Acquired

Immunodeficiency
Syndrome (AIDS) Caused
by HIV
Acquired
Immunodeficiency
Syndrome (AIDS) Caused
by HIV

Mary E. Miller
Acquired Immunodeficiency Syndrome (AIDS) Caused by HIV
Copyright Momentum Press, LLC, 2017.

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First published in 2017 by

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 Abstract
Acquired immunodeficiency syndrome, or AIDS, is a disease of the im-
mune system that is caused by the human immunodeficiency virus (HIV).
AIDS has caused significant loss of life with considerable social and eco-
nomic consequences worldwide. HIV must infect a host cell in order to
replicate, and once infected, the host cell is unable to function properly.
Since HIV infects specific cells of the host immune system, HIV infec-
tion impairs the ability of the patient to fight infections and kill cancer
cells, therefore most deaths associated with HIV infection occur due to
cancer or opportunistic infections. There is no cure for HIV, but advance-
ments in treatments mean that an HIV positive person could experience
a normal lifespan with sustained daily care and medication designed to
prevent HIV replication and spread. These medications primarily target
viral proteins that allow HIV to infect host cells, replicate, and spread in
the body. Work continues to find a way to eliminate HIV from patients
and develop new pharmaceutical targets to address concerns of drug re-
sistant strains of HIV. Worldwide awareness of how the virus infects, is
treated, and spreads within populations is a critical component to control
the current AIDS pandemic.

Keywords
AIDS, ART, CD4, HIV, immunodeficiency, T cell
 Contents
List of Figures and Tables........................................................................ix
Acknowledgment.....................................................................................xi
Introduction.........................................................................................xiii
Chapter 1 Symptoms and Diagnosis of Acquired Immune
Deficiency Syndrome (AIDS).............................................1
Chapter 2 Causes and Contributing Factors of AIDS.........................7
Chapter 3 Treatment and Therapy for AIDS.....................................13
Chapter 4 Future Prospects...............................................................29
Bibliography..........................................................................................33
Glossary................................................................................................35
About the Author...................................................................................39
Index....................................................................................................41
 List of Figures and Tables
Figure 2.1 Image of HIV.....................................................................8
Figure 3.1 HIV attachment...............................................................14
Figure 3.2 HIV replication................................................................17
Figure 3.3 HIV maturation...............................................................23

TABLE
Table 3.1 Gene products of the HIV-1 genome...............................21
Table 3.2 FDA approved drugs for treatment of HIV infection.......24
 Acknowledgment
I would like to thank Malcolm Campbell for the opportunity to make
contributions to this book series. His forward approach to science and
scientific pedagogy is inspiring. I thank my husband David and daughter
Mallory for their patience and support of these efforts. I am fortunate to
work at Rhodes College, which has supported my professional and intel-
lectual development. I take pride that I have worked with outstanding
students, and thank them for inspiring my passion for science education.
My outstanding mentors, colleagues, and collaborators have made it pos-
sible to carry out rigorous research and forward high impact educational
practices. Specifically I thank Mitch Smith, Dan Engel, Jeff Becker, Fred
Cross, and Pam Hanson, whose advice and influence have shaped my
professional success. The editorial staff at Momentum Press has been sup-
portive and kind, and I appreciate their work in the production of this
book. I hope that some aspect of this work is helpful for individuals work-
ing to better understand or manage these devastating diseases.
 Introduction
Acquired immunodeficiency syndrome, or AIDS, is a disease of the
immune system that is caused by the human immunodeficiency virus
(HIV), a member of the Lentivirus genus of the family Retroviridae.
AIDS is a syndrome, or collection, of conditions that occur during ad-
vanced stages of HIV infections. HIV targets specific cells of the human
immune system, crippling the patients ability to fight infections. Fatal
diseases associated with AIDS are cancer or opportunistic infections as
a result of a weakened host immune system. For example, HIV infec-
tion does not cause tuberculosis; but an individual with an HIV-induced
weakened immune system will develop a set of symptoms (a syndrome)
which can include the inability to fight infection, such as the bacteria that
causes tuberculosis. The tuberculosis infection can become so severe that
the patient dies from the bacteria, not the virus directly. Recent advance-
ments in treatment allow patients to manage HIV infection so that, with
proper use and sufficient financial resources, loss of life due to AIDS can
be avoided. A person with HIV can experience a normal lifespan, though
daily care and commitment to appropriate treatment regimens must be
continuously maintained for the life of the patient. There is no cure for
HIV infection.
HIV is thought to have infected humans since the late 1800s, begin-
ning most likely in Africa between 1880s and 1920s, subsequently spread-
ing throughout the world. In 1981, the U.S. Centers for Disease Control
and Prevention (CDC) publication Morbidity and Mortality Weekly Report
(MMWR) was the first official reporting of AIDS, though cases of AIDS
most likely went unnoticed by the CDC during the mid-1970s. The 1981
report described cases of Pneumocystis carinii pneumonia (PCP), a very
rare lung infection, in previously healthy gay men in Los Angeles, CA.
Other infections also appeared in these patients, suggesting impaired im-
munity. Soon after the 1981 MMWR, the CDC received information
about similar cases of PCP, opportunistic infections, and aggressive can-
cers among gay men in other large cities in the United States. By the end
xiv INTRODUCTION

of 1981, 270 cases of severe immunodeficiency (the term AIDS was not
used until 1982) among gay men were reported, with 121 having died
from the conditionan astonishingly high mortality rate. These initial
reports resulted in a misconception by healthcare providers and the public
that the disease was limited to only gay men. This initial and incorrect
perspective created long-term consequences for public awareness about
what caused AIDS and how it was transmitted. The marginalization of
the disease and infected people continued through the following decades
as healthcare providers and citizens struggled to provide medical and emo-
tional support to individuals with AIDS. The first infant case of AIDS
was reported in 1982 from an infected blood transfusion, and 22 infants
with unexplained immunodeficiency with opportunistic infections were
reported. Current blood transfusion procedures protect individuals from
this risk. In 1983, the CDC reported cases of AIDS in female sexual part-
ners of men with AIDS, establishing that the disease was not limited to
gay men. MMWR reports in 1983 were consistent with an infectious
agent as the cause of AIDS, and that this infection was spread by sexual
transmission or exposure to infected blood. In this same year, a statement
known as The Denver Principles was issued, and serves as a Charter state-
ment for the National Association of People with AIDS, an early organi-
zation formed to support individuals with AIDS. Later in that year, the
CDC ruled out casual contact, food, water, air, or environmental surfaces
as routes for transmission of the disease. AIDS was recognized as a world-
wide threat when the World Health Organization (WHO) held its first
meeting to establish international surveillance of the disease. In 1984,
scientists identified HIV as the virus that causes what we now call AIDS.
Research continues to develop better diagnostic tests and treatments for
the disease. By the end of 1985, HIV infection had been reported from
all over the world. Over the next two decades, efforts to battle the AIDS
epidemic continued, demonstrating a historic worldwide effort to educate
individuals on behavioral modifications that can influence disease spread,
and research to treat HIV infections. In 1987, the first antiretroviral treat-
ment for HIV infections was approved for use in the United States. In this
same year, individuals with AIDS were placed on U.S. immigration exclu-
sion lists because AIDS was considered a dangerous, contagious disease.
This policy remained in place until 2010. In 1992, AIDS was the number
 INTRODUCTION
xv

one cause in the United States of death for men from ages 25 to 44, and
in 1994, AIDS was the leading cause of death for all Americans from ages
25 to 44. The WHO reported in 1999 that AIDS was the fourth largest
cause of death worldwide, and first in Africa. In 2002, life expectancy in
sub-Saharan Africa dropped from 62 years to 47 years because of the early
deaths of people suffering from AIDS. Improved treatments of HIV mean
that individuals live longer with HIV associated disease, so the prevalence
of HIV continues to rise. However, year 2005 marked the peak number
of deaths associated with HIV infection.
The number of individuals newly diagnosed as infected with HIV has
dropped by approximately 19% from 2005 to 2014, with 39,315 new
HIV diagnoses in 2015. In a 2012 study from the United States, race
and ethnicity differences were observed in infected populations.A lthough
African Americans comprise only 13% of the investigated population,
they were 45% of new HIV diagnoses. Hispanic/Latinos comprise 18%
of the US population but 24% of new HIV diagnoses. In 2015, 67% of
the new HIV diagnoses were gay or bisexual; heterosexual transmission
occurred in 24% of new diagnoses; not all patients report sexual trans-
mission information. Young people are more likely to become infected,
with individuals aged 1324 making up 16% of the population but 22%
of new HIV diagnoses. Young gay or bisexual men accounted for 84%
of all new HIV diagnoses. In 2014, HIV and AIDS were the 8th lead-
ing causes of death among individuals between the ages of 25 and 34.
When considering HIV infections worldwide, the United States has only
a small proportion of the 36.7 million cases in 2015. Approximately 2.1
million of these cases were new diagnoses, and 65% of these occurred
in sub-Saharan Africa. Other regions with high HIV diagnoses include
Asia, Latin America, the Caribbean, and Eastern Europe. An estimated
1.1 million people died from AIDS-related illnesses in 2015. Although
this is a large number of people, it was fewer than observed in previ-
ous years, largely due to intense efforts to expand antiretroviral treatment
availability. Unfortunately, only 4350% of HIV-infected people received
antiviral treatments during 2015.
When HIV infects humans and causes disease, the virus is moving
through its natural life cycle as an obligate parasite, meaning that the
virus depends on host cells to provide the machinery needed to produce
xvi INTRODUCTION

more viruses. In this sense, the work needed to make copies, or repli-
cate the virus, occurs inside human cells. Cells are the fundamental liv-
ing units in our bodiesand individual cells have the ability to grow,
multiply, and communicate. Groups of individual cells can work together
to function collectively and in a coordinated way, giving rise to higher
order tissues and organs. Viruses are acellular, meaning that they do not
have structures associated with a living cell, and are not able to grow and
multiply on their own. Viruses have simple structures, usually composed
of a genome and associated proteins. Viral proteins carry out a variety of
functions for the virus. For example, some proteins coat and protect the
genome in a structure called a capsid.
Most genomes, including human genomes, are comprised of deoxy-
ribonucleic acid, or DNA. Some viruses, including HIV, have genomes
comprised of ribonucleic acid, or RNA, instead of DNA. Both RNA and
DNA form chains of nucleotides, but RNA carries one additional oxy-
gen atom and includes one nucleotide base (uracil) not found in DNA.
These differences between RNA and DNA change how these molecules
interact with themselves and other molecules. DNA interacts with itself
to form the classic double helix structure we commonly associate with
DNA, and the double helix of DNA can interact with proteins to form
higher order structures called chromatin. Chromatin compacts, protects,
and regulates the behavior of DNA. RNA can fold back on itself, but does
not form long, extended double helices or chromatin. DNA and RNA
also play distinct roles in the process of gene expressionwhere informa-
tion stored in DNA is used to drive the synthesis of functional products,
such as RNA or proteins. The process by which a DNA gene is used
to encode for a protein involves an intermediary step called transcrip-
tion where the DNA is used as template to produce the similar, comple-
mentary, but distinct RNA. The RNA code is used to produce proteins
through a process called translation. Proteins are composed of amino
acid chains, and each amino acid has chemical and structural properties
that collectively determine the proteins overall shape and thus its func-
tion. The structure of a protein dictates how it interacts with other pro-
teins, and what it can do. For example, every protein has distinct chemical
and physical properties so that it binds (physically interacts) with other
proteins or molecules. The ability of cells to interact with each other, or
 INTRODUCTION
xvii

viruses, via proteins located on their surfaces, produces an opportunity

for cellular communication. In other words, proteins on the surface of
each cell, often called receptors, physically interact, change shape, and
initiate signals inside the cell, allowing a cell to recognize another cell or
a virus. In this way, a cell can sense when it has come in contact with a
virus. Therefore, cellular communication and responses require that the
correct protein be expressed in the correct cell at the correct time. Dif-
ferential gene expression means that a cell does not produce every possible
protein encoded in its genome. Cells produce proteins at the right time
and at an appropriate abundance to accomplish the cells functions. This
differential gene expression gives rise to cells with specialized functions,
each able to carry out potentially unique functions because of the protein
composition of the cell. Though only a subset of genes are expressed in
any particular cell, the common mechanism used by all cells means that
the code present in the DNA dictates the code present in the RNA, which
in turn dictates the amino acid sequence of the protein, and therefore
the proteins function. A gene that exists in our DNA is considered a
functional unit of coded information because it contains instructions to
produce a functional product, such as RNA and proteins. Humans have
about 22,000 genes, each encoding different one or more product, each
one distinct in its composition and function. The relationship between
DNA and RNA and protein synthesis is common to all life, and together
the processes of transcription and translation are referred to as the central
dogma of life.
Genetic material is expressed following the rules of central dogma,
regardless whether the virus genome is composed of DNA or RNA. A
viral genome composed of RNA or DNA can be single stranded (ss),
composed of a single chain of nucleotides, or double stranded (ds) where
two chains of nucleotides pair together (the human genome is dsDNA).
Viral genomes can be one continuous piece, or composed of multiple lin-
ear or circular molecules. Viruses that carry DNA as the genetic material
are aptly referred to as DNA viruses. DNA viruses can be ss or ds, and
will be transcribed using host machinery to form RNA as needed. Viruses
that carry RNA are called RNA viruses. If the RNA genome of a virus
must be converted to DNA as part of its normal replication, the virus is
classified as a retrovirus. The process where the RNA genome is used as
xviii INTRODUCTION

template to make complementary piece of DNA is called reverse tran-

scription, in contrast to transcription where DNA is used as template to
make complementary RNA. In all viral infections, the viral genome is
used as template for the synthesis of additional viral genomes using the
same host cell machinery that would replicate the hosts genome. In this
way, the virus is dependent on host cell machinery to replicate. Since HIV
has an ssRNA genome that must be converted to DNA as part of its life
cycle, it is classified as a retrovirus.
 CHAPTER 1

Symptoms and Diagnosis of

Acquired Immune Deficiency
Syndrome (AIDS)

AIDS is a progressive disease of the immune system. In AIDS, HIV in-

fection causes damage to specific cells of the immune system, leading to
symptoms associated with decreased immune function. The symptoms of
AIDS are related primarily to the ability of the HIV virus to infect only
a few types of cells in the human bodyparticularly those cells that ex-
press the receptor cluster of differentiation 4 (CD4). CD4 is expressed
only in a small percentage of cells in the immune system (CD4+, pro-
nounced CD4 positive). To fully understand the symptoms of AIDS and
the pathogenic effect of HIV infection, it is important to understand how
our immune system normally works, the cells that are involved, and the
role that CD4+ cells play in immunity. The human immune system is
complex, where the impairment of one component can have a dramatic
effect on the function of many aspects of immunity. In the case of HIV,
immune system complexity is particularly problematic since the normal
progress of HIV infection destroys the very immune cells needed to fight
infections.
CD4 is expressed on the surface of specific immune cells, mostly T
cells, though there are other types of CD4+ immune cells. T cells are a
type of lymphocyte, which is a type of white blood cell. White blood
cells play a critical role in immune response, and unlike red blood cells,
lymphocytes do not transport oxygen through the body. Both red and
white blood cells are originally formed from hematopoietic stem cells
located in the bone marrow, the soft internal region of the bone that
supports cellular growth and replenishment. Hematopoietic stem cells
2 ACQUIRED IMMUNODEFICIENCY SYNDROME (AIDS) CAUSED BY HIV

reproduce and differentiate into several different cell types, including

lymphocytes. Stem cells differentiate into B cells or T cells, and T cells
are able to migrate to the thymus as part of their maturation. B and T
cells are each capable of interacting with foreign molecules in the body,
and stimulating a response that will help remove them. Molecules that
trigger a response from a B or T cell are called antigens, and antigens are
often proteins encoded by non-human genomes. When a human protein
receptor on a lymphocyte binds to an antigen, the immune cell triggers an
immune response. In this way, antigens encoded by viruses or bacteria can
be identified, targeted, and destroyed by our immune system.
Collectively, a persons population of B and T cells can interact with a
vast variety of antigens. However, any given B cell or T cell produces many
copies of only one type of specific antigen receptor, each of which can
bind to only one specific type of antigen. When an individual B cell physi-
cally binds to its antigen, the B cell rapidly produces more receptor-like
molecules that are secreted from the B cell into the fluids of the body.
These secreted versions of the receptors are called antibodies (Ab) or
immunoglobulins (Ig), which can bind to the same antigen type. B cells
allow the immune system to recognize antigens in the fluids of the body
because Bcells produce antibodies that circulate in our blood and lymph
where they can bind to antigens and target them for removal by an efficient
immune response. Frequently, scientists isolate antibodies as treatment for
disease because these proteins bind tightly to specific proteins of a patho-
gen and target that pathogen for destruction. Antibodies can also be used
as diagnostic tools, since the presence of a pathogen in a patient can be
detected when the patients antibodies bind very tightly to it. Some forms
of tests for HIV infection make use of a patients antibodies in this way.
T cells do not secrete their antigen receptor, nor do they make anti-
bodies. T cells receptors are activated by antigens that are displayed on
the surface of particular types of cells that use a set of proteins called
the major histocompatibility complex (MHC), also in humans re-
ferred to as human leukocyte antigen (HLA). Most cells in our body,
with the exception of red blood cells, display MHC class I (MHC I) on
their surfaces. Specialized lymphocytes produce MHC class II (MHC II)
proteins on their surfaces. These MHC protein complexes function as
an antigen-presenting system for T cells and their receptors. Generally,
 SYMPTOMS AND DIAGNOSIS 3

MHC I molecules display small segments of proteins (called peptides)

that are translated in the same cell that displays the peptide. MHC II
molecules display peptides that were originally produced outside the
cell displaying it. For example, a host cell such as a macrophage might
engulf an invading pathogenic bacterium in order to kill the invading
cell. P
rotein components of the bacteria are bound by MHC II, and
moved to the surface of the macrophage so that the captured bacterial
protein antigen is presented on the outside of the macrophage. When
the bacterial antigen peptide is displayed on the surface of a cell by an
MHCII molecule, a T cell receptor on the surface of the T cell might be
able to recognize and bind to the antigen/MHC complex on the surface of
an antigen-presenting cell. The CD4 protein displayed on the surface of
Tcells helps the T cell receptor bind to antigen presented with MHCII.
CD4 also binds directly to antigen presented by MHC II molecules. If
the population of CD4+ T cells drops in the body, the immune system is
crippled in its ability to recognize antigen-presenting cells, and therefore
is crippled in its ability to mount a vigorous immune response triggered
by pathogenic antigens.
To summarize, when a T cell receptor interacts with an MHC plus
peptide, the T cell receptor activates its T cell and initiates an immune
response. The type of response depends on the type of T cell (and cognate
MHC type) involved. CD4+ cells capable of being infected by HIV in-
clude helper T cells, monocytes, macrophages, and dendritic cells. Helper
T cells recognize MHC II plus antigen, whereas cytotoxic T cells (also
called CD8+ cells) recognize MHC class I plus antigen. Helper T cells
produce cytokines, molecules that are secreted from the cell to stimulate
other immune cells, such as B cells. In this way, appropriate B cell function
requires a healthy population of CD4+ T cells. When HIV infects and
impairs the function of CD4+ cells, it broadly limits the immune system.
People with reduced numbers of CD4+ cells have weakened response
to infections which can lead to opportunistic infections and cancers that
normally are eliminated by a healthy and vigorous immune system.
As HIV infects cells of the immune system, symptoms of infection are
described in three stages. These stages are defined by the amount of virus
present in the patient, or viral load, and the loss of CD4+ T cells of the
host immune system. Stage 1 is considered an acute infection and occurs
4 ACQUIRED IMMUNODEFICIENCY SYNDROME (AIDS) CAUSED BY HIV

between two to four weeks after infection by the virus. Stage 1 symptoms
include flu-like symptoms such as fever, chills, rash, night sweats, sore
throat, muscle aches, swollen lymph nodes, and mouth ulcers. Some in-
dividuals do not feel sick during stage 1, and do not feel any symptoms.
Stage 2 is clinical latency, also referred to as asymptomatic HIV, or a
chronic HIV infection. During stage 2, an individual has very low levels
of HIV replication with very mild or no discernable symptoms. A stage
2 individual can spread the virus, and remains in stage 2 for a variable
amount of time, from weeks to decades. If viral replication is triggered
and the viral load increases, the infection progresses to stage 3 which is
when most patients are diagnosed with AIDS. Stage 3 is when a patients
CD4+ T cell count drops below 200 cells/mm3 (cells per cubic millime-
ter) of blood, whereas a healthy person has 5001600 cells/mm3 CD4+
cells. Symptoms during stage 3 may include fever, chills, sweating, swol-
len lymph glands, weight loss, and fatigue. When the immune system is
compromised in an AIDS patient, the likelihood of opportunistic infec-
tions increases. If an individual in stage 2 is diagnosed with any one of
the following opportunistic infections, their diagnosis is moved to stage 3
even if their CD4+ count is greater than 200 cells/mm3.

Candidiasis of the trachea, bronchi, esophagus, or lungs is caused

by the fungus Candida
Invasive cervical cancer
Coccidioidomycosis pneumonia caused by the fungus Coccidioides
immitis
Cryptococcosis pneumonia caused by the fungus Cryptococcus
neoformans
Cryptospporidiosis diarrheal disease for more than one month
caused by the protozoan Cryptosporidium
Cytomegalovirus diseases, particularly of the retina but also in-
cluding pneumonia, gastroenteritis, and brain infection
HIV related encephalopathy of the brain
Herpes simplex virus associated ulcers for more than one month,
bronchitis, pneumonia, or esophagitis.
Histoplasmosis pneumonia caused by the fungus Histoplasma
capsulatum
 SYMPTOMS AND DIAGNOSIS 5

Isosporiasis intestinal disease for more than one month caused by

the protozoan Isospora belli
Kaposis sarcoma cancer caused by Kaposis sarcoma herpesvirus or
human herpesvirus 8
Many types of lymphoma (cancer of the lymph system)
Tuberculosis of the lungs caused by the bacterium Mycobacterium
tuberculosis
Mycobacterium avium complex
Pneumonia caused by the parasite Pneumocystis carinii
Pneumonia that recurs in one or both lungs
Progressive multifocal leukoencephalopathy of the brain and spi-
nal cord caused by the John Cunningham (JC) virus.
Salmonella septicemia that is recurring gastrointestinal disease
caused by Salmonella infection of the entire body
Toxoplasmosis of the brain caused by the protozoan Toxoplasma
gondii
Wasting Syndrome due to HIV with involuntary loss of more than
10% of body weight with diarrhea and weakness for more than 30days

Several tests exist to detect the presence of HIV in a patient. Three types
of tests focus on the patients antibodies which bind to HIV protein
antigens. These antibody-based tests work between 3 to 12 weeks after
infection, with approximately 97% of infected individuals developing an-
tibodies to HIV in this time frame. A negative test would require retesting
the same person 3 months after initial exposure to the virus. Fifty viruses
per mL of patient blood is the limit of detection using current tests, so
even individuals with undetectable amounts of HIV in their blood can
still carry the virus. Examples of the antibody test are the OraQuick HIV
Test and the Home Access HIV-1 Test System. A second type of HIV
diagnostic test is called a combination test, or fourth generation test. A
combination test looks for host antibodies to the HIV, as described above,
but also uses commercially available antibodies known to bind to HIV
proteins to identify HIV components in a patients blood sample. The
combination test can work between 2 to 6 weeks post exposure. A third
test is called the nucleic acid test (NAT) for HIV in the blood. NAT de-
tects the viral genome, and not the hosts immune response to the virus.
6 ACQUIRED IMMUNODEFICIENCY SYNDROME (AIDS) CAUSED BY HIV

The NAT test is capable of measuring viral load within patients and is
effective between 1 and 4 weeks post exposure. The NAT test is more
expensive, and not used for routine screening. In all three tests, a nega-
tive result does not mean that the patient is virus-free; it just indicates a
failure to detect virus. After consultation with a physician, individuals
might want to be retested a few weeks after a negative result. Further-
more, HIV-positive patients can develop an HIV superinfection, which
happens when a second strain of HIV infects the same person. Continued
testing in patients already diagnosed as HIV-positive can detect a super-
infection. This second HIV strain can displace the original strain, or both
HIV strains can coexist in the patient. In both AIDS and super infection
cases, the weakened immune system makes other infections occur more
frequently and more intensely.
 Index
Acquired immune deficiency C-C chemokine receptor type 5
syndrome (AIDS) (CCR5), 14, 15, 25
causes and contributing factors of, C-X-X chemokine receptor type 4
711 (CXCR4), 14
diagnosis of, 45 Capsid, 7
future prospects, 2930 CD4+ cells, 1, 3, 10, 14, 26
symptoms of infection of, 34 CD8+ cells, 3
tests to detect presence of HIV, 56. Cell membrane, 7
See also specific tests Chronic HIV infection. See
treatment and therapy, HIV-1 Asymptomatic HIV
replication Circulating recombinant forms
targeting ability of virus to attach (CRF), 9
and enter host cells, 1315 Cluster of differentiation 4 (CD4),
targeting viral assembly, 1, 3, 21
exit from host cell, and Combination test, for HIV
maturation,2228 infection,5
targeting viral gene Combivir, 24
expression,1722 Crixivan, 25
targeting viral genome Cytokines, 3
duplication and integration, Cytotoxic T cells, 3
1517
Agenerase, 25 Direct cell-cell infection, 15
Allosteric integrase (IN) inhibitors Duplication, of viral genome, 1517
(ALLINIs), 29
Aminoglycoside antibiotics, 20 Edurant, 25
Antibodies (Ab), 2 Emtriva, 24
Antibody-based tests, 5 Env, 1314, 2022
Antigens, 2 Epivir, 24
Antiretroviral therapies (ART), 13 Epzicom, 24
during and after delivery, 27
combinations treatment, 2526 Fortovase, 25
complication of HIV treatment Fourth generation test, for HIV
with, 2627 infection, 5
FDA-approved drugs, 2425 Fullerene cone, 7
Aptivus, 25 Fusion and entry inhibitors, 25
Asymptomatic HIV, 4 Fuzeon, 25
Attachment of HIV, targeting, 1315
Gag-Pol. See p160
B cells, 2, 3 Gag proteins, 2021, 22
Bone marrow, 1 Gastrointestinal T cells, 11
Breastfeeding, HIV and, 10 Gene expression, targeting, 1722
42 INDEX

Gene therapy, 30 Kaletra, 25

Glycoprotein 120 (gp120), 14, 20, 22 Kilodaltons, 20
Glycoprotein 160 (gp160), 20, 21
Glycoprotein 41 (gp41), 14, 20, 22 Latent, 16
Glycosylation, 14 Lexiva, 25
Long terminal repeats (LTRs), 16
Helper T cells, 3 Lymphocyte, 1
Hematopoietic stem cells, 12
Hepatitis G virus, 26 Major histocompatibility complex
HIV-1, 8, 910 (MHC), 2
genome products, 21 class I (MHC I), 23
replication, treatment and therapy, class II (MHC II), 23
1328 Manaviroc, 15
HIV-2, 9 Matrix proteins, 23
HIV infection. See also Acquired Maturation
immune deficiency syndrome of HIV, 2228
(AIDS) inhibitors, 29
antiretroviral therapies for. See
Antiretroviral therapies Needle, reusing, 10
attachment process, 1315 Nef, 2022
causes, 1, 11 NFKappa B, 18
cells of immune system, 16 Non-nucleoside inhibitors, 16
complication of HIV treatment Non-nucleoside reverse transcription
with ART, 2627 inhibitors (NNRTI), 25
FDA-approved drugs for, 13, 2425 Norvir, 25
prevention of, 27 Nucleic acid test (NAT), 56
transmission of, 910 Nucleoside inhibitors, 16
vaccines to, 30 Nucleoside reverse transcription
Hivid, 24 inhibitors (NRTI), 24
Home Access HIV-1 Test System, 5
Host cell, 710 OraQuick HIV Test, 5
virus exit from, 2228
Host protein receptors, 7 P160, 20, 21, 23
Human leukocyte antigen (HLA). p17, 20
See Major histocompatibility p2, 20
complex (MHC) p24, 20
p55, 20
Immune reconstitution inflammatory p6, 20
syndrome (IRIS), 2627 p7, 20
Immunoglobulins (Ig). Peptides, 3
SeeAntibodies(Ab) Peptidomimetic inhibitor
Integrase (IN), 16, 17, 20, 22 U-75875,29
Integrase strand transfer inhibitors, 25 Placental transfer, during child
Integration, of viral genome, 1517 birth,10
Intelence, 25 Pol, 20
Invirase, 25 Post-exposure prophylaxis (PEP), 27
Isentress, 25 Pre-exposure prophylaxis (PrEP), 27
ISG15, 29 PrEPTruvada, 27
 INDEX
43

Prezista, 25 Tivicay, 25
Protease (PR), 20, 2223 Trizivir, 24
Protease inhibitors (PI), 25 Truvada, 24
Provirus, 16, 18
Vaccines, 30
Red blood cells, 1 Videx EC, 25
Rescriptor, 25 Vif, 2021, 24
Retrovir, 24 Viracept, 25
Rev, 1921 Viral assembly, 2228
Reverse transcriptase (RT), Viral envelope, 7
16, 20, 22 Viral gene expression, targeting,
Reyataz, 25 1722
RNaseH, 16, 20 Viral load, 3
Viral particles, 7
Selzentry, 25 Viral RNA, 18
Sexual intercourse, 910 Viramune, 25
Simian (monkey) immunodeficiency Viramune XR, 25
virus (SIV), 9 Viread, 25
Splicing, 19 Virological synapses, 15
ssRNA genome, 7, 19, 22 Virulence, 9
duplication and integration, Vitekta, 25
targeting, 1517 Vpr, 2021, 2324
Stem cells, 12 Vpu, 2022
Superinfection, 6 Vpx, 24
Sustiva, 25
White blood cells, 1
T cells, 12
receptor, 3 Zerit, 25
Tat, 1821 Ziagen, 25
 OTHER TITLES IN OUR HUMAN DISEASES
AND CONDITIONS COLLECTION
A. Malcolm Campbell, Editor
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Gradual Loss of Mental Capacity from Alzheimers by Mary E. Miller
Hemophilia: The Royal Disease by Todd T. Eckdahl
Sickle Cell Disease: The Evil Spirit of Misshapen Hemoglobin by Todd T. Eckdahl
Auto-Immunity Attacks the Body by Mary E. Miller
Huntingtons Disease: The Singer Must Dance by Todd T. Eckahl
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by Mary E. Miller
Infectious Human Diseases by Mary E. Miller

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