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How Does Hiv Weaken The Immune System

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How Does Hiv Weaken The Immune System – Helper T cells play a key role in our immune system, helping us defend against bacterial and fungal infections. They are also the host cells for the HIV virus, and the loss of these important cells can lead to AIDS.

Currently, approximately 35 million people worldwide are infected with HIV/AIDS, including over 3 million children. An additional 2 million people become infected with the virus every year. In the United States, over 1 million people are infected with HIV, and an estimated 1 in 6 people are unaware that they are infected with HIV.

How Does Hiv Weaken The Immune System

HIV infection can occur when the HIV virus enters a person’s mucous membranes or bloodstream. The virus is able to recognize and infect certain types of immune cells, specifically attacking cells called helper T cells or CD4+ T cells. Helper T cells play a key role in the body’s defense against bacterial and fungal infections.

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During the first phase of HIV infection, called the acute phase, large amounts of virus are produced in helper T cells, destroying many of these cells in the process.

People often report flu-like symptoms such as fever, sore throat and body aches, as well as a skin rash early in the infection. Eventually, levels of the virus and helper T cells stabilize and the infected person experiences fewer symptoms.

Within a few months of initial infection, viral loads are generally low and can remain low for years, even without treatment.

Over time, however, the amount of virus increases and the level of helper T cells decreases. When T cell counts drop low enough, individuals are much more susceptible to opportunistic infections. This stage of HIV infection is called AIDS.

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Like other viruses, HIV infects host cells to produce more viruses. HIV attacks the cells of the immune system, particularly T cells, which are a type of white blood cell. In the first step of the HIV life cycle, the virus enters the body and then identifies the host T cell through interactions between receptor proteins (called CD4) on the surface of the T cell and the viral envelope protein (Env) on the surface of the viral membrane. Another T-cell surface protein, called a coreceptor (specifically CCR5 or CXCR4), also binds to Env proteins, causing large conformational changes in Env and leading to fusion of the viral and host cell membranes. The HIV virus’s conical capsid, which contains two copies of the virus’s single-stranded RNA genome, is then embedded in the host cell. Shortly after the HIV capsid enters, the viral RNA genome begins to be copied into double-stranded DNA in a process known as reverse transcription. Reverse transcription is carried out by a viral protein called reverse transcriptase (RT), using host tRNA to activate the reaction and dNTPs to build new DNA strands. Meanwhile, the HIV capsid is transported to the nucleus through interactions with microtubule-based motor proteins.

HIV is a retrovirus and one of the characteristics of this type of virus is the integration of its genome with the host genome. Integration is mediated by a viral protein called integrase. Once inside the nucleus, reverse transcription is completed. The capsid shell breaks apart, releasing a double-stranded DNA copy of the HIV genome. The integrase then binds and cleaves a fragment of DNA from a nearby host and inserts viral DNA at that site. In some cells, viral proteins begin to be produced soon after integration, while in other cells the viral DNA remains dormant for days, months, or even years. When viral DNA is activated (or transcribed), it serves as a blueprint for turning the cell into a virus factory. While some viral RNAs end up in the ribosomes, where they are read and direct the production of viral proteins, other viral RNAs are transported to the cell membrane, where they are packaged into new virions.

Once the infected cell has built the various components of the virus, they must be assembled and released at the cell membrane. These components include two identical copies of the RNA genome, tRNA from the host cell and multiple copies of the Env protein (which is embedded in the cell membrane), the Gag polyprotein, viral protease, RT, and integrase.

1) Assembly. During this phase, various components are recruited to specific locations on the cell membrane. The Gag polyprotein is a key component that largely directs the assembly of the infectious particle. While one end of Gag binds to the RNA genome, the other end binds to the plasma membrane. Thousands of gags are assembled and tightly packed during assembly.

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2) Budding and release. The packaging of the Gag polyprotein causes the plasma membrane to begin to bulge, eventually forming a spherical, lollipop-like particle. At this point, proteins known as ESCRT are recruited and cut the “neck” of the cell membrane, releasing the virus from the cell.

3) Puberty. The Gag polyprotein is basically several different viral proteins connected by short linkers. During maturation, the Gag polyprotein is cleaved and cleaved, a process carried out by the HIV protease. This results in the release of the matrix protein (MA) which binds to the cell membrane and is responsible for recruiting the viral Env protein to the budding site, the capsid protein (CA) which forms the conical capsid shell, the nucleocapsid protein (NC) which binds and condenses the viral The RNA of the genome and the p6 protein, which plays a role in the budding of the virus. During maturation, CA proteins form a conical envelope around the HIV genome.

How does HIV infection occur? The molecular animation below shows the process by which the HIV virus infects a T cell and turns it into a virus factory.

Please note that the animation shown here is a work in progress and will continue to be updated, refined and improved in the coming years. Additional animations will show how antiretroviral drugs affect the life cycle and how innate immunity can block HIV infection.

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To combat viral infections, the mammalian immune system has evolved many defense mechanisms, some of which act against HIV and other retroviruses by attacking various aspects of their life cycle, limiting their replication. The following limiting factors are some of the best-studied examples.

APOBEC3G (A3G) is a protein produced by the host cell and packaged into budding viruses. After these viruses infect a new host cell, A3G causes a large number of changes to the HIV genome, rendering the virus non-infectious due to catastrophic errors in its genetic sequence. This process is shown in the animation on the left.

As shown in the animation above, HIV counteracts A3G restriction by encoding a protein called the viral infectivity factor (Vif). Vif hijacks the host’s molecular machinery and uses it to destroy A3G, preventing A3G from being packaged into new HIV virions.

Tripartite motif proteins (TRIM5) are restriction factors that block retroviral infections by binding to viral capsids soon after entering the host cell and preventing reverse transcription.

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TRIM5 is a mammalian restriction factor that can potently block viral replication. It is part of the innate immune system. TRIM5α (purple) can bind to the HIV capsid envelope (yellow), which covers and protects the viral genome. Structural studies have shown that TRIM5 can form a cage-like structure surrounding the capsid. There are three proposed mechanisms by which TRIM5 may inhibit HIV infection: 1) induction of premature uncoating of the viral capsid, 2) recruitment of ubiquitin, which leads to unproductive virus unwinding, 3) virophagy, in which the TRIM5 cage directs degradation of the viral capsid by digestive enzymes contained in a membrane structure called a lysosome. Medically Reviewed by Cameron White, MD, MPH – Ann Pietrangelo and Kristen Cherney – Updated June 30, 2023

HIV destroys CD4 cells, which are responsible for keeping people healthy and protecting them against disease and infection. As HIV gradually weakens the body’s natural defenses, signs and symptoms may appear.

HIV attacks cell types that would normally fight off invaders like HIV. As the virus replicates, it damages or destroys the infected CD4 cell and produces more virus, which infects more CD4 cells. CD4 cells are also called T cells or helper cells.

Without treatment, this cycle can continue until the immune system becomes severely compromised, putting the person at risk for serious illness and infection.

The Immune Response Against Pathogens

Acquired immunodeficiency syndrome (AIDS) is the final stage of HIV infection. At this stage, the immune system is significantly weakened and the risk of contracting opportunistic infections is much greater.

However, not everyone infected with HIV will develop AIDS. The sooner a person receives therapy, the better the outcome.

The immune system prevents diseases and infections from occurring in the body. White blood cells protect the body against viruses, bacteria and other organisms that can cause disease.

A few days after exposure to the virus, an HIV-infected person may develop a flu-like illness that lasts for several weeks. It is associated with the first stage of HIV infection, called the acute stage of infection or acute HIV.

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A person infected with HIV may not have many serious symptoms at this stage, but they are usually serious

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