HIV and AIDS Continuing Education
© 2009 by Aspira Continuing Education. All rights reserved. No part of this material
may be transmitted or reproduced in any form, or by any means, mechanical or
electronic without written permission of Aspira Continuing Education.
1. Differentiate between HIV and AIDS
2. Identify causes
3. Learn epidemiology
4. Learn the historical framework related to the development of
HIV/AIDS
5. Become familiar with the impact HIV/AIDS on culture
6. Identify and recognize common stigmas associated with HIV/AIDS
7. Increase familiarity with the relationship between HIV/AIDS and
mental health
8. Increase familiarity with the relationship between HIV/AIDS and
substance abuse
9. Develop the ability to identify the characteristics and method of
assessment and treatment of people who live with HIV/AIDS.
Table of Contents:
1. Definitions
2. Causes
3. Epidemiology
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4. History
5. Stigma
6. HIV/AIDS and Mental Health
7. HIV/AIDS and Substance Abuse
8. Cognitive Disorders
9. Summary
10. References
1. Definitions
Human immunodeficiency virus (HIV) is a lentivirus (a member of the
retrovirus family) that can lead to acquired immunodeficiency syndrome
(AIDS), a condition in humans in which the immune system begins to fail,
leading to life-threatening opportunistic infections. Previous names for the
virus include human T-lymphotropic virus-III (HTLV-III),
lymphadenopathy-associated virus (LAV), and AIDS-associated retrovirus
(ARV). Infection with HIV occurs by the transfer of blood, semen, vaginal
fluid, pre-ejaculate, or breast milk. Within these bodily fluids, HIV is present
as both free virus particles and virus within infected immune cells. The four
major routes of transmission are unprotected sexual intercourse,
contaminated needles, breast milk, and transmission from an infected mother
to her baby at birth (Vertical transmission). Screening of blood products for
HIV has largely eliminated transmission through blood transfusions or
infected blood products in the developed world (Appay V, Sauce D, January
2008. "Immune activation and inflammation in HIV-1 infection: causes and
consequences". J. Pathol).
HIV infection in humans is now pandemic. As
of January 2006, the Joint United Nations
Programme on HIV/AIDS (UNAIDS) and the
World Health Organization (WHO) estimate that
AIDS has killed more than 25 million people
since it was first recognized on December 1,
1981. It is estimated that about 0.6 percent of the
world's population is infected with HIV. In
2005 alone, AIDS claimed an estimated 2.4–3.3
million lives, of which more than 570,000 were
children. A third of these deaths are occurring in
sub-Saharan Africa, retarding economic growth
and increasing poverty. According to current
estimates, HIV is set to infect 90 million people
in Africa, resulting in a minimum estimate of 18 million orphans.
Antiretroviral treatment reduces both the mortality and the morbidity of HIV
infection, but routine access to antiretroviral medication is not available in
all countries. HIV primarily infects vital cells in the human immune system
such as helper T cells (specifically CD4+ T cells), macrophages, and
Human
immunodeficiency virus
Scanning electron micrograph
of HIV-1 (in green) budding
from cultured lymphocyte.
Multiple round bumps on cell
surface represent sites of
assembly and budding of
virions.
dendritic cells. HIV infection leads to low levels of CD4+ T cells through
three main mechanisms: firstly, direct viral killing of infected cells;
secondly, increased rates of apoptosis in infected cells; and thirdly, killing of
infected CD4+ T cells by CD8 cytotoxic lymphocytes that recognize infected
cells. When CD4+ T cell numbers decline below a critical level, cellmediated
immunity is lost, and the body becomes progressively more
susceptible to opportunistic infections (Appay V, Sauce D, January 2008.
"Immune activation and inflammation in HIV-1 infection: causes and
consequences". J. Pathol).
Eventually most HIV-infected individuals develop AIDS (Acquired
Immunodeficiency Syndrome). These individuals mostly die from
opportunistic infections or malignancies associated with the progressive
failure of the immune system. Without treatment, about 9 out of every 10
persons with HIV will progress to AIDS after 10-15 years. Many people
deteriorate much sooner. Treatment with anti-retrovirals increases the life
expectancy of people infected with HIV. Even after HIV has progressed to
diagnosable AIDS, the average survival time with antiretroviral therapy (as
of 2005) is estimated to be more than 5 years. Without antiretroviral therapy,
death normally occurs within a year. It is hoped that current and future
treatments may allow HIV-infected individuals to achieve a life expectancy
approaching that of the general public (Appay V, Sauce D, January 2008.
"Immune activation and inflammation in HIV-1 infection: causes and
consequences". J. Pathol).
Acquired immune deficiency syndrome or acquired immunodeficiency
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 (Appay V, Sauce D (January 2008). "Immune activation and
inflammation in HIV-1 infection: causes and consequences". J. Pathol.)
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 (Appay V, Sauce D, January 2008. "Immune
activation and inflammation in HIV-1 infection: causes and consequences".
J. Pathol).
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. Genetic research indicates that HIV originated in west-central
Africa during the late nineteenth or early twentieth century. AIDS was first
recognized by the U.S. Centers for Disease Control and Prevention in 1981
and its cause, HIV, identified in the early 1980s (Appay V, Sauce D, January
2008. "Immune activation and inflammation in HIV-1 infection: causes and
consequences". J. Pathol).
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 programs in attempts
to slow the spread of the virus (Appay V, Sauce D, January 2008. "Immune
activation and inflammation in HIV-1 infection: causes and consequences".
J. Pathol).
2. Causes
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 (Appay V, Sauce D, January 2008. "Immune activation
and inflammation in HIV-1 infection: causes and consequences". J. Pathol).
Scanning electron micrograph of HIV-1, colored green, budding from a cultured lymphocyte.
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 CCR5-
Δ32 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 (Mastro TD, de Vincenzi I, 1996.
Probabilities of sexual HIV-1 transmission).
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. Sexual assault greatly increases the risk
of HIV transmission as protection is rarely employed and physical trauma to
the vagina occurs frequently, 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 fourfold. 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 (Mastro TD, de Vincenzi I, 1996.
Probabilities of sexual HIV-1 transmission).
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. Infection is unlikely in a single encounter. High rates
of infection have been linked to a pattern of overlapping long-term romantic
relationships. This allows the virus to quickly spread to multiple partners
who in turn infect their partners. A pattern of serial monogamy or occasional
casual encounters is associated with lower rates of infection. HIV spreads
readily through heterosexual sex in Africa, but less so elsewhere. One
possibility being researched is that schistosomiasis, which affects up to 50
per cent of women in parts of Africa, damages the lining of the vagina
(Mastro TD, de Vincenzi I, 1996. "Probabilities of sexual HIV-1
transmission).
Exposure to blood-borne pathogens
(CDC poster from 1989 highlighting the threat of AIDS associated with drug use)
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 HIV-infected person is thought to be about 1
in 150. 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 sub-
Saharan 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
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HIV infections come from transfusion of infected blood and blood products
(Source: The World Health Organization).
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 % (Source:
The World Health Organization).
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 (Source: The World Health
Organization).
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.
10
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During the acute phase, HIVinduced
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 (Source: The World Health Organization).
Estimated per act risk for acquisition
of HIV by exposure route.
Exposure Route
Estimated infections
per 10,000 exposures
to an infected source
Blood Transfusion 9,000
Childbirth 2,500
Needle-sharing injection drug use 67
Percutaneous needle stick 30
Receptive anal intercourse* 50
Insertive anal intercourse* 6.5
Receptive penile-vaginal intercourse* 10
Insertive penile-vaginal intercourse* 5
Receptive oral intercourse*§ 1
Insertive oral intercourse*§ 0.5
* assuming no condom use
§ source refers to oral intercourse
performed on a man
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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 (Source: The World
Health Organization).
3. Epidemiology
Estimated prevalence of HIV among young adults (15-49) per country at the end of 2005
The AIDS pandemic can also be seen as several epidemics of separate
subtypes; the major factors in its spread are sexual transmission and vertical
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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
(Source: The World Health Organization).
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 worstaffected
countries; for example, in 2006 it was estimated that it had dropped
from 65 to 35 years in Botswana (Source: The World Health Organization).
Changes in life expectancy in some hard-hit African countries. Botswana
Zimbabwe Kenya South Africa Uganda
