Human Immuno Deficiency Virus ( Hiv )

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
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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

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
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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

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 to HIV–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 TRIM5α
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 Δ32
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 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

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 ...
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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

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

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
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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:

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

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

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
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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

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

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 Helpwriting.net ...
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

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
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

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

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

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

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

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

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) X² Y² 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 Helpwriting.net ...
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

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

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

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 ∆ 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 ∆ 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

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

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

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

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, and AIDS:
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

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 (naïve) subsets of CD4+ and CD8+ T cells, and that this effect was
inhibited with a mAb against the β1 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 α4–integrin in CNS immunocompetence 2.3.3 α4–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

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

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 ∆ 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

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

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 RORγt – 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–RORγt–Foxp3) and all four TFs (Tbet–GATA3–RORγt–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

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
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

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 µl monoclonal antibodies (mAbs) in 3 tubes. Tube 1
for T 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 ® Elite ʻʻCoulterʼʼ 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

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 (α) and
beta (β) chains. The fully matured T–cells population expressing αβ T–cells receptors (TCR)
composed of the T–cells which expresses CD4 or CD8, and the CD4– or CD8– γδ 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 β2 domain of the (MHC) class II
molecule however for the CD8 the ligand is α3 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 αβ 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

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
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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

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 ... Show more content on Helpwriting.net ...
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 naïve 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 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

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
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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

Human Immuno Deficiency Virus ( Hiv )

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