Running Head: Immunology
Running Head: Immunology
Running Head: Immunology
Immunology
Name:
Institution of Affiliation
Immunology 2
Question 1
The 40-year-old patient was diagnosed with influenza virus after his swab was
analyzed in the laboratory. He had been reported to have flu like symptoms which include
fever, running nose and coughing. This virus is having been reported to be a worldwide threat
to human and animal health and is likely to cause a pandemic with high death rates (Petrova
& Russell, 2017). This virus attacks the respiratory system for replication such as
tracheobronchial tree and the nasal mucosa (Broecker et al., 2018). The infection starts with
adsorption of the virus to the target cells. The virus has two factors that facilitate infection
one of these is neuramidase which facilitates the release of the virus to the target cells. The
other is hemagglutinin which plays a role in facilitating the attachment of the virus to the
surface of cells, through binding to the sialic acid receptors on epithelial cell surface.
The antibodies that act against neuramidase are normally not effective while the one
that act against the hemagglutinin are very efficacious and protect the body against infection.
Once the cells are infected the virus replicates and causes serious health threats to the patient.
Once this happens the host immune response then responds to protect and eliminate the virus
from the body. The main target of the influenza virus are the epithelial cells in the in the
respiratory system. The first line of defense for this virus is innate immunity which is
responsible for the early intervention in containment of the virus before more protection is
offered by adaptive immunity (Iwasaki & Pillai, 2014). Innate immunity acts by forming
physical barriers such as collectins and cellular immune response. This immunity is
controlled by cytokines and chemokines released by the infected cell as well as antigen
presenting cells.
This immune response acts in two ways, in the first step the infected cells and antigen
presenting cells stimulate innate immunity by secretion of type one interferon (Kreijtz,
Immunology 3
Fouchier & Rimmelzwaan, 2011). This type one interferon is secreted by infected cells on the
interferon receptors of this cells or the adjacent cells. The antiviral signaling cascade is
stimulated and the signal transducers Janus kinase 1 and tyrosine kinase 2 are
phosphorylated. These kinases become activated and phosphorylate signal transducer and
activator of transcription STAT 1 and STAT 2 which then form a complex with interferon
gamma regulatory protein9(IRF9). The resultant product is interferon stimulated gene factor-
3 transcription complex (ISGF-3). This complex plays a role in the transcription of genes that
encode antiviral proteins which establish and viral resistant state in the cells thereby
inhibiting replication of the influenza virus. Type one interferon is eliminated in the body
Therefore, the first step plays a role in inhibiting the replication of the virus and thus
it provides enough time required for the adaptive immunity to become active and eliminate
the virus. In the second step the antigen presenting cells and infected cells stimulate the
natural killer cells activity which then destroys the infected cells so that they don’t release the
complex 1. In turn the sialic acid receptors bound by haemagluttin proteins become expressed
on the influenza virus infected cells surface leading to the direct destruction of infected cells.
During this period the antigen presenting cells also activate the adaptive immunity through
secretion of virus specific plasma cells that are involved in eliminating the infection.
Question 2
Innate immunity cannot work solely to help the host eliminate the influenza virus
infection in the body. Once the body is attacked by disease causing pathogens the body’s
immune system responds by to protecting the body against infection. The immune system
accomplishes this by detecting and distinguishing the healthy cells for the infected ones. This
Immunology 4
is a complex system that coordinates two mechanisms to achieve the desired protection of the
host. These mechanisms are innate and adaptive immunity (Sun, Sun, Xiao, & Sun, 2019).
The adaptive immune response consists of lymphocytes the T and B cells that have specific
Adaptive e immunity is important as it ensures that the body keeps memory of the
infection and sets necessary measures to avoid reinfection. The formed immunological
response memory results in stronger and faster response if the virus infects the host again. On
the other hand, innate immunity is the first immune response against the pathogens before
adaptive immunity become active and eliminate the infection. Innate immunity basically
functions to provide time for adaptive immunity to recognize the virus before reacting and
eliminating it. Additionally, innate immunity is only specific for molecules and molecular
patterns found in general pathogens thereby it cannot help the host overcome the infection.
Innate immunity also has minimal diversity in terms of the receptors that are used
which can only recognize antigen patterns. In innate immunity there is no customization of
new receptors to adapt immune response. Adaptive immunity has great diversity and new
determinants. Therefore, adaptive and innate immunity have to work in coordinated action to
help the host in fighting the infection because they all play a role in ensuring that the host
Question 3
Adaptive immunity is the second line of defense which acts to protect the host against
infection by the influenza virus (Petrova & Russell, 2017). This immunity is initiated by virus
Immunology 5
specific CD4 and CD8 cells which cause cellular immunity and humoral immunity which is
facilitated by virus specific antibodies. These cells act by recognizing the virus, then multiply
and fight it together leading to its destruction and protection of the host. Innate immunity
cannot solely help the host to overcome the infection its specificity in recognizing pathogens
is not effective and thus it can’t recognize some of the viruses. It functions to activate the
adaptive immune response which occurs much later. Before the adaptive immune response
Adaptive immunity overcomes the influenza virus infection in the host by two
strategies these are humoral immunity and cellular immunity. Humoral immunity occurs
when Influenza virus in the host stimulates the secretion of virus specific antibodies secreted
by B cells. This are specific antibodies secreted to attack the hemagglutinin and neuramidase
protein of the influenza virus respectively. Antibodies are produced to attack the
hemagglutinin protein by binding to its receptor that is located in the protein and thus
inhibiting the receptor medicated endocytosis which is the binding of the virus to the host
cells. This immunity provided by this antibody is specific to a particular strain of the virus.
This immunity against the influenza virus infection provides a long-lasting immunological
memory that protects the body if a virus that resembles the previous strain infects the
Additionally, the other antibodies secreted to attack the neuramidase protein of the
virus do this by inhibiting the last phase if the virus replication cycle thus preventing the
spread of the virus in the host. These antibodies function through inhibition of the enzyme
activity of the protein leading to the neutralization of the virus. The spread of the virus
becomes limited and thus the duration and severity of the infection is reduced. Furthermore,
these antibodies stimulate antibody dependent cellular toxicity which functions in the
elimination of the cells infected by the virus. On the other hand, the host elicits cellular
Immunology 6
immune response against the influenza virus through CD4 and CD8 T cells that are specific
These two cells have a role in controlling the immune response and lysis of the virus
respectively. The activity of this cells is stimulated through the recognition of virus epitopes
in the class two molecules of the major histocompatibility complex and the reaction with
antigen presenting cells. The activity of the antibodies is increased through the switching of
the antibody classes and hypermutations in the somatic cells that affect the variable regions pf
the antibody. This then results in the maturation of the of the antibodies that are specific to
the influenza virus. After the infection of host by influenza virus memory is induced in the
CD4 cells which the helps the body in fighting the virus if it reoccurs.
Question 4 A
The influenza virus contains some antigens that possess large repetitive and sugar
molecules that lead to the stimulation of B cell immune response. To protect the body from
this infection B cell response is stimulated and reactivated in the respiratory tract after
infection and even in the incidence of reoccurrence of the virus (Lam & Baumgarth, 2019).
The activation of the B cells is done by innate immunity signals such as type one interferon.
These cells relocate to the mediastinal lymph nodes in the respiratory system where B-1 and
B-2 cells differentiate into IgM, IgA, IgG antibodies (Lu et al., 2016). This happens within
the three days of influenza virus infection in the body. The differentiation occurs through
plamablasts secreting antibodies and germinal centers that develop in the B cell follicles. The
plamablasts in the extrafollicular foci are involved in the B cell response of eliminating the
virus. The germinal centers establish long term plasma cells secreted by antibodies
Question 4B
The development of B cells in this patient begins the stems cells that are derived from
the bone marrow. Development continues through the spleen up to the final stage of
assembly and signaling of receptor of the B cell antigen. During this process the
immunoglobulin genes which are the heavy and light chain are rearranged in the pro- B and
pre- B stages. These B cells undergo positive and negative selection to ensure that they
develop properly. The positive selection involves antigen independent signaling of both the
pre-B cell receptor and B cell receptor (Nemazee, 2017). These receptors have to bind to the
On the other hand, negative selection involves the binding of the B cell receptor to
self-antigens present in the bone marrow. If the bond formed is strong the B cell undergoes
receptor editing, clonal deletion and receptor editing. The process of negative selection
ensures that the mature B cells don’t bind with self-antigens found in the bone marrow. The
stages in the development begin with the stem cell which forms the early pro B cells this
then develops into the late pro B cell which is followed by the formation of large B cell. The
large B cell then develops into a small B cell that then forms immature B cell. The formation
of the immature B cells is completed with two transitional stages through the relocation to the
spleen and at this stage they are referred to as T1 B cells. This T1 B cells then develop into
T2 B cells which undergo differentiation to form either marginal zone B cells or follicular B
cells and this is determined by the signals received from the B cell receptors (Kleiman, Jia,
Loguercio, Su, & Feeney, 2016). This differentiation is the final step that forms the mature B
Question 5
Infection by the influenza virus has caused a worldwide threat to the health of
individuals. This virus has been reported to cause deaths every year and the people who
survive their first infection with this virus stimulate an immunological memory which
protects the host from the reoccurrence of an infection brought about by the similar virus
strain (Nachbagauer & Krammer, 2017). This knowledge is the foundation of the provision of
the vaccine that is issued to individuals to protect them from infection by this virus. If the
patient in this case study had been immunized with influenza vaccine then the immunological
memory formed by the vaccine will protect him from the infection. However, if the patient
was infected by an influenza virus strain that was different from the one used in vaccination
then the patient will be infected severely by the virus as the body will recognize this as new
Most of the vaccines administered to people resemble the previous epidemic strains
or known strains so the if the patient undergoes infection by a different strain the he will
suffer severity of the illness (Maamary, Wang, Tan, Palese, & Ravetch, 2017). If the patient
is in this case study was affected by the same strain virus used in the vaccine then the vaccine
will offer protection, the hosts adaptive immune response will act by stimulating effector
mechanisms which act by either regulating the virus replication or inactivating their toxicity.
These immunological effectors include antibodies that are secreted by B cells and they play a
role in protection by binding to the influenza virus and eliminating it. Additionally, the
cytotoxic CD8+ T cells are also produced and they play a role in in recognizing and lysing
the cells that are infected by the virus thereby preventing spread of the infection in the body
(Cobey & Hensley, 2017). The T helper cells are also secreted and they assist in the
This T cells are important as they stimulate the secretion of antibodies that have high
affinity to the antigens of the influenza virus thus facilitating immunological response. The
CD4+ cells play a role in initiating antibody response which is required by the T cells to offer
protection to the host (Kramer, 2015). Additionally, innate immunity also plays a role in
protecting this vaccinated patient against infection by the influenza virus. Innate immunity
activates and shapes the functions of the adaptive immunity in responding to the infection. It
plays a role in stimulating the T cells and B cells through the action of antigen presenting
cells mainly the dendritic cells which are needed in initiating these effectors.
These dendritic cells circulate in then body and when they come into contact with the
influenza virus in the body they mature and stimulate the expression of specific certain
receptors. After this they relocate to secondary lymph nodes where they induce the T cell and
B cell response to adaptive immunity. Therefore, these dendritic cells play an important role
in stimulating antigen specific signals to the T lymphocytes to which then activates the naïve
T cells. These signals are the initial vaccine response needed to induce an inflammatory
response and is done by innate immunity (Okamoto, Tsukamoto, Kouwaki, Seya, & Oshiumi,
2017). For the vaccine to provide longiterm protection against infection then the memory
cells of the immune system should be able to effectively and rapidly reactivate in the event
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