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(Diagram of the HIV Virus. Vector Stock Vector - Illustration of Drug, Experiment: 27191723, n.d.)

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Human immunodeficiency virus (HIV) is a single-stranded, enveloped retrovirus, meaning it uses the genetic material within it (RNA) and injects it into host cells to replicate.HIV targets the immune system, effectively disabling it from doing its natural function. With an impaired immune system, the human body is no longer able to combat infections and effectively heal from injuries, leaving infections to spread unchecked throughout, causing degradation across the body's systems and organs, which can be fatal if left untreated.

(World Health Organization, 2024)

exists in two forms: HIV-1 and HIV-2. Viruses require the use of a host cell to replicate since they lack some of the organelles required to multiply by themselves. HIV contains two strands of RNA, which carry its genetic information. It also contains the enzymes reverse transcriptase, protease, and integrase, which are essential in converting its RNA into DNA and inserting that DNA into the host cell’s genetic material. These components are encapsulated by the capsid, a shell-like formation made from protein. The virus is also surrounded by a cell membrane gained from the host cell's own membrane. The surface of the virus's membrane contains important glycoproteins that attach to host cells.

(Tankeshwar, 2010)

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Transmission of HIV primarily occurs through sexual contact; however, it can spread through the use of shared needles, contaminated blood, and it can also be passed down from mother to child. HIV transfers through the exchange of bodily fluids since the virus targets immune cells present all across the body.

(HIV.gov, 2022)

The surface of the HIV contains glycoproteins essential to the virus since they give it the ability to bind with host cells. The viral envelope refers to the glycoprotein structures that form the envelope spike complex, which attaches to the host cells. The glycoproteins involved are gp120 and gp41. The glycoprotein envelope binds to the CD4 glycoprotein within a host cell. These receptors are found primarily in immune system cells such as macrophages, dendritic cells, and especially CD4+ T-cells, also known as helper T-cells, which are an essential part of the adaptive immune system. Once attached with the CD4 glycoproteins, conformational changes in the envelope initiate coreceptor binding. The Variable loop 3 attached to the gp120 glycoproteins can bind with either the ccr5 or the cxcr4 coreceptors; the type of coreceptors varies depending on the type of immune cell the virus is binding with. Once coreceptor binding occurs, membrane fusion can take place. The gp41 glycoprotein penetrates the host cell membrane, fusing the HIV viral envelope to the cell. (Wilen et al., 2012)

The RNA within the virus is released into the host cell and undergoes the process of reverse transcription to synthesize viral DNA. With the use of the enzyme reverse transcriptase, the RNA is transformed into viral DNA. (Wilen et al., 2012)

Once the proviral DNA enters the nucleus of the host cell it binds with the host DNA, resulting in the creation of proviral DNA. As a result of the proviral DNA, the host cell begins producing viral RNA, which is then used to provide RNA and polyproteins for new HIV viruses. The RNA and polyproteins move towards the cell membrane, where it is packaged and packed with viral proteins. As it leaves the host cell, it uses the host cell membrane to create its own membrane, forming immature HIV. As the new virus separates from the host cell, the protease enzyme from the virus cuts new polyproteins to synthesize a matured HIV virus.

(National Institute of Allergy and Infectious Diseases, 2018)

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CD4+T cell depletion and Immune system dysfunction

During replication of the virus, the cell membrane of the host cell becomes compromised since it was in the creation of a new HIV. This directly affects cell integrity and creates an influx of extra cellular fluid entering the cell, causing it to burst under pressure. If the cell somehow survives the viral replication, the viral DNA within the host cell cannot be destroyed unless the host cell is also destroyed through apoptosis (programmed cell death)

(National Institute of Allergy and Infectious Diseases, 2018)

HIV viruses require the presence of cells that hold the CD4 glycoprotein and also either the CCR5 or the CXCR4 coreceptors to undergo fusion with a host cell. These co-receptors are primarily found in immune system cells. Specifically, CCR5 coreceptors are found within monocytes, dendritic cells, and activated T-cells where whereas CXCR4 are primarily found in helper CD4+T-cells, otherwise known as helper T-cells. In the initial infection of HIV, the virus is classified as R5-tropic, meaning that it prefers the CCR5 receptors within cells; however, as the virus undergoes replication, it can develop mutations resulting in a new strain of HIV, X4- tropic HIV which live alongside the original strain and target specifically CXCR4 coreceptors. (Mosier, 2008)

As Immune cells are the primary target of HIV, this causes a massive reduction in the presence and production of cells that are vital in the homeostasis of the immune system and the body's defense mechanisms for infections. As HIV continues to multiply within the body the immune system will become dysfunctional leading to acquired immunodeficiency syndrome or AIDS.

(Jabea Ekabe et al., 2022)

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There are three stages of HIV infection.

1) Acute infection begins within 2-4 weeks post infection. During this period people may develop symptoms such as headaches, fevers, and rashes; however, some individuals may be asymptomatic and show no clear signs of infection. Acute infection is when HIV replicates exponentially, spreading quickly throughout the body, targeting the cells' immune system, which contain the CD4 glycoproteins it requires to bind with. As HIV spreads through the bloodstream, it becomes increasingly more infectious.

(National Institutes of Health, 2021)

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The Immune response is the body's defense against harmful pathogens that can cause infection. There are two forms of immune response, the innate and the adaptive; both have key roles in the protection of the body.

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The innate defense is the immediate response defense system. The innate immune system is present at birth and

It includes external barricades such as the integumentary system, mucus membranes such as saliva from the mouth, and internal defenses such as monocytes, red blood cells, cytokines, and many more. The innate defense also includes systems such as the inflammatory response, fever, and chemical signaling.

(Justiz & Jan, 2024)

The innate immune response is nonspecific, meaning it responds similarly to all threats and does change depending on the pathogen that is present. (Alberts et al., 2002)

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The adaptive immune response is the body's line of defense to the pathogens that the innate immune response could not handle. What the Innate immune response lacks in being able to specify responses for varying pathogens, the adaptive immune responses make up for it by being able to create specified responses to different pathogens. It also can remember parts of the pathogen so that it will be able to combat it more effectively in the future if reinfection were to occur.

(Doitsh & Greene, 2016)

Adaptive immunity is acquired throughout the individual's lifetime as they gain exposure to the external environment. The adaptive Immunity system is barely functioning during birth, leaving the child with immunities gained from the mothers' genes.

The adaptive immune response is highly specific, and the antibodies used to combat pathogens are produced by lymphocytes. Two main cell types are involved in this system, the B cells and T cells.

The adaptive immune system can function across the body via the use of the humoral immunity and the cellular defenses.

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Antigens are foreign molecules that trigger immune responses within the body. Antigens are usually derived from pathogens, which could pose a threat to the immune system. These antigens are detected by B-cells, which have antigen receptors to create antibodies that can combat the antigens and prevent infections. A B-cell is triggered by the presence of an antigen and will differentiate into antibody secreting plasma cells. The B cells also require the help of the CD4+ T cell, also known as the Helper T-cell, to release cytokines in order to differentiate. (A et al.., 2001)

The B cell can differentiate into two cells, the previously mentioned plasma cells and the memory B cells. Plasma cells are specialized for the synthesis of antibodies. The structure of their organelles, such as the endoplasmic reticulum and Golgi apparatus, supports their function. Antibodies are released throughout the body, where they can identify and eliminate the specific pathogens.

(Shrestha, 2024)

The memory B cells function to provide and maintain immunological memory of the antigen that initiated the immune response. For that reason, Memory B cells have long life spans. In case of a future encounter with the same pathogen, the memory B cell allows the immune system to react faster, preventing infection.

(Shrestha, 2024)

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Cellular immunity is moderated by T lymphocytes, also known as T cells. T cells are produced in the bone marrow; however, they mature within the thymus. at this stage, they can differentiate into 3 forms, each varying in function.

The cytotoxic T cells, also known as killer T cells, are responsible for neutralizing infected cells. Helper T-cells help enhance the functions of other immune cells, such as B cells. Like mast cells, helper T cells can release cytokines, which trigger the activation of macrophages, inflammatory response, and the activation of T and B cells.

Memory T-cells assist in rapid activation when the previously identified pathogen is present. (Britannica, 2015)

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Immunological memory begins at first contact with a new antigen. At first contact or the primary response, there is no active development of antigens however, B cells begin differentiation. the increase of antigen concentration to the destruction of antigen can span over days as the body tries to find the correct antibody. During this stage, memory cells are being produced to remember which antibodies are used to neutralize the pathogen.

(Abolhassani, 2019)

In a secondary response, memory cells hold the data to create the required antibodies to neutralize the pathogens. since the body remembers which antibodies are required, the production rate is much faster with a shorter lag period. The levels of antibodies present are also high and can last longer in comparison to the primary response.

(Abolhassani, 2019)

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There are mechanisms of innate immune response, physical and chemical barriers, phagocytes, natural killer cells, interferons, and inflammation and fever.

Physical and biochemical borders include skin and organ membranes, which provide external protection from foreign pathogens and minimize the risk of a pathogen entering the body. The skin provides a physical barrier to prevent pathogens from entering, and secretory glands, such as saliva, contain enzymes that can break down pathogens. Mucus created by goblet cells can create barriers and entrap pathogens, preventing them from reaching vulnerable areas such as organs. Mechanical barriers such as sneezing, coughing, and vomiting can help expel pathogens that have entered the body before the spread.

(Science learning hub, 2010)

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If pathogens manage to penetrate the physical and chemical barriers, phagocytes are the next line of defense. Phagocytes are specialized cells that can undergo the process of phagocytosis. Phagocytosis is the process of certain immune system cells engulfing and neutralizing pathogens. for this to occur, the pathogen and the phagocyte must come in contact with each other. once in contact, the pathogen can bind to the receptors on the surface of the phagocyte. The phagocyte then begins to surround the pathogen, engulfing it. The engulfed pathogen becomes encapsulated in a phagosome, which is a bubble-like structure. The encapsulated pathogen is then broken down by lysosomes, which are organelles that contain enzymes that assist in the breakdown of cellular material. The waste product is discharged from the phagocyte. Some examples of common phagocytes are monocytes, macrophages, mast cells, and dendritic cells.

(The Editors of Encyclopedia Britannica, 2018)

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Natural killer T cells monitor, identify, and neutralize infected cells by monitoring for changes on the surface proteins., release perforins, which are responsible for triggering membrane repairs, forming pores on the target cells, and releasing enzymes into infected cells to trigger apoptosis. When cells become infected or cancerous lose their major histocompatibility complex (MHW). When a natural killer cell comes across a cell with an abnormal, missing or compromised MHW, it will initiate a kill response to destroy the infected or mutated cell so that the infection or mutation does not spread. The natural killer cells release perforin, which is responsible for making pores in the surface of the infected cells, allowing for the entry of enzymes that will promote apoptosis.

(Paul & Lal, 2017)

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Interferons are small proteins released by infected cells or by phagocytic cells that have engulfed viruses. Once interferon is released, it binds to receptors on normal cells, which activate the production of antiviral proteins responsible for preventing viral replication within host cells. This can effectively stop the further development of infections. Interferons can also recruit the assistance of other immune cells, such as phagocytes and natural killer T cells in the immune response. (Kopitar-Jerala, 2017)

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Inflammation is the body's response to prevent infection and promote healing to the site of injury. when inflammation occurs, it generally means that the body is fending off foreign pathogens, preventing them from replicating and infecting the body. When a pathogen damages cells, it can release chemokines, which signal mast cells to release histamines. Histamines are what trigger the vasodilatation resulting in cardinal signs of inflammation: rubor (red), tumor (swelling), dolor(pain), and Calor (heat). The influx of blood cells to the site of injury promotes healing and also helps prevent infection.

(Britainnica, n.d.)

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Fever occurs when the body purposefully increases its core body temperature to combat the spread of infection. Fever is triggered by immunological mediators that trigger the hypothalamus.

(Balli et al., 2023)

With an increase in body temperature, infectious pathogens will have impaired abilities to replicate and survive, as many infections can only thrive within certain temperature ranges. The increase in temperature also enhances the body's immune functions by increasing cell metabolism and activating immune response cells, such as natural killer cells, T and B lymphocytes, and macrophages.(Cleveland Clinic, 2019)

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2) Chronic infection occurs after the acute stage. In this stage, viral replication decreases as the cells of the immune system are depleted. The chronic stage of HIV can span over several years; depending on the management of the infection, some may live with it for decades.

(National Institutes of Health, 2021)

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3) AIDS / Acquired Immunodeficiency Syndrome is the final stage of HIV infection. At this point, detrimental amounts of damage have occurred to the immune system, leaving the body with no secondary line of defense, resulting in the body being extremely vulnerable to opportunistic infections. The CD4 cell count has dropped to below 200 cell/mm^3 whereas a health individual can range from 500 to 1400 cell/mm^3. (WebMD, 2007). People are likely to succumb to the effects of the opportunistic infections within three years. (National Institutes of Health, 2021)

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