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Chronic Care Programme
Treatment guidelines
HIV/Aids
Chronic condition
Alternative names
Consultations protocols
Preferred treating provider
Notes
 preferred as indicated by option
 referral protocols apply
Provider
General Practitioner
Physician
Paediatrician
Cardiologist
Neurologist
Neurosurgeon
Maximum consultations per annum
 Initial consultation
 Follow-up consultation
Tariff codes
New Patient
Option/plan
GMHPP
Gold Options
G1000, G500 and
G200.
Blue Options
B300 and B200.
GMISHPP
Existing patient
Stable
Unstable
Controlled
Uncontrolled
1
1
3
1
0183; 0142; 0187; 0108
1
5
Investigations protocols
ICD 10 coding
G40.-G41.
General
Acquired Immune Deficiency Syndrome(AIDS) is a set of symptoms and infections resulting
from the damage to the human immune system caused by the human immunodeficiency virus
(HIV). This condition progressively reduces the effectiveness of the immune system and leaves
individuals susceptible to opportunistic infections and tumors. HIV is transmitted through direct
contact of a mucous membrane or the bloodstream with a bodily fluid containing HIV, such as
blood, semen, vaginal fluid, preseminal fluid, and breast milk. This transmission can involve anal,
vaginal or oral sex, blood transfusion, contaminated hypodermic needles, exchange between
mother and baby during pregnancy, childbirth, or breastfeeding, or other exposure to one of the
above bodily fluids.
AIDS is now a pandemic. In 2007, an estimated 33.2 million people lived with the disease
worldwide, and it killed an estimated 2.1 million people, including 330,000 children. Over
three-quarters of these deaths occurred in sub-Saharan Africa, retarding economic growth and
destroying human capital. Most researchers believe that HIV originated in sub-Saharan Africa
during the twentieth century. The disease was first identified by the U.S. Centers for Disease
Control and Prevention in 1981 and its cause identified by American and French scientists in
the late 1980s. Although treatments for AIDS and HIV can slow the course of the disease, there
is currently no vaccine or cure. Antiretroviral treatment reduces both the mortality and the
morbidity of HIV infection, but these drugs are expensive and routine access to antiretroviral
medication is not available in all countries. Due to the difficulty in treating HIV infection,
preventing infection is a key aim in controlling the AIDS epidemic, with health organizations
promoting safe sex and needle-exchange programmes in attempts to slow the spread of the virus
Signs and symptoms
The symptoms of 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 elements of the immune
system that HIV damages. Opportunistic infections are common in people with AIDS. HIV
affects nearly every organ system. People with AIDS also have an increased risk of developing
various cancers such as Kaposi's sarcoma, cervical cancer and cancers of the immune system
known as lymphomas. Additionally, people with 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 AIDS patients develop depend in part on the
prevalence of these infections in the geographic area in which the patient lives.
Pulmonary infections
X-ray of Pneumocystis jirovecii caused pneumonia. There is increased white (opacity) in the
lower lungs on both sides, characteristic of Pneumocystis pneumonia
Pneumocystis pneumonia (originally known as Pneumocystis carinii pneumonia, and still
abbreviated as PCP, which now stands for Pneumocystis pneumonia) is relatively rare in healthy,
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 immediate cause of death. In developing
countries, it is still one of the first indications of AIDS in untested individuals, although it does
not generally occur unless the CD4 count is less than 200 cells per µL of blood.
Tuberculosis (TB) is unique among infections associated with HIV because it is transmissible to
immunocompetent people via the respiratory route, is easily treatable once identified, may occur
in early-stage HIV disease, and is preventable with drug therapy. However, multidrug resistance
is a potentially serious problem. Even though its incidence has declined because of the use of
directly observed therapy 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
>300 cells per µL), TB typically presents as a pulmonary disease. In advanced HIV infection, TB
often presents atypically with extrapulmonary (systemic) disease a common feature. Symptoms
are usually constitutional and 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.
Gastrointestinal infections
Esophagitis is an inflammation of the lining of the lower end of the esophagus (gullet or
swallowing tube leading to the stomach). In HIV infected individuals, this is normally due to
fungal (candidiasis) or viral (herpes simplex-1 or cytomegalovirus) infections. In rare cases, it
could be due to mycobacteria.
Unexplained chronic diarrhea in HIV infection is due to many possible causes, including common
bacterial (Salmonella, Shigella, Listeria or Campylobacter) and parasitic infections; and
uncommon opportunistic infections such as cryptosporidiosis, microsporidiosis, Mycobacterium
avium complex (MAC) and viruses, astrovirus, adenovirus, rotavirus and cytomegalovirus, (the
latter as a course of colitis). In some cases, 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 diseases
Toxoplasmosis is a disease caused by the single-celled parasite called Toxoplasma gondii; it
usually infects the brain causing toxoplasma encephalitis but it can infect and cause disease in the
eyes and lungs.
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 called JC 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 AIDS patients. It progresses rapidly, usually causing death within
months of diagnosis. 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 and is 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.
Cryptococcal meningitis is an infection of the meninx (the membrane covering 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; left untreated, it can be
lethal.
Tumors and malignancies
Kaposi's sarcoma
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 signals of the AIDS epidemic.
Caused by a gammaherpes 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,
gastrointestinal 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. In some cases
these lymphomas are AIDS-defining. Epstein-Barr virus (EBV) or KSHV cause many of these
lymphomas.
Cervical cancer in HIV-infected women is considered AIDS-defining. It is caused by human
papillomavirus (HPV).
In addition to the 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 carcinomas. 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 is extensively used to treat AIDS, the incidence of
many 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
AIDS patients often develop opportunistic infections that present with non-specific symptoms,
especially low-grade fevers and weight loss. These include infection with Mycobacterium aviumintracellulare and cytomegalovirus (CMV). CMV can cause colitis, as described above, and
CMV retinitis can cause blindness. Penicilliosis due to Penicillium marneffei is now the third
most common opportunistic infection (after extrapulmonary tuberculosis and cryptococcosis) in
HIV-positive individuals within the endemic area of Southeast Asia.
Diagnosis
Scanning electron micrograph of HIV-1, colored green, budding from a cultured lymphocyte.
AIDS is the most severe acceleration of infection with HIV. HIV is a retrovirus that primarily
infects vital organs of the human immune system such as CD4+ T cells (a subset of T cells),
macrophages and dendritic cells. It directly and indirectly destroys CD4+ T cells. Once HIV has
killed so many CD4+ T cells that there are fewer than 200 of these cells per microliter (µL) of
blood, cellular immunity is lost. Acute HIV infection progresses over time to clinical latent HIV
infection and then to early symptomatic HIV infection and later to AIDS, which is identified
either on the basis of the amount of CD4+ T cells remaining in the blood, and/or the presence of
certain infections, as noted above.
In the absence of antiretroviral therapy, the median time of progression from HIV infection to
AIDS is nine to ten years, and the median survival time after developing AIDS is only 9.2
months. However, the rate of clinical disease progression varies widely between individuals, from
two weeks up to 20 years. Many factors affect the rate of progression. These include factors that
influence the body's ability to defend against HIV such as the infected person's general immune
function. Older people have weaker immune systems, and therefore have a greater risk of rapid
disease progression than younger people. Poor access to health care and the existence of
coexisting infections such as tuberculosis also may predispose people to faster disease
progression. The infected person's genetic inheritance plays an important role and some people
are resistant to certain strains of HIV. An example of this is people with the homozygous CCR5Δ32 variation are resistant to infection with certain strains of HIV. HIV is genetically variable and
exists as different strains, which cause different rates of clinical disease progression.
Sexual transmission
Sexual transmission occurs with the 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, as HIV can be transmitted through both insertive and receptive oral sex. The risk of
HIV transmission from exposure to saliva is considerably smaller than the risk from exposure to
semen, 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, facilitating the transmission
of HIV.
Other sexually transmitted infections (STI) increase the risk of HIV transmission and infection,
because they cause the disruption of the normal epithelial barrier by genital ulceration and/or
microulceration; and by accumulation of pools of HIV-susceptible or HIV-infected cells
(lymphocytes and macrophages) in semen and vaginal secretions. Epidemiological studies from
sub-Saharan Africa, Europe and North America suggest that 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 index case 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 being infected with HIV from a single prick with a needle that has been used on an HIVinfected person is thought to be about 1 in 150 (see table above). Post-exposure prophylaxis with
anti-HIV drugs can further reduce this risk. This route can also affect people who give and
receive tattoos and piercings. Universal precautions are frequently not followed in both subSaharan Africa and much of Asia because of both a shortage of supplies and inadequate training.
The WHO estimates that approximately 2.5% of all HIV infections in sub-Saharan Africa are
transmitted through unsafe healthcare injections. Because of this, the United Nations General
Assembly has urged the nations of the world to implement precautions to prevent HIV
transmission by health workers.
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, according
to the WHO, 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.
Perinatal transmission
The transmission of the virus from the mother to the 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 25%. However, when the mother
takes antiretroviral 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. Breastfeeding also increases the risk of transmission by about 4 %.
Misconceptions
A number of misconceptions have arisen surrounding HIV/AIDS. Three of the most common are
that AIDS can spread through casual contact, that sexual intercourse with a virgin will cure 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 AIDS infection, and that open discussion of
homosexuality and HIV in schools will lead to increased rates of homosexuality and AIDS.
The Pathophysiology.
The pathophysiology of AIDS is complex, as is the case with all syndromes. Ultimately, HIV
causes AIDS by depleting CD4+ T helper lymphocytes. This weakens the immune system and
allows opportunistic infections. T lymphocytes are essential to the immune response and without
them, the body cannot fight infections or kill cancerous cells. The mechanism of CD4+ T cell
depletion differs in the acute and chronic phases. During the acute phase, HIV-induced cell lysis
and killing of infected cells by cytotoxic T cells accounts for CD4+ T cell depletion, although
apoptosis 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 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. The reason for the preferential loss of mucosal CD4+ T cells is that a majority of mucosal
CD4+ T cells express the CCR5 coreceptor, whereas a small fraction of CD4+ T cells in the
bloodstream do so. HIV seeks out and destroys CCR5 expressing CD4+ cells during acute
infection. A vigorous immune response eventually controls the infection and initiates the
clinically 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 persisting
throughout the chronic phase. Immune activation, which is reflected by the increased activation
state of immune cells and release of proinflammatory cytokines, results from the activity of
several HIV gene products and the immune response to ongoing HIV replication. Another cause
is the 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. This results in the systemic
exposure of the immune system to microbial components of the gut’s normal flora, which in a
healthy person 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. However,
direct killing by HIV alone cannot account for the observed depletion of CD4+ T 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. 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 AIDS
Cells affected
The virus, entering through which ever route, acts primarily on the following cells:
1. Lymphoreticular system:
1. CD4+ T-Helper cells
2. CD4+ Macrophages
3. CD4+ Monocytes
4. B-lymphocytes
2. Certain endothelial cells
3. Central nervous system:
1. Microglia of the nervous system
2. Astrocytes
3. Oligodendrocytes
4. Neurones - indirectly by the action of cytokines and the gp-120
The effect
The virus has cytopathic effects but how it does it is still not quite clear. It can remain inactive in
these cells for long periods, though. This effect is hypothesized to be due to the CD4-gp120
interaction.



The most prominent effect of the HIV virus is its T-helper cell suppression and lysis. The
cell is simply killed off or deranged to the point of being function-less (they do not
respond to foreign antigens). The infected B-cells can not produce enough antibodies
either. Thus the immune system collapses leading to the familiar AIDS complications, like
infections and neoplasms (vide supra).
Infection of the cells of the CNS cause acute aseptic meningitis, subacute encephalitis,
vacuolar myelopathy and peripheral neuropathy. Later it leads to even AIDS dementia
complex.
The CD4-gp120 interaction (vide supra) is also permissive to other viruses like
Cytomegalovirus, Hepatitis virus, Herpes simplex virus, etc. These viruses lead to further
cell damage i.e. cytopathy.
Molecular basis
For details, see:



Structure and genome of HIV,
HIV replication cycle
HIV tropism
Treatment
There is currently no vaccine or cure for HIV or AIDS. The only known methods of prevention
are based on avoiding exposure to the virus or, failing that, an antiretroviral treatment directly
after a highly significant exposure, called post-exposure prophylaxis (PEP). PEP has a very
demanding four week schedule of dosage. It also has very unpleasant side effects including
diarrhea, malaise, nausea and fatigue.
Antiviral therapy
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 optimal HAART
options consist of combinations (or "cocktails") consisting of at least three drugs belonging to at
least two types, or "classes," of antiretroviral 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. In developed countries where HAART is available,
doctors assess the viral load, rapidity in CD4 decline, and patient readiness while deciding when
to recommend initiating treatment.
HAART allows the stabilization of the patient’s symptoms and viremia, but it neither cures the
patient of HIV, nor alleviates the symptoms, and 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 AIDS occurs at a median of between nine to ten years and the
median survival time after developing AIDS is only 9.2 months. HAART is thought to increase
survival time by between 4 and 12 years.
For some patients, which can be more than fifty percent of patients, HAART achieves far less
than optimal results, due to medication intolerance/side effects, prior ineffective antiretroviral
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. The reasons
for non-adherence and non-persistence are varied. Major psychosocial issues include poor access
to medical care, inadequate social supports, psychiatric disease and drug abuse. HAART
regimens can also be complex and thus hard to follow, with large numbers of pills taken
frequently. Side effects can also deter people from persisting with HAART, these include
lipodystrophy, dyslipidaemia, diarrhoea, insulin resistance, 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 AIDS.
Future research
It has been postulated that only a vaccine can halt the pandemic because a vaccine would possibly
cost less, thus being affordable for developing countries, and would not require daily treatments.
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. A number of studies have shown that measures to prevent
opportunistic infections can be beneficial when treating patients with HIV infection or AIDS.
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 immunosuppression 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.
Alternative medicine
Various forms of alternative medicine have been used to treat symptoms or alter the course of the
disease. 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 that there is no evidence that these herbs have any effect on the
progression of the disease, but may instead produce serious side-effects.
Some data suggest that multivitamin and mineral supplements might reduce HIV disease
progression in adults, although there is no conclusive evidence on if they reduce mortality among
people with good nutritional status. Vitamin A supplementation in children probably has some
benefit. Daily doses of selenium can suppress HIV viral burden with an associated improvement
of the CD4 count. Selenium can be used as an adjunct therapy to standard antiviral treatments, but
cannot itself reduce mortality and morbidity.
Current studies indicate that that alternative medicine therapies have little effect on the mortality
or morbidity of the disease, but may improve the quality of life of individuals afflicted with
AIDS. The psychological benefits of these therapies are the most important use
Medicine formularies
Plan or option
GMHPP
Gold Options
G1000, G500 and
G200
Blue Options
B300 and B200
GMISHPP
Blue Option B100
[Link to appropriate Mediscor formulary]
[Core]
n/a
Epidemiology
The AIDS pandemic can also be seen as several epidemics of separate subtypes; the major factors
in its spread are sexual transmission and vertical transmission from mother to child at birth and
through breast milk. Despite recent, improved access to antiretroviral treatment and care in many
regions of the world, the AIDS pandemic claimed an estimated 2.1 million (range 1.9–
2.4 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. An
estimated 2.5 million (range 1.8–4.1 million) people were newly infected in 2007, including
420,000 children.
Sub-Saharan Africa remains by far the worst affected region. In 2007 it contained an estimated
68% of all people living with AIDS and 76% of all AIDS deaths, with 1.7 million new infections
bringing the number of people living with HIV to 22.5 million, and with 11.4 million AIDS
orphans living in the 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 AIDS
continued to be the single largest cause of mortality in this region. South Africa has the largest
population of HIV patients in the world, followed by Nigeria and India. South & South East Asia
are second worst affected; in 2007 this region contained an estimated 18% of all people living
with AIDS, and an estimated 300,000 deaths from AIDS. India has an estimated 2.5 million
infections and an estimated adult prevalence of 0.36%. 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.
Prognosis
Without treatment, the net median survival time after infection with HIV is estimated to be 9 to
11 years, depending on the HIV subtype, and the median survival rate after diagnosis of AIDS in
resource-limited settings where treatment is not available ranges between 6 and 19 months,
depending on the study. In areas where it is widely available, the development of HAART as
effective therapy for HIV infection and 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 antiretroviral
therapy, death normally occurs within a year. Most patients die from opportunistic infections or
malignancies associated with the progressive failure of the immune system. The rate of clinical
disease progression varies widely between individuals and has been shown to be affected by
many factors such as host susceptibility and immune function health care and co-infections, as
well as which particular strain of the virus is involved
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Papadopulos-Eleopulos E, Turner VF, Papadimitriou J, et al (2004). "A critique of
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example):
o , (2000). "The Durban Declaration". Nature 406 (6791): 15–6.
doi:10.1038/35017662. PMID 10894520. Retrieved on 2008-05-03.
o Cohen J (1994). "The Duesberg Phenomenon: A Berkeley virologist and his
supporters continue to argue that HIV is not the cause of AIDS. A 3-month
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1642–1649.
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and Infectious Diseases. Retrieved on 2006-09-07.
o O'Brien SJ, Goedert JJ (1996). "HIV causes AIDS: Koch's postulates fulfilled".
Curr. Opin. Immunol. 8 (5): 613–8. PMID 8902385.
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143.
Smith TC, Novella SP (2007). "HIV denial in the Internet era". PLoS Med. 4 (8):
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144.
Watson J (2006). "Scientists, activists sue South Africa's AIDS 'denialists'". Nat.
Med. 12 (1): 6. doi:10.1038/nm0106-6a. PMID 16397537.
145.
Baleta A (2003). "S Africa's AIDS activists accuse government of murder". Lancet
361 (9363): 1105. doi:10.1016/S0140-6736(03)12909-1. PMID 12672319.
146.
Cohen J (2000). "South Africa's new enemy". Science 288 (5474): 2168–70.
doi:10.1126/science.288.5474.2168. PMID 10896606.
Further reading
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2007 AIDS epidemic update (pdf). UNAIDS. Retrieved on 2008-03-21.
UNAIDS Annual Report - Making the money work (pdf). UNAIDS. Retrieved on 200803-21.
Financial Resources Required to Achieve, Universal Access to HIV Prevention,
Treatment Care and Support (pdf). UNAIDS. Retrieved on 2008-03-21.
Practical Guidelines for Intensifying HIV Prevention (pdf). UNAIDS. Retrieved on 200803-21.