Running Head: Immunology

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Running head: Immunology 1

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,
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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

through degradative mechanisms.

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

mature virus. They do this by through methods facilitated by major histocompatibility

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
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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

antigen receptors used in recognizing and fighting pathogens.

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.

Adaptive immunity is required as it is highly specific and it differentiates between pathogen

and non-pathogen structures detecting even the minute differences.

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

receptors can be processed by genetic recombination to recognize epitopes and antigenic

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

overcomes the infection even if it reoccurs later.

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
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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

starts to react, it plays a role to control infections.

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

host (Ye et al., 2019).

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
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immune response against the influenza virus through CD4 and CD8 T cells that are specific

to the virus (Fiebiger, Maamary, Pincetic, & Ravetch, 2015).

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

extrafollicular foci which causes rapid clonal multiplication leading to production of

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

(Bahadoran et al., 2016.


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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

maturation. This process is regulated through several occurrences including expression,

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

B cells to ensure that development occurs through proper signals.

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

cells or naïve B cells.


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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

infection (Nogales & DeDiego, 2020).

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

production and maintenance of the B cells and CD8+ T cells.


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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

the infection by the virus occurs (Thulin & Wang, 2018).


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References

Bahadoran, A., Lee, S. H., Wang, S. M., Manikam, R., Rajarajeswaran, J., Raju, C. S., &

Sekaran, S. D. (2016). undefined. Frontiers in Microbiology, 7.

Broecker, F., Liu, S. T., Sun, W., Krammer, F., Simon, V., & Palese, P. (2018).

Immunodominance of antigenic site B in the Hemagglutinin of the current H3N2

influenza virus in humans and mice. Journal of Virology, 92(20).

Cobey, S., & Hensley, S. E. (2017). Immune history and influenza virus

susceptibility. Current Opinion in Virology, 22, 105-111.

Fiebiger, B. M., Maamary, J., Pincetic, A., & Ravetch, J. V. (2015). Protection in antibody-

and T cell-mediated autoimmune diseases by antiinflammatory IgG Fcs requires type

II FcRs. Proceedings of the National Academy of Sciences, 112(18), E2385-E2394.

Iwasaki, A., & Pillai, P. (2014). Innate immunity to influenza virus infection. Nature Reviews

Immunology, 14(5), 315-328.

Kleiman, E., Jia, H., Loguercio, S., Su, A. I., & Feeney, A. J. (2016).

undefined. Proceedings of the National Academy of Sciences, 113(27), E3911-

E3920.

Krammer, F. (2015). undefined. Biotechnology Journal, 10(5), 690-701.

Kreijtz, J., Fouchier, R., & Rimmelzwaan, G. (2011). Immune responses to influenza virus

infection. Virus Research, 162(1-2), 19-30.

Lam, J. H., & Baumgarth, N. (2019). The multifaceted B cell response to influenza

virus. The Journal of Immunology, 202(2), 351-359.

Lu, C., Murakowski, D. K., Bournazos, S., Schools, T., Sarkar, D., Halper-Stromberg, A., …

Nussenzweig, M. C. (2016). Enhanced clearance of HIV-1-infected cells by broadly

neutralizing antibodies against HIV-1 in vivo. Science, 352(6288), 1001-1004.


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Maamary, J., Wang, T. T., Tan, G. S., Palese, P., & Ravetch, J. V. (2017). Increasing the

breadth and potency of response to the seasonal influenza virus vaccine by immune

complex immunization. Proceedings of the National Academy of Sciences, 114(38),

10172-10177.

Nachbagauer, R., & Krammer, F. (2017). Universal influenza virus vaccines and therapeutic

antibodies. Clinical Microbiology and Infection, 23(4), 222-228.

Nemazee, D. (2017). Mechanisms of central tolerance for B cells. Nature Reviews

Immunology, 17(5), 281-294.

Nogales, A., & DeDiego, M. L. (2020). Influenza virus and vaccination. Pathogens, 9(3),

220.

Nüssing, S., Sant, S., Koutsakos, M., Subbarao, K., Nguyen, T. H., & Kedzierska, K. (2018).

Innate and adaptive T cells in influenza disease. Frontiers of Medicine, 12(1), 34-47.

Okamoto, M., Tsukamoto, H., Kouwaki, T., Seya, T., & Oshiumi, H. (2017). Recognition of

viral RNA by pattern recognition receptors in the induction of innate immunity and

excessive inflammation during respiratory viral infections. Viral Immunology, 30(6),

408-420.

Petrova, V. N., & Russell, C. A. (2017). The evolution of seasonal influenza viruses. Nature

Reviews Microbiology, 16(1), 47-60.

Sun, H., Sun, C., Xiao, W., & Sun, R. (2019). Tissue-resident lymphocytes: From adaptive

to innate immunity. Cellular & Molecular Immunology, 16(3), 205-215.

Thulin, N., & Wang, T. (2018). The role of Fc gamma receptors in broad protection against

influenza viruses. Vaccines, 6(3), 36.

Ye, L., Schnepf, D., Becker, J., Ebert, K., Tanriver, Y., Bernasconi, V., … Staeheli, P.

(2019). Interferon-λ enhances adaptive mucosal immunity by boosting release of

thymic stromal lymphopoietin. Nature Immunology, 20(5), 593-601.


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