HIV In The African American Community

HIV In The African American Community
The prevalence of HIV in the African American community is unmatched by any other population. African Americans accounted for 49% of all HIV
related deaths in 2010 (CDC, 2014). In my specialty area of family practice, I have encountered only one non–minority patient with HIV; all others
have been African–American. This population needs to be of high consideration for disease education. African Americans are typically unaware of
resources available to prevent the transmission of this disease, as well as testing available to them in their communities. African American children,
especially, are at greater risk for HIV due to lack of knowledge and earlier age of engaging in sexual intercourse. They are typically unaware that their
behavior can yield such a negative outcome (CDC, 2012). Many urban schools lack proper funding to accommodate a sexual education curriculum. It
is of increased importance to raise awareness, educate and provide a plan of care for the African American teenage and adult population, as the
incidence of this disease rises daily. ... Show more content on Helpwriting.net ...
(2011) was a multi–continent, randomized, controlled trial to evaluate the effectiveness of antiretroviral therapy on the speed of the disease process
among HIV–1 infected and HIV–1 uninfected partners. In the study, 1,763 HIV mixed status couples were grouped into either early antiretroviral and
delayed therapy groups. Inclusion criteria consisted of the HIV–1 infected participant having a CD4 count between 350 and 550 with no previous
antiretroviral therapy usage, except to prevent mother–baby transmission. Participants attended three monthly sessions and then quarterly sessions until
ill or requiring an additional amount of antiretroviral drugs (Cohen et al, 2011). The uninfected partners were tested each quarter for seroconversion,
the period in time in which antibodies become detectable. The research study concluded that early antiretroviral therapy initiation had a greater
effect on CD4 count than delayed antiretroviral therapy. The average CD4 count in the early therapy group originated at 400 and increased to 603
after 12 months of ART. A decline of CD4 cells were noted in the delayed group (Cohen et al, 2011). The authors concluded that a higher incidence of
HIV transmission was noted in African countries and adverse effects were more likely to occur in the early therapy group. Early therapy had a positive
effect on the HIV–1 uninfected and HIV–1 infected
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CD4 Cells Essay
CD4 cells are targets for contracting HIV as a transmembrane protein that is part of the virus has a high affinity for CD4 cells, this protein is gp41
(Coico, & Sunshine, 2009, P. 269). Dendritic cells, CD4+ T cells, and macrophages all contain CD4 and therefore, are targeted by HIV. Another
glycoprotein that is introduced by HIV is gp120. Gp120 and gp41 are bound to each other and, once gp41 is bound to the CD4 molecule, gp120
binds to a second molecule, allowing HIV to invade the cell (Coico, & Sunshine, 2009, P. 269). The CD4+ cell that becomes the target of the gp120
is determined by the coreceptor on the gp120 molecule (Coico, & Sunshine, 2009, P. 269). After the CD4 cells has a gp120 bound to it, the cell
membrane is then ... Show more content on Helpwriting.net ...
Opportunistic infections are worse and occur more regularly in people who have diminished immune systems (HIV/AIDS, 2017, Para. 1). Opportunistic
infections associated with AIDS are often the result of the individual not being able to control and defend against normal pathogens due to the reduced
immune system (Coico, & Sunshine, 2009, P. 272). These opportunistic infections lead to death of the cells and can result in the death of the individual.
According to the CDC, some of the most common opportunistic infections for individuals who suffer from HIV and AIDS include tuberculosis,
lymphoma, toxoplasmosis of the brain, and recurrent pneumonia (HIV/AIDS, 2017, Table 1). Cancers and other diseases are also considered to be
opportunistic infections from HIV and AIDS.
Treatment and Drug Resistance With the advances made in medicine, there are treatment options available for individuals who suffer from HIV and
AIDS. The first treatment for HIV was a nucleoside that inhibited reverse transcriptase and is name azidothymidine (Coico, & Sunshine, 2009, P. 273).
With the fast rate that HIV can cause mutations, drug resistance occurs rapidly and is different in each individual who is infected. Treatments are not
affective against HIV if the particular virus is resistant to the treatment; however, more recent treatments have shown improvements where individuals
can be on them for years before a drug resistant reaction is observed (Pennings, 2013, P. 1). The highly

Viruses Are Parasites Using Its Host 's Cells
Viruses are parasites using its host 's cells to replicate its own genome (Freeman, 2011). Viruses have either a deoxyribonucleic acid (DNA) or
ribonucleic acid (RNA) genome that affects its specific named genome. Types of RNA viruses include positive strand, negative strand, double strand
and RNA transcriptase. RNA viruses have evolved into effective pathogens that mutate at high rates. This allows them an advantage over their host to
effectively evade the immune system through several mechanisms, such as mimicry, avoiding cell lysis, and phagocytosis. Their ability to bypass a
cell 's normal process of proof–reading and error correction is what makes RNA viruses such effective pathogens. Almost all RNA viruses are termed
emerging infectious diseases because they are already known, but are increasing rapidly in new areas. There are a few emerging infectious RNA
viruses that have reappeared into the population and have the potential to cause an epidemic.
Ebola hemorrhagic disease, rabies, influenza and HIV are examples of RNA viruses and a few of these viruses have yet to be thoroughly researched. An
example of an RNA virus that mutates and evolves at a high rate is the influenza virus. The influenza virus can mutate in two different ways; antigenic
shift which is an abrupt change and by antigenic drift which is a smaller, more gradual change that occurs through point mutations (Uyeki 2014). These
changes are what help the virus to evade the host 's immune system. Another

Biol 537 Immunology Research Paper
Molly Fields
Qing Deng
BIOL 537 Immunology
Term Paper
Due: April 16, 2015
Immunopathogenesis of 'Vyloria'
When a virus invades the human body there is an assortment of responses from the immune system relying largely on the particular pathogen type.
Viruses invade the host with the purpose of replication to ensure survival. My cytosolic virus is a single stranded RNA virus. The virus is surrounded
by an envelope with a lipid membrane. Inside the envelope are matrix proteins, integrase, protease, reverse transcriptase and the RNA genome. All
viruses contain three proteins necessary for their survival; one for replication, one for packaging and delivering it to more host cells and a protein that
modifies the function or structure of the host ... Show more content on Helpwriting.net ...
They go through negative selection after V(D)J recombination where the self–reacting cells are eliminated. Positive selection is in the periphery and
where B cells become mature B–cells. Unlike T–cells, B–cells also go through hypermuation and class switching in the lymph nodes after they are
activated. This helps them be more specific for antigens. B–cells either proliferate into memory B–cells or plasma cells that secrete antibodies.
Antibodies opsonize, neutralize or fight by complement fixation against the virus. The memory cells are used if an infection of the same virus occurs

HIV: Spread Of AIDS In The Human Body
HIV stands for human immunodeficiency virus, HIV is a very dangerous disease, if left untreated, it can lead to the disease AIDS (acquire
immunodeficiency syndrome). It can affect anyone, at any time if they put themselves in a situation where they could be at risk. Unlike other viruses,
the human body can't get rid of this virus, so once a person has HIV, they have it for the rest of their life. Although it can be a dangerous disease, it is
very preventable. There are several important facts about HIV that people should know; these include the spread of infection in the body, ways to
prevent the infection and the type of medication to use to prevent further spread of the HIV virus.
HIV attacks the body's immune system, by destroying CD4 cells also knows as T cells, that are a type of white blood cells that help the body immune
system fight off infections. T cells have proteins that helps the HIV virus bind. If HIV is left untreated, it can reduce the numbers of infected CD4
cells in the body, making the person's more prone to infections ("CD4 Count, HIV, andAIDS: Test and Results–– What They Mean," n.d.). Over time,
HIV can completely destroy these cells and the body can no longer fight off infectious disease. When the body begins losing its ability to fight
infections and the CD4 cell ... Show more content on Helpwriting.net ...
AIDS stands for acquiring immunodeficiency virus.When a person has AIDS the person body is unable to fight off infections. A person with AIDS
has to take antibiotic prophylaxis to prevent infection from occurring ("How HIV Causes AIDS," n.d.). People who are not infected with HIV have
roughly 800 to 1,200 CD4 cells per cubic millimeter of blood When Diagnosed with AIDS a person can have fewer than 50 CD4 cells in their entire
body ("CD4 Count, HIV, and AIDS: Test and Results–– What They Mean," n.d.). It is important to get treatment right away when a person is
diagnosed with

Cd4 Count Test
Why am I having this test?
The CD4 count test is performed if you have been diagnosed with human immunodeficiency virus (HIV) infection or acquired immunodeficiency
syndrome (AIDS). For AIDS patients, the purpose of the test is:
To determine the current status and outlook of the disease.
To determine when to begin antiviral therapy for HIV or AIDS and to monitor this treatment.
The CD4 count test can also be used to help confirm a diagnosis of certain types of leukemia.
If you have HIV, your health care provider may recommend that this test be performed every 3–6 months.
What is being tested?
This test checks for any reduction in the level of CD4 cells in the blood. CD4 cells are a type of white blood cells that fight infection. They are also
known as T–helper cells. These cells are ... Show more content on Helpwriting.net ...
This test, along with the viral load test, can help determine your risk for developing other infections. The viral load test measures the level of HIV in
the blood.
Increasing amounts of CD4 cells indicate that your antiviral therapy is working.
What kind of sample is taken?
A blood sample is required for this test. It is usually collected by inserting a needle into a blood vessel.
How do I prepare for this test?
There is no preparation required for this test.
What are the reference values?
How are the results reported?
You may have to wait for a few days for the test results to be finalized. Your test results will be reported as a range of values and percentages. You
will compare your results to normal ranges and percentages that were established after testing a large group of healthy people. Reference ranges may
vary among different people, labs, and hospitals. For this test, reference ranges and percentages are:
T cells
Percent: 60–95.
Number of cells per microliter (mcL): 800–2,500.
T–helper (CD4) cells
Percent: 60–75.

Number of cells per mcL: 600–1,500.
T–suppressor (CD8) cells
Percent:

The Human Immunodeficiency Virus ( Hiv )
The Human Immunodeficiency virus (HIV) is a virus that causes Acquired Immunodeficiency Syndrome (AIDS). HIV and AIDS gravely reduces a
person's immune system allowing them to be more susceptible to serve infections. At the end of 2009, the Center for Disease Control and Prevention
(CDC) estimated 1,148,200 people over the age of 13 in the United States were infected with HIV. The CDC estimates that the incidence every year is
50,000 people. (2) The main treatment therapy is highly active antiretroviral therapy (HARRT). This therapy utilizes nucleoside/nucleotide reverse
transcriptase inhibitors, non–nucleoside reverse transcriptase inhibitors, and protease inhibitors to prevent replication of HIV. This extends the latency
period of HIV,... Show more content on Helpwriting.net ...
HIV uses the coreceptors, CCR5 and C–X–C chemokine receptor type 4 (CXCR4), on the CD4+ helper T–cell to infect the cell. (19) After the virus
has infected the cell it integrates its own DNA with long terminal repeats into the host genome. Researchers are currently studying zinc finger
nucleases (ZFNs) to create this в€† 32 mutation in the CCR5 and CXCR4 gene as way of preventing further infection. Along with use of ZFNs to
remove long terminal repeats of the provirus HIV from the host genome. This review will discuss the molecule techniques used for diagnoses and
possible treatment for HIV–1 using ZFNs.
How it invades CD4+ helper T– cells
HIV first binds to CD4+ helper T–cell with the gp120 protein on the HIV virus and the chemokine receptor, CCR5, on the CD4+ helper T–cell. (6)
The viral core then enters the cell and the virion's protein membrane fuses with the cell membrane. The virus then injects its RNA into the cytoplasm
where reverse transcription occurs so synthesize HIV DNA, also called provirus. The provirus is then transferred into the nucleus were it is integrated
into the host genome. The infected cell then transcribes and translates the provirus. The viral proteins and some of the viral RNA gather at the edge
of the cell membrane and bud off from the infected cell. The newly formed HIV virus goes on to infect other CD4+ helper T–cells, while the infected
cell dies. (6) The virus can evolve to use the

What Role Does Cd4 Play In The Human Immune System
The human immune system plays a major role in every person's body. It protects the body against foreign particles that could lead to diseases, such as
bacteria and viruses. A white blood cell protein, called CD4, play a key role in the human immune system. Without the help of CD4 proteins, bodies
would not be able to receive the signal to activate the body's immune response against foreign contaminants entering the body. CD4 proteins are found
in white blood cells, which play a very important role in the human immune system. CD4 is also a glycoprotein. They can be found on the surface of
immune cells, such as T–helper cells, that serve as receptors. They are receptors for one of the most commonly known infections, HIV AIDS. CD4
cells, also known as T–helper cells, are an essential part of the human immune system. When a foreign particle enters the body, CD4 cells send
signals to other types of immune cells, which trigger them to then destroy the infectious particle. If a body's CD4 cell count is reduced, the body is
left vulnerable to many diseases and infections that it would otherwise have been able to protect itself against. CD4 is also a glycoprotein on ... Show
more content on Helpwriting.net ...
Cytokines are cell signaling molecules that aid cell to cell communication in immune responses and stimulate the movement of cells towards sites of
inflammation, infection, and trauma. Researchers at UC Davis have found that early exposure to inflammatory cytokines can "paralyze" CD4 cells.
This CD4 paralysis could play a role in preventing autoimmunity. Autoimmunity is misdirected immune responses that can cause the immune system to
go awry and attack the body itself. By shutting down CD4 cells, it prevented an autoimmune response. This research shows the potential to paralyze the
immune system to prevent autoimmunity, or to adjust and teach it to accept transplanted cells and

Genetic Determinants Of Hiv Infection
Genetic determinants of HIV infection:
HIV has two major types: HIV–1 and HIV–2. HIV–1 has four groups M, N, O and P. These groups are further classified into subtypes. Group M is a
major infecting group worldwide contributing to 90% of HIV–1 infections. Group M is classified into nine subtypes (A, B, C, D, E, F, G, H, J and K).
Subtype B is predominantly found in America and Western Europe. The susceptibility toHIV–1 infection, transmission of disease, and response to
retroviral therapy depend on the genetic determinants of the host cell. These genetic determinants vary in populations and among patients. These
genetic variants regulate chemokine co–receptors and ligands that involve in the entry of the virus, major histocompatibility complex, killer cells Ig
like receptor and cytokines, and TRIM5О± motif and apolipoprotein B mRNA–editing enzyme, catalytic polypeptide–like 3G (Kaur and Mehra, 2009).
In genome–wide association studies performed in European population, it was shown that Human leukocyte antigen (HLA) class I variation (Eg.
HLA–B*5701) is the major contributor to viral set point and CD4+ T cell decline (Fellay et al., 2010). Cohort study of genetic polymorphism in
chemokine receptors in Indian population has shown that protective CCR5 О”32 variant is rare and CCR5HHE carrying *59402A has the high
likelihood of infections (Kaur and Mehra, 2009). HIV Sequence Database contains annotated HIV sequences

Hiv Virus Research Paper
The human immunodeficiency virus gets its name by the sole species it affects and the characteristic damage it does to the body, which is also
known as HIV. Viruses are notorious for the mode in which they reproduce; a virus enters the body, seizes the body's cells, and uses it as a host. This
is the only way for viruses to replicate. HIV takes over the body's T cells, also known as CD4 cells, which are important to defend the body from
various antigens. Normally, T cells would respond to infection and diseases by neutralizing, creating antibodies to fight off the antigen the next time it
comes around, or lessen the effects it has on the body. Infections such as pneumonia that would make a regular person incredibly ill could be fatal to
someone ... Show more content on Helpwriting.net ...
Two to four weeks after infection a person can experience flu–like symptoms. This is when the virus begins to rapidly replicate, and during this time is
when the HIV virus count is highest and the CD4 count drops rapidly. The lower the CD4 count the more susceptible the body is to other infections.
Although HIV can be spread during any stage, there is a higher chance of spreading the virus because of the high virus load per cubic millimeter of
blood. The second stage is known as clinical latency also known is inactivity, dormancy, asymptomatic HIV, and chronic HIV infection. Amid this
aspect of infection the virus is active in the body, but there are low levels in the blood. Contagion is still existent, so precautions are pertinent.
Affected humans can reach chronic HIV infection stage rapidly, but can be prolonged for a more than a decade with proper treatment. The final stage
of HIV infection is known as AIDS, which means acquired immunodeficiency syndrome, meaning that the CD4 cell count is less than 200 per cubic
millimeter of blood. Normal CD4 counts range from 500–1600 per cubic millimeter. During this stage the body can no longer protect itself from
antigens. Common infections such as the common cold can ultimately be fatal to the

Themis Genetic Summary
Chabod et al. published "A Spontaneous Mutation of the Rat Themis Gene Leads to Impaired Function of Regulatory T Cells Linked to Inflammatory
Bowel Disease", aiming to establish the importance of the Themis gene, as well as its close interactions with regulatory T cell (2012). This discovery
would allow future studies to focus on the Themis gene as a new candidate for studying the pathology behind chronic inflammatory diseases that target
the immune system in humans (Chabod et al. 2012). Chabod et al. hypothesized that the Themis gene plays a key role in the maintenance of digestive
tract homeostasis and is pivotal to the suppressive abilities of natural CD4 regulatory T cell (2012). Inversely, Chabod et al. hypothesized that a
defective Themis... Show more content on Helpwriting.net ...
In this experiment, the scientists compared the amount of autoantibodies present in the digestive system of BN rats and BNm rats. An extraction of
sera from BNm rats revealed the presence of autoantibodies that recognize and attacked wall components of arterioles and venules, as well as muscular
layers of the intestine (Chabod et al. 2012). Furthermore, the intestinal tracts of BNm rats were noticeably marked with macroscopic lesions, multifocal
infiltration, and granulomas (Chabod et al. 2012). In comparison, BN rats lacked the same autoantibodies found the mutated rats and tended to have
less intestinal abrasions and abnormalities (Chabod et al. 2012). To determine whether CD4 T cells contributed to the development of IBD, the
researchers experiments with wild type BN rats that were thymectomized and given anti–CD4 treatment (Chabod et al. 2012). The experimented rats
showed no signs of IBD, indicating that mutation in the Themis gene is required for the development of IBD seen in BNm rats (Chabod et al. 2012).
This further supports the researchers' notion that a mutated Themis gene, along with subsequent reduction of viable CD4 T cells, is closely related to
the occurrence of

Smoking: Statistics and Linear Regression Equation.
Problems on Regression and Correlation Prepared by: Dr. Elias Dabeet Q1. Dr. Green (a pediatrician) wanted to test if there is a correlation between
the number of meals consumed by a child per day (X) and the child weight (Y). Included you will find a table containing the information on 5 of the
children. Use the table to answer the following: Child Number of meals consumed per day (X) child weight (Y) XВІ YВІ XY Ahmad 11 8 121 64 88
Ali 16 11 256 121 176 Osama 12 9 144 81 108 Husien 19 13 361 169 247 Total 58 41 882 435 619 a. Determine the simple linear regression equation. b.
Determine the correlation coefficient. Interpret it in words. c. What is the expected child weight if the number of... Show more content on
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experiencing hypertension, given that the person is a moderate smoker; 2. non–smoker or experiencing hypertension. 3. a smoker, given that the person
is experiencing no hypertension. Q9. 1418 men were cross–classified according to their smoking status and their lung cancer status as in the following
table: Lung Cancer Present Absent Total Smoker Yes 688 650 1338 No 21 59 80 Total 709 709 1418 If one of these men is selected at random, find the
probability that he is a) a smoker b) having lung cancer. . c) non–smoker or having lung cancer. d) having lung cancer, given that he is a smoker. e) a
smoker, given that he does not have lung cancer. h) Are the events " being a smoker " and " having lung cancer " independent? Why? Q10. A lab test
is 95 percent effective at detecting a certain disease when it is present. When the disease is not present, the test is 99 percent effective at declaring the
subject negative. If 8 percent of the population has

Human Immuno Deficiency Virus ( Hiv )
Immunopathology of Human Immuno deficiency virus (HIV) Introduction – a bit about the history of the discovery of the virus, then how it came to
be known as aids, where the virus is thought to come from, include transmission Human immuno deficiency virus, (HIV) belongs to the genus
Lentivirinae, a Retroviridae, which is a family of enveloped retro viruses. It was first described in 1983, when a case of acquired immune deficiency
syndrome (AIDS) was reported, two years earlier. The disease was characterised by immunocompromised patients that were more susceptible to
opportunistic pathogens, along with a dramatic decrease in the CD4 T cell count. It has since been discovered that there are two types of HIV, HIV–1,
and HIV–2. Each one endemic in different parts of the world, however HIV–1 is more virulent, and is responsible for the most cases of AIDS
worldwide. http://www.ncbi.nlm.nih.gov/books/NBK27126/ These viruses persist and continue to replicate for many years before causing overt signs
of disease. Unlike many other pathogens, HIV is only able to be transmitted through body fluids as they cannot survive outside of a host, so are
described as being blood–borne. Common methods of transmission include sexual intercourse, contaminated needles injected intravenously, transfusion
with contaminated blood, and transmission across the placenta from the mother to the foetus. http://www.ncbi.nlm.nih.gov/books/NBK27114/#A1325
Both viruses appear to have spread to humans from other

The Prevalence Of Hiv Among Women
C.2. Study Population/Design {this paragraph need to be reduced by 3 lines} This study is a prospective, special exposure cohort study. The study
population will include HIV seropositive pregnant women, postpartum women within 6 weeks after delivery (due to the fact that most HIV–infected
pregnant women do not usually come back for postpartum visits after delivery), and infants of seropositive pregnant women till 6 months old in
Gambia. The study will be conducted in three years. The prevalence of HIV among women in Gambia is higher (7.6 per 1000) than other West African
countries (3.1 per 1000). Our eligibility criteria include reproductive ages of women from 15–45 years old, HIV seropositive pregnant women, and
participants from the three regions of Brikama, Janjanbureh, and Basse In Gambia (unicef, 2013). We intend recruiting 224~250 participants, based
on the sample size calculation below (to accommodate potential losses to follow ups), nationwide in urban hospital clinics from the largest antenatal
centers in Gambia (Please send me the correct link [2]). An informed consent will be obtained and signed by participants. Afterwards, a detailed
questionnaire about their demographic variables, physical examination findings, HIV staging, and mode of delivery, breastfeeding and laboratory tests
will be performed (Lambert et al., 1997). The specimen will be collected and stored, and the women will be seen on subsequent antenatal or postnatal
visits for follow up. The selection

A Research Study On Human Immunodeficiency Virus
Abstract
Human Immunodeficiency Virus infects approximately 50,000 people every year in the United States. This virus causes the Acquired
Immunodeficiency Disease that leaves patients more susceptible to opportunistic infections. Conventional treatment focuses on extending the latent
phase of AIDs for as long as possible by interfering with HIV replication. Individuals that are homozygous for a naturally occurring в€† 32 deletion
mutation in the CCR5 gene have high resistance to HIV–1 infections because the virus is unable to attach and affect the cell. Engineered zinc finger
nucleases are currently being analyzed to see if they are capable of modifying CD4+ helper T–cells into a resistant strain of CD4+ helper T–cells
against HIV–1. A patient from Berlin in 2009 inadvertently received a CCR5– negative hematopoietic stem/ progenitor cells from a donor that was
homozygous for the CCR5 в€† 32 mutation. This provided the infected patient with a lifelong supply of HIV
–1 resistant CD4+ helper T–cells and
eventually led the patient into remission. Molecular techniques are currently being used to test and monitor HIV using amplification methods. This
review will discuss the molecular techniques used for diagnosing, monitoring and possible treatment of HIV–1.
Introduction The Human Immunodeficiency Virus (HIV) is a retrovirus, whose natural progression of infection leads to a severely compromised
immune system known as Acquired Immunodeficiency Syndrome (AIDS). At the end of

The Virus Responsible for the AIDS Disease
The virus which is responsible for the disease of AIDS or the Acquired Immunodeficiency Syndrome is named as HIV or the Human
Immunodeficiency Virus. HIV is one of the members of viruses called the retrovirus. Explain this later These viruses are capable of duplicating the
RNA into DNA.The virus has two exact copies of single–stranded RNA as the basic genome in the very center of the organism. The genome is
surrounded by a membrane that is made of membrane–bound proteins and lipids. One of the membrane–bound proteins is called the T–cells which
help the virus becoming physically attached. When it became attached, the virus that is brought inside by the T–cell could result for the internal core to
become exposed and damaged. Then the enzyme attached to the RNA, starts to make a base–pair single–strand copy of the RNA into DNA. The single
strand of DNA is also duplicated by the same enzyme to form double–stranded DNA. This DNA enters one of the 46 chromosomes within our cells and
used it as pattern to produce new virus particles. These new virus particles can be released from the infected cell and infect the adjacent cells.) HIV can
hide for a very long period of time in the cells of the body and attacks the main part of the immune system – the T–cells or the CD4 cells. HIV cannot
enter unbroken skin. HIV can be transmitted through direct exchange of body fluids. Sexual intercourse is the most common form of HIV
transmission. Blood to blood contact, such as sharing needles for

T Cell Gene Therapy : The Center Of Research With Stem...
The CCR5 co–receptor is not only the center of research with stem cell transplant, but has also been a recent target of gene therapy research. Gene
therapy is a fairly new technology where genes (edited or normal) are transplanted in humans to produce a specific response. One avenue of research
that is currently being studied is T cell gene editing focused on the CCR5 delta32 mutation in HIV infected patients using the CRISPR/cas9 system.
There is some research using TALENS, but evidence with CRISPR/cas9 will be discussed here (Ye, 2014). The CRISPR technique that edits gene
sequences has been also researched for use in Hepatitis B, Epstein Bar Virus, Malaria, and Human Papilloma Virus. Simply put, the CRISPR/cas9
system can be ... Show more content on Helpwriting.net ...
The researchers created and studied the best way for the CRISPR/cas9 system to be delivered into CD4 cells. The best delivery mode for the
CRISPR/cas9 was assessed to be an adenovirus known as the Ad5F35, and the optimal time for exposure for maximal gene editing was found to be 8
days. The CRISPR/cas9 was introduced to the cells by the Ad5F35 adenovirus and eight days passed to allow the system to modify the genetic makeup.
Following transduction of the CD4 cells with the genetically engineered CCR5 mutation, the cells remained HIV resistant. This study claims to be the
first to successfully use an adenovirus to transduce genetically modified DNA into CD4 cells to provide resistance to HIV. In theory, these modified
CD4 cells can then be transplanted in HIV patients so that their fighter cells will be resistant to HIV infection. (Li, 2015).
Another recent study involved transplanting these modified T cells into mice using the CRISPR/cas9 to see if the engineered cells would transfer
resistance to HIV. After transplanting the T cells and exposing the mice to HIV, the mice tested resistant to the virus (Zu, 2017).
The author in the initial CRISPR study, Li, believed it to be important to create a way to genetically change the CXCR4 co–receptor as well as the
CCR5 co–receptor so that the virus cannot utilize any receptor to enter the host cell (Li, 2015). In a study done in 2017, scientists developed a way to
alter the genetic makeup of the CXCR4 co–receptor. Instead of

Interstitial Migration Of Lymphocytes.
3. Interstitial migration of lymphocytes in non–lymphoid organs. 3.1. T cells– Targeting infected or transformed cells in an inflammatory milieu is a
complex and multifactorial process. To mediate their effector functions, primed CD8+ and CD4+ T cells need to migrate into the inflamed organs and
initiate adaptive immune responses. After homing into the inflamed tissue, T cells require presentation of the cognate antigen–MHC complex on the
surface of the target cells before effector functions can be initiated. In case of T cells, the identification and neutralisation of these target cells can be
challenging, as the number of target cells in most cases is much lower than the tissue resident and/or inflammatory immune cells within the milieu.
Moreover, successful initiation of effector T cell function results in lower abundance of target cells therefore T cells need to scan larger regions within
the tissue for increasingly rare target cells. Similarly, the complex inflammatory environment presents several other challenges that may impede
successful navigation of effector T cells like the presence of various chemotactic cues, pathogen–associated molecular patterns (PAMPs),
damage–associated molecular patterns (DAMPs) and alterations in the extracellular matrix (ECM). To successfully navigate through such a complex
inflammatory milieu, T cells have devised novel migratory strategies. Extravasating T cells in the tissue polarise and migrate at high velocities within
the inflamed

Hiv Aids Research Paper
Liz Soto
Dr. Calderon
Biology 1A Lab
10/17/16
HIV/AIDS
HIV which stands for human immunodeficiency virus is a virus that attacks the human infection fighting CD4 cells of the immune system. AIDS
which stands for acquired immunodeficiency syndrome, is the most advanced stage of the HIV infection. If HIV is left untreated it leads up to AIDS,
and that is when the immune system is too weak to fight off infections or even certain cancers. HIV is spread through certain body fluids such as
blood, semen, pre–seminal fluid, vaginal fluids, rectal fluids, and breast milk. In the United States HIV is commonly spread by having sex with
someone who is infected or by sharing drug injection needles. HIV is not airborne so you cannot get infected by a simple ... Show more content on
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Gp120 is exposed on the surface of the HIV envelope. GP120 is important for when the virus enter because they attach to certain cell surface
receptors. These receptors are essential because they are the ones that bind to CD4 cells. The binding of these receptors start a change in the
gp120 protein. Gp120 is coded by the HIV gene, so this means that gp120 plays a vital role in the ability of HIV to enter CD4 cells. Gp120 was
among the first targets in finding and HIV vaccine. There are two kinds of HIV, HIV 1 and HIV 2. HIV 1 is the most common in the world and
HIV 2 is typically found only in West Africa. HIV 1 is responsible for stain M in its gene and is mostly responsible for the spread of the virus
making it an epidemic. Today, there is an estimated of 32 million people with HIV. HIV is treated with a combination of three different drugs called
antiretroviral. This helps to keep the amount of HIV in your body low and from getting sick alot. Overall, HIV does not necessarily become AIDS,
with proper treatment you will never reach the AIDS virus. Till this day, there is yet to be a cure for HIV. Scientist are still trying to find a cure that
could possibly help on stopping the replication of the HIV disease once it eneters the human blood

Wound Healing Case Study
Wound healing is an intricate process, whereas the skin may heal itself after an injury. At the time of injury, the inflammatory phase begins and is
noted as a significant time, because this process prepares the wound environment for recovery. Since Mr. Jones laceration is five days old, suturing the
laceration may not be appropriate. The wound was not stitched and allowed to heal by primary intention (first intention), because scarring is minimized
during this process and no tissue loss is noted. Mr. Jones wound will have to heal by primary intention. Cleaning the laceration daily and applying a
clean dressing will invoke healing. Since Mr. Jones will be a risk for infection, the continuation of antibiotics will be beneficial. Mr. Jones... Show more
content on Helpwriting.net ...
Since AIDS (acquired immune deficiency syndrome) is a disease of the immune system caused by HIV, which is a retrovirus that causes acute
immunosuppression. HIV can produce an increase in fatal diseases which includes wasting syndromes and central nervous system disintegration.
People with acquired immune deficiency syndrome (AIDS) develop opportunistic infections once the immune system becomes severely compromised.
A patient's CD4 T–cell is directly related to the risk of developing an opportunistic infection. Additionally, HIV most frequently infects CD4 cells.
The CD4 cell count is a key gauge of the health of the immune system. CD4 levels lower than 200 will be at risk for an opportunistic infection.
.Patients with AIDS routinely receives a test called the CD4 test. This blood test is taken to count several types of cells. Moreover, this test do not
count CD4 cells, it is a calculation based on total white blood cells and the proportion of cells that are CD4. The blood sample is tested to count
several types of cells. Interpretation of this test does not count the CD4 cells directly. Instead, the laboratory makes an estimate based on total white
blood cells and the percentage of cells that are CD4. Therefore, the CD4 count is not exact. When the CD4 cells has gone down, it is indicative of a
weakened immune system. The lower the CD4 cells, the more probable the patient will become sick. A patient loses the ability to fight infection when
the CD4 cells have gone down. Once the patient has lost the ability to fight off germs, an opportunistic infection such as pneumonia, skin infections,
oral disorders, diarrhea, AIDS related dementia, Kaposi sarcoma, and CNS disorders may occur. Routinely patients are advised to check CD4 cells
every three to six months when initiating antiretroviral treatment and once levels has increased, test every six to twelve

Research Study on the Interaction Among Platelets and...
Subjects
The study subject was divided into 4 groups. Group I: 21 patients with hepatic schistosomiasis (12 male and 9 females). Group II: 18 patients with
HCV infection (10 male and 8 females). Group III: 23 patients with concomitant hepatic schistosomiasis and HCV infections (13 male and 10 females).
Group IV: 20 healthy individuals as controls (12 male and 8 females). Full history taking including contact with water canal water were collected from
the study subject
Abdominal ultrasound
Ultrasonography was conducted to all study subject to assess the hepatic physical condition including the grading of portal tract thickening in S.
mansoni positive patients and the extent of liver cirrhosis.
Liver function tests
Serum levels of AST,... Show more content on Helpwriting.net ...
HCV–RNA levels were analyzed by real time polymerase chain reaction using a commercial kit (Bioer, Technology Co., Ltd) according to the
manufacturer's instructions.
Flow–cytometeric analysis
Platelets rich plasma (PRP) were separated and freshly tested for CD41, CD42, CD62P and CD63 expression using fluorescein isothiocyanate (FITC)
and phycoerythrin (PE) conjugated monoclonal antibodies (mAbs) (BD Biosciences. Com, Pharmingen TM). The flow cytometry for the immune
cells, EDTA treated blood was labeled with 10 Вµl monoclonal antibodies (mAbs) in 3 tubes. Tube 1 forT cell contained CD3–peridin chlorophyll
protein (PerCP), CD4–fluorescein isothiocyanate (FITC) and CD8–phycoerythrin (PE). Tube 2 for NK cells contained CD16/CD56 PE and CD 3
FITC. Tube 3 for B cells contained CD19 FITC and CD22 PE (all Becton Dickson, San Jose, Calif). A non specific Isotype Control was used in each
sample. All antibodies were of IgG1k Isotype Flowcytometer Epics В® Elite К»К»CoulterКјКј system was used for analysis. Results were expressed
as a specific percentage of positive markers, calculated by subtracting the non specific fluorescence of the Isotype control form the specific fluorescence
of the mAbs. For subtraction, the manufacturer's software was used [15].
Statistical analysis
Statistical analysis was performed using Instat software. ANOVA test was

Case Study Of Multiple Sclerosis (MS)
Multiple Sclerosis (MS), is an autoimmune disease in which the surrounding protective coating layer of the axon, myelin, is degraded, resulting in the
formation of inflamed lesions (also referred to as plaques) around the regions of the brain and spinal cord. The myelin sheath is not only a protective
layer, but it also increases the speed of electrical impulses transfer across the body via saltatory conduction. Depending on the severity of damage to the
myelin, it can slow down or distort messages travelling along nerve fibres, some signals may not pass through at all, as damage may eventually
degrade and impair the axon itself. This attack is carried out by cytotoxic T cells (CD8+) , which are activated by tip–dendritic cells. It has been
observed in case studies where in the presence of increased concentration of CD8+, there is a positive correlation to the increased damage brought to
the myelin. However, there are alternative studies that imply that because the myelin presenting peptide CD4+ is involved in the onset of
inflammation, the CD8+ may be the one attempting to prevent the attack on the myelin. Still no one is sure of the cause, or is fully aware of the true
functions of the receptors involved. ... Show more content on Helpwriting.net ...
The tip–dendritic cell has an added function in which it is able to load a myelin peptide, extending the transfer from CD4+ to CD8+. This brings about
a secondary autoimmunity as the CD8+ is able to respond to oligodendrocytes and cause them to lysis because the CD8+ is able to recognise myelin
protein on these oligodendrocytes which constitute the myelin

The Human Immune System Of Multiple Structures
The human immune system consists of multiple structures. These structures include the following: tonsils and adenoids, thymus, lymph nodes, spleen,
appendix, lymphatic vessels, and bone marrow. HIV involves many structures/components of the immune system, so it is important to understand the
structures and function of each involved component. Calles, Evans, and Terlonge (2010) clearly explain the parts of the immune system affected by HIV.
To begin the immune system uses antigens to help fight against infection by working with antibodies to produce an immune response (Calles, Evans, &
Terlonge, 2010). Furthermore, the immune system produces lymphocytes (i.e. also known as white blood cells). There are two types of lymphocytes
produced, B cells and T cells. B cells remain in bone marrow (i.e. where B and T cells are made) and T cells move to the thymus (Calles, Evans, &
Terlonge, 2010). After their migration, T cells finish cell development, become immunocompetent, replicate, and differentiate. There are two important
functions of T cells, which include maintenance of the immune system and destroying cells with certain antigens. There are distinct T cells which are
identified by surface markers (Calles, Evans, & Terlonge, 2010). Concerning HIV, CD4+ are impacted the most. These cells are responsible for
triggering B cells and macrophages when an antigen is present (Calles, Evans, & Terlonge, 2010). Furthermore, T cells discharge cytokines, which are
involved in

Tcr Recognition
T–cells are one of the key factors in the adaptive immune system which specifically recognize the virus infected and tumors cells. These cells
recognize antigens (epi–topes or tumor antigens) using protein known as T–cells receptor TCR which is heterodimer and is consisted of an alpha (О±)
and beta (ОІ) chains. The fully matured T–cells population expressing О±ОІ T–cells receptors (TCR) composed of the T–cells which expresses CD4 or
CD8, and the CD4– or CD8– ОіОґ expressing T–cells receptor cells. The specificity of the CD4+ and CD8+ T–cells is directed by the expression of
the co–receptors, CD4 and CD8. The ligand for CD4 is the ОІ2 domain of the (MHC) class II molecule however for the CD8 the ligand is О±3 domain
of MHC class I moluecule. Therefore,... Show more content on Helpwriting.net ...
Therefore, TCRs are unable to target tumor antigens such as carbohydrate or lipid antigens. However, genetically modified T–cells expressing CARs
(chimeric antigen receptors) avoid the TCRs limitation and can recognize intact antigen i.e. cell surface proteins, carbo–hydrate and lipid tumor
antigen. Moreover, tumor can also down regulation expression of HLA. The T–cells expressing CARs can be used regardless of the HLA types in
adaptive T–cells therapy. Interaction of the unique О±ОІ TCR of the T–cells to the specific antigen presented on either class I or II MHC molecule of
antigen presenting cells (APCs) result in the activation of the T–cells. This type of activation is called "Signal 1", which is not sufficient for optimal
activation and proliferation of the T–cells. Therefore, an optimal activation and proliferation requires an additional co–stimulatory "signal 2", provided
by CD28 molecules on the surface of the APCs. Interaction of the CD28 molecule to its ligand B7–1(CD80) and B7–2 (CD86) increases the
proliferation of the

The Role Of Initiation And Ligand Interaction Of Resting...
2.2.3 Role of VLA–4 in Costimulation Integrin receptor/ligand interactions provide a potent costimulatory signal to CD3–mediated T cell activation
(Davis et al., 1990; Nguyen et al., 2008). Specifically, the VLA–4 mediated interaction of resting human CD4+ T lymphocytes with FN has been
shown to promote CD3–mediated T cell proliferation (Shimizu et al., 1990). Coimmobilization with mAb to CD3 and FN consistently resulted in
strong T cell proliferation. Other investigators showed that immobilized FN enhances anti–CD3 induced proliferation of both CD45RAdim (memory)
and CD45RAHI (naГЇve) subsets of CD4+ and CD8+ T cells, and that this effect was inhibited with a mAb against the ОІ1 subunit of VLA–4.
Additionally, Nojima et al. showed that the A and B epitopes of VLA
–4 play a key role in VLA–4 mediated T cell costimulation (Nojima et al., 1990).
2.3 Role of О±4–integrin in CNS immunocompetence 2.3.3 О±4–integrin Antagonism in EAE As previously described, leukocytes activated in the
periphery are able to adhere to the endothelium of blood vessel walls in order to traffic into the CNS, where re–activation by antigen presentation from
perivascular APC leads to inflammation. In 1992, Yednock et al., which would later develop a successful therapy for RRMS patients, made a
revolutionary finding. They reported that lymphocytes and monocytes bound selectively to inflamed EAE brain vessels and that this could be reversed
with antibodies against VLA–4 (Yednock et al., 1992). When tested in

Human Immunodeficiency Virus And Acquired Immune...
Human Immunodeficiency Virus and Acquired Immune Deficiency Syndrome
In 1981, the first cases in the United States of Acquired Immune Deficiency Syndrome (AIDS) developed in Los Angeles and New York (Fraser,
Burd, Liebson, Lipschik, & Peterson, 2008). The illness presented itself among several homosexual males who developed rare opportunistic infections
such as Pneumocystis carinii pneumonia and Kaposi's sarcoma (Sharp & Hahn, 2011). At the time, medical professionals deemed the infections to be
"gay–related infectious diseases" (Pence, 2008). However, three months after this diagnosis, medical professionals revealed the presence of the same
infection among newborns whose mothers used intravenous drugs (Pence, 2008). In 1984, scientist ... Show more content on Helpwriting.net ...
Pathophysiology The Human Immunodeficiency Virus has two types, (type 1 and type 2), followed by nine different subtypes based on the simian
location from which each strand originated (Sharp & Hahn, 2008). According to Sharp and Hahn (2008), Human Immunodeficiency Virus Type 1 is the
most common cause of Acquired Immune Deficiency Syndrome worldwide and originates from the Simian Immunodeficiency Virus found in
sub–Saharan African chimpanzees and gorillas. Specifically, group M represents the most common strand of Human Immunodeficiency Virus Type 1
(Sharp & Hahn 2008). The original contraction of SIV–1 in humans followed the consumption of bush meat collected from hunting HIV infected
chimpanzees and gorillas (Sharp & Hahn, 2008). Once in the human body, the Simian Immunodeficiency Virus became the Human Immunodeficiency
Virus (Sharp & Hahn, 2008). Although originally acquired through the consumption of infected simian blood, the most predominant contracting factor
in today's society is through unprotected sexual intercourse, whether oral, anal, or vaginal, and the exchange of infected blood (Fraser et al., 2008).
The Human Immunodeficiency Virus is a retrovirus originally encoded in ribonucleic acid or RNA (Fraser et al., 2008). HIV virions travel through
the blood stream and other bodily fluids in order to infect

Muurine T Cell Transfer Model Of Colitis
In patients with IBD (European Journal of Immunology 2012 & Human Immunology paper) and in experimental murine T cell transfer models of
colitis ( American Journal of immunology), environmental stimulants to the cells of the mucosal immune system (such as commensal microorganisms)
have been shown to elicit pro–inflammatory and anti–inflammatory cytokine production. The figure below effectively shows the crucial transcription
factors and cytokines generated by the T helper cell subsets in IBD–affected mucosa, also portraying significance of individual cell response pathways.
Inflammation in IBD is caused by the loss of homeostasis between CD4+ CD25+ Foxp3+ regulatory cells (Treg) and proinflammatory effector Th17
cell, therefore the role... Show more content on Helpwriting.net ...
Additionally the European journal of Immunology 2012 demonstrates that Purinergic signalling and associated ectonucleotidases, such as CD39 and
CD73, have been implicated in the pathogenesis of IBD and also found that there was elevated levels of CD73+CD4+ T cells in the peripheral blood
and intestinal lamina propria of patients with active IBD which returned to baseline levels following anti–TNF treatment. Therefore, expression of
CD73 by peripheral CD4+ T cells is heightened by TNF, and lessened by an anti–TNF monoclonal antibody (e.g. infliximab). These CD73+CD4+ cell
populations conveyed CD45RO, elevated levels of RORC, IL–17A, and enrichment in TNF, whilst there was lower levels of FOXP3 and/or CD25.
Th17 cells vastly permeate the inflamed intestine of IBD patients, where they produce cytokines such as interleukins (IL–17A), rapidly stimulating the
inflammatory process. Therefore it can be confidently deduced increased CD73+CD4+ T–cells leads to higher concentrations of the T–helper type 17
phenotype seen in active IBD patients, and could thus be used to monitor IBD during treatment. Tumour Necrosis Factor (TNF) also plays a central
role in the pathogenesis of IBD as it has been shown to exert various

ICL Case Study
ICL was first defined by Center for Disease Control and Prevention in 1992 as low CD4 cell counts in the absence of HIV and other secondary
causes of immunodeficiency. Idiopathic CD4 Lymphopenia is a rare immunological disorder associated with persistent Low CD4 counts. The mean
age at diagnosis is 41 years with slight male predominance [1]. Diagnosis Criteria for ICL includes low CD4 count < 300 cells or <20% of the total
Lymphocyte count in the absence of HIV infection and secondary evidence of Immunodeficiency conditions associated with low CD4 counts [1] but if
there is concomitant anemia and thrombocytopenia then other causes must rule out. In contrast to HIV, there is a slow progressive decline in CD4
counts and number of CD8 counts... Show more content on Helpwriting.net ...
ICL is a diagnosis of exclusion so secondary causes of Lymphopenia must be excluded to arrive at the diagnosis. The most common secondary causes
are viral and bacterial infections, chemotherapy and cytotoxic drugs, malignancy and autoimmune conditions. There is no consensus for diagnostic
investigations ICL but the work up should be dictated by the presenting opportunistic infection and generally should include CD4, CD8, natural killer,
and B–cell subsets, immunoglobulin levels, HIV 1–2 serology and PCR, HTLV 1 and 2 testing, EBV and cytomegalovirus PCRs, and an autoantibody
panel. The diagnosis is especially challenging in the presence of autoimmune diseases, since lymphopenia can be secondary to autoimmunity and vice
versa, with transient immunosuppressant therapy–induced lymphopenia further complicating matters [4]. Although no published guidelines for
management of ICL exist, it is logical to assume that primary and secondary prophylaxis and treatment of opportunistic infections should form the
mainstay of therapy. Prophylaxis strategies generally follow recommendations for HIV. Interleukin 2 and hematopoietic cell transplantation have been
successfully used to augment the CD4 count in ICL whereas interleukin 7 are currently being studied [3]. There is a study done in December 2015
which used Interleukin 7 for treatment for ICL and it showed significant good results. Polyethylene Glycol Interleukin 2 has been used in the treatment
of

Pros And Cons Of Antiretroviral Therapy
Antiretroviral therapy; advantages and disadvantages:
As have been described above, HIV can have a potential effect on immunological cells, which are important to protect the body from additional
infections such as Tuberculosis (TB), Cytomegalovirus (CMV) and other viral or bacterial infections. An effective treatment is needed to reconstruct
what HIV has damaged. Antiretroviral therapy (ART) is a common treatment to stop the viral replication and decrease the disease progression, which
may lead to a vast decline of the morbidity and mortality. The standard treatment involves a combination of at least three drugs; often known as a
highly active antiretroviral therapy (HAART) where the most common types are Nucleoside reverse transcriptase ... Show more content on
Helpwriting.net ...
Recent studies suggested that CD4 domain specific monoclonal antibody such as mAb (15A7) and Ibalizumab have a great revolution in HIV–1
treatment area. The majority of previous mentioned treatments constitute to either restore the immune response or decline the plasma vireamia,
however, this type of treatment is more likely to interfere with the HIV–1 structure. Before explaining how this category of drugs works, it is necessary
to clarify the reaction between HIV–1 glycoproteins and CD4. Once the virus enters the body, HIV–1 envelope glycoprotein (gp120) attaches to a
cellular CD4 receptor. As CD4/gp120 is formed, it allows gp120 to attache to chemokine receptor–5 (CCR5) or CX chemokine receptor–4 (CXCR4)
allowing gp41, another viral envelope molecule, to insert into the target cell membrane leading to fusion the viral envelope and cellular membrane
(Christopher et al., 2010). Ibalizumab is CD4 domain–2 monoclonal antibody using as an effective treatment to enhance the CD4 counts. In a study
which set out to determine the antiviral efficacy of Ibalizumab on HIV–1 positive patients not on (ART), (Christopher et al., 2010) found that the CD4
counts increase after one day of drug initiation even before the viral load decline. This suggested that the rise of CD4 counts is possibly due to
redistribution of CD4 cells from lymphoid tissues rather than regeneration of these cells. Notably, niegher

Explain The Pathophysiology Of Hiv Virus
Pathophysiology of the human immunodeficiency virus
Nancy R. Calles, MSN, RN, PNP, ACRN, MPH Desiree Evans, MD, MPH DeLouis Terlonge, MD
Objectives
1. 2. 3. 4. 5. Provide an overview of the healthy immune system. Describe the human immunodeficiency virus (HIV). Describe the major components of
the HIV life cycle. Identify the various HIV types and subtypes. Discuss HIV's effects on the immune system.
Overview
The human immunodeficiency virus (HIV) is a retrovirus belonging to the family of lentiviruses. Retroviruses can use their RNA and host DNA to
make viral DNA and are known for their long incubation periods. Like other retroviruses, HIV infects the body, has a long incubation period (clinical
latency), and ultimately causes the signs ... Show more content on Helpwriting.net ...
Found throughout the body, phagocytes rid the body of worn–out cells, initiate the immune response by presenting antigens to lymphocytes, are
important in immune response regulation and inflammation, and carry receptors for cytokines. Dendritic cells, another type of phagocyte, also are
antigen–presenting cells. They have long, threadlike extensions that help trap lymphocytes and antigens and are found in the spleen and lymph nodes.
Neutrophils are granulocytic phagocytes that are important in the inflammatory response.
Figure 1. Organs of the Immune System
B Lymphocytes
The main function of B lymphocytes is humoral (antibody) immunity. Each B cell can recognize specific antigen targets and can secrete specific
antibodies. Antibodies function by coating antigens, which makes the antigens more vulnerable to phagocytosis (engulfing and ingestion of invading
organisms by leukocytes and/ or macrophages), or by triggering the complement system, leading to an inflammatory response. Antibodies are highly
specialized serum protein molecules. They are grouped into five classes, each having a specialized function: immunoglobulin G (IgG), IgA, IgM, IgE,
and IgD.
Complement
The complement system consists of 25 proteins. Complement can induce an inflammatory response when it functions with antibodies to facilitate

phagocytosis or weaken the

Hiv And Its Effects On Children
HIV
What is HIV?
HIV stands for human immunodeficiency virus. Infection by this virus frequently leads to AIDS – acquired immunodeficiency syndrome. Viral
infection initially causes a flu–like illness characterized by fever, sore throat, headache, rash, gastrointestinal discomfort, and body aches (mylagias).
The virus tends to stay dormant for months or years while it is slowly killing immune cells – especially CD4 cells.
Individuals with high viral loads and low CD4 cell counts have high viral infectivity and tend to develop opportunistic infections – atypical infections
that generally affect immunocompromised hosts. AIDS is a common cause of death worldwide, buts its medical treatment in developed countries has
led to a significant ... Show more content on Helpwriting.net ...
The virus tends to lie dormant for months or years, slowly and progressively killing immune cells. Patients eventually develop opportunistic infections
as their CD4 counts decrease below 200.
How common is HIV infection?
HIV is relatively common in the United States and responsible for a fair amount of deaths. This condition is a frequent cause for referral to an
infectious disease specialist.
In 2015, worldwide – approximately 37 million adults and children had HIV or AIDS, 2 million were newly infected that year, and 1 million people
died of the condition. Sub–Saharan Africa makes up about 75% of the word's HIV–infected population. Approximately 3.3 million children have HIV
/AIDS in the world – most of these patients are born in sub–Saharan Africa and Southeast Asia.
The prevalence of HIV seems to be stabilizing overall, however some countries are still demonstrating an increase. Since 2001, there has been about a
38% decrease in the incidence of HIV infection.
What are the symptoms and signs of HIV infection?
Symptoms of acute HIV infection are flu–like and typically include:
Fever
Enlarged and painful lymph nodes – lymphadenopathy
Rash
Sore throat
Body aches
Headache
Weight loss

Night sweats
Anorexia – loss of appetite
These typically subside and the virus then hibernates in the lymphatic system. Months or years later, the CD4 cells become significantly depleted

Innate Response : The Innate Immune Response
There are two branches of the immune response: the innate immune response and the adaptive immune response. The innate immune response consists
of multiple leukocytes that recognize pathogen associated molecular patterns (PAMPs) [1]. These PAMPs are non–specific, conserved motifs present
on a broad range of pathogens, and are recognized through various pattern recognition receptors (PRRs) on leukocytes, which trigger a
pro–inflammatory response [1]. Conversely, the adaptive immune response is composed of only two leukocytes, B lymphocytes and T lymphocytes.
Both subsets of lymphocytes have the capacity to generate an immune response specific to the invading pathogen [1]. In order for this to occur, the
adaptive immune system must be able to recognize specific foreign antigens, as opposed to conserved motifs. Thus, stringent regulation of both B and T
lymphocytes must occur in order to prevent recognition of self–antigens as foreign; this process is termed self–tolerance. Self–tolerance occurs through
two mechanisms. The first is central tolerance, which takes place in the thymus (T cells) and bone marrow (B cells) [2]. Central tolerance selects for
individual B and T cells, which do not recognize self–antigens presented to them in the primary lymphoid organs, to continue maturation [2]. The
second is peripheral tolerance, which occurs outside of primary lymphoid organs, where B and T lymphocytes are further selected for self–reactivity to
antigens that were not presented to

Vaccine : Chromium Release Assay For Measure Cd4 +
At each stage of testing the following assays will be used to monitor the immune response to the vaccine: Chromium release assay to measure CD8+
response, thymidine incorporation assay to measure CD4+ proliferation and ELISPOT to measure B cell responses. Tumour regression will be looked
for using MRI techniques and visually on the skin. In all phases of clinical trials, patients that can no longer benefit from approved treatments will be
used. Stage 3 and 4 patients only will be used due to potential side effects. Patients that do not respond to treatment after 6 months will be removed from
the program. Patients that do respond will participate in the trials until death and will be monitored every 6 months, with maintenance vaccines... Show
more content on Helpwriting.net ...
During phase 4, sentry studies will take place.
Manipulated DCs frequently have trouble migrating to lymph nodes; therefore the vaccine will be administered via an intranodal injection at the
closest lymph node to the tumour. Since DC vaccines have little to no toxicity, as many DCs that can be prepared as possible will be injected. The
vaccine will be injected 4 times biweekly. Ipilumumab and MDX–1106 will be given once every 3 weeks via intravenous infusion for 12 weeks. Niacin
will be taken once every day in the form of a tablet for 12 weeks.
This vaccine will be used in conjunction with the anti–CTLA–4 antibody, Ipilumumab, to keep T cells active for longer by blocking CTLA–4 T cell
inhibitory signals. Anti–PD–1 antibodies such as MDX–1106 will also be used to block the PD–1 ligand from binding the PD–1 receptor. This receptor
when activated can promote T cell apoptosis and also reduce T–reg apoptosis. Tumour cells frequently upregulate PD–1 to downregulate the immune
system in the tumour microenvironment, so the use of this antibody is almost essential when trying to produce active immunotherapy. Niacin will also
be given to patients to increase blood flow within the tumour, in turn allowing increased access to the tumour site for immune cells. Radiotherapy will
be

Genetic Engineering Technology
Modern genetic engineering technologies are advancing, and genetically modifying a genome is becoming a reality. The Clustered Regularly
Interspaced Short Palindromic Repeats (CRISPR) and CRISPR–associated system (CAS9) genome editing system is the most advanced in use.
CRISPR can edit a genome more accurately and with higher precision than any other system. The intended use of the CRISPR/CAS9 system is to
insert a gene, delete a gene, or silence a gene, leading to powerful applications (Christensen and Choy 2017a). For example, scientists plan to use this
technology to change the genome and resulting phenotype in the efforts to eliminate potentially lethal diseases. One such disease is Human
Immunodeficiency Virus (HIV) and Acquired... Show more content on Helpwriting.net ...
CRISPR was first exploited in 2007, by a food ingredient company. Their focus was on applications of the system to fermented milk bacteria
(Streptococcus thermophilus) in the production of yogurt and cheese. By utilizing the CRISPR system, the company was able to vaccinate the bacteria
used in their product against unwanted bacteriophages (Stachler and Marchfelder 2016a). Since then, the greater applications of the system have been
realized.
CRISPR is an adaptive natural immune system used by bacteria to protect against bacteriophages that replicate within the bacterium. It starts when a
bacteriophage lands on the membrane of a bacterium cell, where it injects its DNA into the cell. Shortly after the DNA is injected, the infected
bacterium detects the presence of bacteriophage DNA, leading to a production of a complex. The complex consists of the CAS9 nuclease and a
twenty–base sequence short guide RNA known as sgRNA. The complex wraps around the bacteriophage DNA, and travels along until it reaches a
targeted sequence indicated by the RNA. The sgRNA searches for complementary bases, only attaching at that region of the genome, ensuring the
proper location. Upon reaching the location, the CAS9 enzyme will proceed to make a double stranded cleave through the DNA, disabling the
bacteriophage and protecting the bacteria (Richter et al. 2012a).
Bioengineers have generated a custom sgRNA within a CAS9 nuclease to search for a specific gene location within the

Logic Based Mechanistic Model Of CD4 And T Cell Phenotypes
In this study, we sought to investigate possible CD4+ T cell phenotypes under diverse environmental conditions, and how the dosage of extracellular
inputs (cytokines and TCR) regulates these phenotypes. To study these questions, we build a knowledge driven logic based mechanistic model of
CD4+ T–cells. We performed extensive search of published literature to build the model, however it is possible that model may have missing links or
components. Logic based models found to be useful in the absence of detailed biochemical information and were previously used to model gene
regulation, and signal transduction (Ref.). Next, using all inputs compositions, we systematically characterized the network behaviors. We found that
the network arrived ... Show more content on Helpwriting.net ...
Thus, the clear differentiation of Th17 will depend on dosage of IL6. In a recent study it was found that RORОіt – Foxp3 co–expressing cells were
enriched in the large intestine (Ohnmacht et al., 2015, Fang and Zhu, 2017). Furthermore, Th17–Treg phenotypes were also observed in vivo in
autoimmune diabetes model and in vitro in lamina propria (Ichiyama et al., 2008; Zhou et al., 2008; Evans and Jenner, 2013). Moreover, Th1–Treg
intermediate phenotypes were observed during Th1 polarizing infections (Stock et al., 2004; Koch et al., 2009, Oldenhove et al., 2009; Evans and
Jenner, 2013).
In addition to the hybrid phenotypes co–expressing two lineage specifying T cells, we also obtained phenotypes with the activity of more than two
TFs, i.e., Th1–Th2–Treg, Th1–Th17–treg, and Th1–Th2–Th17–Treg. It was shown previously that the basal levels of Tbet and GATA3 can be
expressed by subset of Treg cells and the dynamic balance of these TFs helps in maintaining immune tolerance (Yu et al., 2015). Here, we predict the
novel phenotypes that can activate three TFs (Tbet–GATA3–Foxp3, Tbet–RORОіt–Foxp3) and all four TFs (Tbet–GATA3–RORОіt–Foxp3). However,
in these phenotypes Tbet and GATA3 have the higher activity levels than the activity levels of Foxp3.
By analyzing all possible input compositions, we obtained the minimal and maximal inputs for each phenotype. The minimal composition include
minimum number of inputs that can stimulate a phenotype, on the

Hiv And Aids : A Deadly Virus Essay
HIV and AIDS Explained
Sebastian V. Aparicio
NorthWest Career and Technical Academy
The human immunodeficiency virus commonly known as HIV, is a deadly virus if left untreated. Unfortunately there's no cure, but ever since the
outbreak 30 years ago in the United states, there have been many advances in drugs.5 The death of HIV has decreased, as well as the amount of people
getting diagnosed. All in all, HIV has a unique life cycle with stages that it advances to, and has caused unwanted stigma and discrimination throughout
the United States.
HIV follows specific steps in order to infect the host. In the first step of the HIV life cycle, binding occurs. In this step, HIV attaches itself to a
specific white blood cell known as CD4.1 These cells are responsible for sending signals to activate the immune system response in helping detect
harmful pathogens.2 Fusion of the HIV and CD4 envelope then allows HIV to enter the CD4 cell.1 Once in the cell, reverse transcriptase is
released in order to convert HIV RNA into HIV DNA.1 Because of that, HIV is now able to enter the CD4 nucleus. HIV then uses another enzyme
integrase which allows HIV DNA to combine with CD4 DNA.1 Soon after, HIV proteins are made from the machinery of CD4; those proteins are the
blueprints in making more HIV.1 The new HIV proteins and RNA assemble into new immature HIV once in the surface of the cell.1The last step is
budding, in this step the new HIV goes outside of

Human Immunodeficiency Virus ( Hiv )
Human Immunodeficiency Virus (HIV) is a retro virus that causes AIDs by infecting the T Helper cells of the body's immune system. The AIDS virus
is the final stages of the HIV virus. HIV is a lentivirus genus, which is a subgroup of the retrovirus that causes the AIDS virus. Even with proper
treatment, an infected person has a life expectancy of less than ten years.As the virus weakens the human immune systems, this effectleaves the patient
compromised and at risk to opportunistic infections that the body would have once had the ability to fight, such as the flu, colds, and pneumonia. HIV
attacks the cells in our immune system such as the helper T cells and is directly related to the CD4*T cells, macrophages, and dendritic cells. The
HIV infection diminishes the levels of CD4*T cells. When the CD4*T cells drop to a critical low level, the body then becomes progressively more
susceptible to opportunistic infections. Two types of HIV have been characterized: HIV–1 and HIV–2. HIV–1 is the virus that was initially discovered
and termed both LAV and HTLV
–III. It is a more virulent strain, more infective, and is the cause of the majority of HIV infections globally. The lower
infectivity of the HIV–2 strain compared to HIV–1 implies that fewer of those exposed to HIV–2 will be infected per exposure. Because of its
relatively poor capacity for transmission, HIV–2 is largely confined to West Africa. (Wikipedia, 2014) Transmission routes for passing the HIV
infection are

Inhibitory Effects Of Psoriasis In Mice
The paper I chose to provide a summary of was one that examined the use of stem cells in order to decrease psoriasis in mice. The researchers
specifically used Mesenchymal stem cells (MSCs), which are those found in the umbilical cord blood. They are multipotent and therefore are able to
differentiate into many different types of tissues. These stem cells, in particular, have an "inhibitory effects on innate and adaptive immune cells"
(Lee). The hallmark of a diagnosis of Psoriasis is the visible skin irritation with red plaques on the epidermal level of the skin. The cause of the
plaques is from cytokines and chemokines, which signal cells secrete proinflammatory responses encouraging a spike of immune cells in the region. The
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Yet another difference is the treatment period, where this treatment lasted for only five days in comparison to 15 in the other treatment method. The
mice treated in the imiquimod group were either injected with embryonic stem cells the day prior to the first treatment of imiquimod or no stem cells
were given at all during the study period.
After the completion of the trial period for both of the inflammation inducing methods, researchers harvested the ears and performed real–time PCR on
them. This process required dendritic cells and CD4+ cells. In order to isolate the dendritic cells, researchers harvested cells from the bone marrow.
The collection of CD4+ cells in the mice took cells from the infected back skin. They then looked at the effect of co–culturing naГЇve CD4+ cells with
the dendritic cells. Isolating the RNA in the CD4+ cells after the culturing period provided the researchers the RNA needed to complete real–time PCR
and determined the antiproliferative effect of the treatment with MSCs. In addition, the researchers harvested spleens, lymph nodes and the skin on the
mice's back to test with flow cytometry.
The researchers found that when they injected the mice with MSC, the normal inflammatory response that IL–23 has was not functional. The
epidermal skin level did not increase in thickness, nor increase in immune cell infiltration, both of which are the normal responses to IL–23 treatment.

The Median Survival Time Of Cd4 + Lymphocyte Count At 200...
The overall estimated survival time from CD4+ lymphocyte count at 200 x 106/L to death was 43.4 months, which was a little longer than that from
San Francisco Homosexual Cohort Study (3). The median survival time of 38 months from CD4+ lymphocyte count at 200 x 106/L to death in San
Francisco Homosexual Cohort Study was quite similar to the result from the study of 17 Korean homosexual men (39.7 months). In Multicenter AIDS
Cohort Study, 71 % of HIV infected persons with CD4+ lymphocyte count in the range of 101 – 200 x 106/L were alive for 2.5 years from 1989 to
1993 (4). In this study, 70.6 % of subjects survived for 2 years and 66.6 % of subjects survived for 2.5 years from the date of CD4+ lymphocyte count
at 200 x 106/L to death.
The median survival time of 19.8 months from the estimated date of CD4+ lymphocyte count at 50 x 106/L to death was somewhat longer than that
reported by Elizabeth G. (16 months, >25% at 2 years)(12). Robert Yarchoan showed that the median survival time of HIV infected persons with CD4+
lymphocyte count less than 50 x 106/L was 12.1 months (95% confidence interval: 7.2 –19.4 months) (13). According to the previous report that
AIDS–defining diseases occurred at CD4+ lymphocyte count of 50 x 106/L for diagnoses, we compared our result of survival time from CD4+
lymphocyte count at 50 x 106/L to death with other AIDS survival studies. Ninety–seven percentages of AIDS patients survived at 6 months and 86%
of them at 12 months in France (14). The

HIV In The African American Community

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