothers have no value because of the presence of maternal antibody to HIV in the child’s blood. HIV infection can only be diagnosed by PCR, testing for HIV pro-viral DNA in the children’s lymphocytes.
The majority of HIV infections are acquired through unprotected sexual relations between partners. The primary mode of HIV infection worldwide is through sexual contact between members of the opposite sex. During a sexual act, only male or female condoms can reduce the chances of infection with HIV. Typical condom use reduces the risk of heterosexual HIV transmission by approximately 80% over the long-term. The benefit is likely to be higher if condoms are used correctly on every occasion. The male latex condom, if used correctly without oil-based lubricants, is the single most effective available technology to reduce sexual transmission of HIV. Manufacturers recommend that oil-based lubricants such as petroleum jelly, butter, and lard not be used with latex condoms, because they dissolve the latex, making the condoms porous. If necessary, manufacturers recommend using water-based lubricants. Oil-based lubricants can however be used with polyurethane condoms.
The female condom is an alternative to the male condom and is made from polyurethane, thus allowing the use of oil-based lubricants. They are larger than male condoms and are designed to be inserted into the vagina. The female condom contains an inner ring, which keeps the condom in place inside the vagina – inserting the female condom requires squeezing this ring. However, availability of female condoms is very low and the price remains prohibitive for many women. Studies suggest that, where female condoms are available, overall protected sexual acts increase relative to unprotected sexual acts, making them an important HIV prevention strategy.
Studies of couples where one partner is infected show that with consistent condom use, HIV infection rates for the uninfected partner are below 1% per year. Prevention strategies are well-known in developed countries, however recent studies in Europe and North America have suggested that a substantial minority of young people continue to engage in high-risk practices and that despite HIV-AIDS knowledge, young people underestimate the risk of becoming infected.
Male circumcision lowers the risk of HIV infection among heterosexual men by up to 60%. It is expected that this procedure will be actively promoted in many of the countries affected by HIV, although doing so will involve confronting a number of practical, cultural and attitudinal issues. Some experts fear that a lower perception of vulnerability among circumcised men may result in more sexual risk-taking behavior, thus negating its preventive effects.
Exposure to Infected Body Fluids
Health care workers can reduce exposure by employing precautions to reduce the risk of exposure to contaminated blood. These precautions include barriers such as gloves, masks, protective eye-ware or shields, and gowns or aprons which prevent exposure of the skin or mucous membranes to blood-borne pathogens. Frequent and thorough washing of the skin immediately after being contaminated with blood or other bodily fluids can reduce the chance of infection. Sharp objects like needles, scalpels and glass, should be carefully disposed of to prevent needle stick injuries with contaminated items. Since intravenous drug use is an important factor in HIV transmission in developed countries, strategies such as needle-exchange programs are used to reduce the infections caused by drug abuse.
Current recommendations state that when replacement feeding is acceptable, feasible, affordable, sustainable and safe, HIV-infected mothers should avoid breast-feeding their infant. However, if this is not the case, exclusive breast-feeding is recommended during the first months of life and discontinued as soon as possible.
Current treatment for HIV infection consists of highly active anti-retroviral therapy (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 optimal HAART options consist of combinations (or “cocktails”) consisting of at least three drugs belonging to at least two types, or “classes,” of anti-retroviral agents. Typical regimens consist of two nucleoside analogue reverse transcriptase inhibitors (NARTIs or NRTIs) plus either a protease inhibitor or a non-nucleoside reverse transcriptase inhibitor (NNRTI). Because HIV disease progression in children is more rapid than in adults, and laboratory parameters are less predictive of risk for disease progression, particularly for young infants, treatment recommendations are more aggressive for children than for adults. HAART allows the stabilization of the patient’s symptoms and viremia, but it neither cures the patient of HIV, nor alleviates the symptoms. Patients with high levels of HIV-1, often HAART resistant, return once treatment is stopped. Moreover, it would take more than the lifetime of an individual to be cleared of HIV infection using HAART. Despite this, many HIV-infected individuals have experienced remarkable improvements in their general health and quality of life, which has led to the plummeting of HIV-associated morbidity and mortality. In the absence of HAART, progression from HIV infection to HIV-AIDS occurs at a median of between nine to ten years and the median survival time after developing HIV-AIDS is only 9.2 months. HAART is thought to increase survival time by between 4 and 12 years.
For more than ½ of patients, HAART achieves less than optimal results, due to medication side effects, prior ineffective anti-retroviral therapy and infection with a drug-resistant strain of HIV. Non-adherence and non-persistence with therapy are the major reasons why some people do not benefit from HAART. Major problems include poor access to medical care, inadequate social supports, psychiatric disease and drug abuse. HAART regimens can also be complex and hard to follow, with large numbers of pills taken frequently. Side effects can also deter people from persisting with HAART, including lipodystrophy, dyslipidaemia, diarrhea, insulin resistance, and an increase in cardiovascular risks and birth defects. 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 HIV-AIDS.
Estimated prevalence of HIV among young adults (15-49) can be seen as several epidemics of separate subtypes; the major factors in its spread are sexual transmission and transmission from mother to child at birth and through breast milk. Despite recent, improved access to anti-retroviral treatment and care in many regions of the world, the HIV-AIDS pandemic claimed an estimated 2.1 million lives in 2007 of which an estimated 330,000 were children under 15 years. Globally, an estimated 33.2 million people lived with HIV in 2007, including 2.5 million children and an estimated 2.5 million people were newly infected in 2007, including 420,000 children. Sub-Saharan Africa remains by far the worst affected region. Unlike other regions, most people living with HIV in sub-Saharan Africa in 2007 (61%) were women. Adult prevalence in 2007 was an estimated 5.0%, and HIV-AIDS continued to be the single largest cause of mortality. South and southeast Asia are second worst affected. In 2007 this region contained an estimated 18% of all people living with HIV-AIDS, and an estimated 300,000 deaths from HIV-AIDS. Life expectancy has fallen dramatically in the worst-affected countries; for example, in 2006 it was estimated that it had dropped from 65 to 35 years in Botswana.
Various forms of alternative medicine are used to treat symptoms and alter the course of the AIDS. Acupuncture has been used to alleviate some symptoms such peripheral neuropathy but cannot cure the HIV infection. Several randomized clinical trials testing the effect of herbal medicines have shown no evidence that these herbs effect progression of the disease.
Some data suggest that multivitamin and mineral supplements may reduce HIV disease progression in adults, although there is no conclusive evidence they reduce mortality among people with good nutritional status. Vitamin A supplementation in children seems to have benefit. Daily doses of selenium can suppress HIV viral burden with an associated improvement of the CD4 count. Selenium can be used as an adjunctive therapy to standard antiviral treatments, but cannot itself reduce mortality and morbidity.
Alternative medicine therapies may improve the quality of life of individuals afflicted with HIV-AIDS.
It has been postulated that only a vaccine can halt the pandemic because a vaccine would possibly cost less, being affordable in developing countries, and would not require daily treatment. However, even after almost 30 years of research, HIV-1 remains a difficult target for a vaccine.
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. Vaccination against hepatitis A and B is advised for patients who are not infected with these viruses and are at risk of becoming infected. Patients with substantial immuno-suppression are also advised to receive prophylactic therapy for Pneumocystis jiroveci pneumonia (PCP), and many patients may benefit from prophylactic therapy for toxoplasmosis and Cryptococcus meningitis as well.
Without treatment, the median survival time after infection with HIV is estimated to be 9 to 11 years, depending on the HIV subtype. The median survival rate after diagnosis of HIV-AIDS in resource-limited settings where treatment is not available ranges between 6 and 19 months. In areas where it is widely available, the development of HAART as effective therapy for HIV infection and HIV-AIDS reduced the death rate from this disease by 80%, and raised the life expectancy for a newly-diagnosed HIV-infected person to about 20 years.
As new treatments continue to be developed and because HIV continues to evolve resistance to treatments, estimates of survival time are likely to continue to change. Without anti-retroviral therapy, death normally occurs within a year. Most patients die from opportunistic infections or malignancies associated with the progressive failure of the immune system.