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How Does Hiv Infect Cells

How Does Hiv Transmit In The Body

How HIV infects us: Mucous membranes, dendritic cells, and lymph nodes | Khan Academy

This is the basic pathway of HIV. The virus can get inside the body through our bodily fluids, particularly blood, semen for men, vaginal fluid for women, and even breast milk from infected mothers.

Since the virus targets the bodys immune system, its first victim or host cell would be the T-helper cells . It attaches and invades these white blood cells and takes control of the cell overall. Once the virus manages to infiltrate the DNA of the CD4 cells, it can now replicate and make copies of the infected CD4 cells, spreading it all over the body via your bloodstream.

The CD4 cells are then destroyed, and the HIV that rides on the host cell then takes over the duplication and spread of the virus. If left untreated, your CD4 cell count goes down to severely low levels, indicating the advancement of your HIV infection to AIDS.

One can categorize HIV infection into 3 acute, chronic, and the advanced stage called AIDS.

Interval Of Mild Or No Symptoms

After the first symptoms disappear, most people, even without treatment, have no symptoms or only occasionally have a few mild symptoms. This interval of few or no symptoms may last from 2 to 15 years. The symptoms that most commonly occur during this interval include the following:

  • Swollen lymph nodes, felt as small, painless lumps in the neck, under the arms, or in the groin

  • White patches in the mouth due to candidiasis

  • Anemia

Some people progressively lose weight and have a mild fever or diarrhea.

These symptoms may result from HIV infection or from opportunistic infections that develop because HIV has weakened the immune system.

Why Does The Immune System Fail To Fight The Hiv Virus

There are various reasons which can contribute to the failure of the immune system to control HIV infection and prevent AIDS development. By infecting CD4+ T cells, HIV is able to replicate predominantly in activated T cells and paralyse one of the main components of adaptive immune system. HIV can also establish latent infection in CD4+ T cells and remain invisible to CD8+ T cells and therefore replication can occur later in the infection and generate new virions. Antigenic mutation within the T-cell epitopes can affect the binding capacity of MHC molecules to the viral peptides, resulting in the inability of the TCRs to recognise the MHC-peptide complex. Finally, HIV is able to hide from anti-HIV antibodies by expressing non-immunogenic glycans on key antibody epitopes.

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Diagnosis Of Hiv Infection

  • Tests to detect antibodies to the HIV virus in a sample of blood or saliva

  • Tests to detect HIV RNA in a sample of blood

Early diagnosis of HIV infection is important because it makes early treatment possible. Early treatment enables infected people to live longer, be healthier, and be less likely to transmit HIV to other people.

Doctors usually ask about risk factors for HIV infection Transmission of HIV Infection Human immunodeficiency virus infection is a viral infection that progressively destroys certain white blood cells and can cause acquired immunodeficiency syndrome . HIV is transmitted… read more and about symptoms .

Doctors also do a complete physical examination to check for signs of opportunistic infections, such as swollen lymph nodes and white patches inside the mouth , and for signs of Kaposi sarcoma of the skin or mouth.

Entryhiv Enters A Cell

What HIV Does

The outer surface of the virus is covered with proteins. Human cells also have proteins on their outer surface, called receptors. These receptors come in millions of different shapes. The HIV virus has proteins on its surface that fit perfectly into the receptors on the surface of certain cells, including CD4 cells, like a key in a lock. Once HIV attaches to these receptors, the virus can fuse with the cell. Then the contents of the virus are inserted into the cell.

Before HIV can infect a cell, it has to bind to not just one, but two receptors on the surface of the CD4 cell. One of these is called the CD4 receptor. The second is called a co-receptor. There are several different co-receptors, including two called CCR5 and CXCR4.

Many drugs are being developed to stop HIV from getting inside a cell. Drugs that stop HIV from joining to the CD4 receptor and fusing with the cell surface are called fusion inhibitors.

Drugs that block HIV from using a cells co-receptors are called receptor blockers or co-receptor antagonists. They can have more specific names, based on the receptor they block. For example, CCR5 inhibitors interfere with the interaction between HIV and the CCR5 co-receptor on CD4 cells.

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Adaptive Immune Response To Hiv

Cellular immune response to HIV. The cellular immune response is induced upon the entry of HIV into the target cells and synthesis of viral proteins . MHC class I on the cell surface displays the intracellularly degraded HIV peptide fragments for recognition by T-cell receptors on CD8+ T cells . CD8+ T cells lyse HIV infected cells and secrete cytokines, i.e. interferon- , tumor necrosis factor , and chemokines, i.e. MIP-1 , MIP and RANTES, that inhibit virus replication and block viral entry into CD4+ T cells. Development of CD8+ T cells is crucial for control of HIV replication. This results in declining viraemia after primary infection. In the early stages of infection, CD4+ T cells lose their proliferative capacity and therefore their contribution to viral control is minor. However, during chronic infection CD4+T cells are present and secrete interleukin-2 or cytokines, such as IFN-, to control viraemia.

Figure 3.

Hivs Affect On Receptor Usage

To speculate as to why HIVs have evolved plasticity in their interactions with co-receptors is important. The ability to use multiple functionally redundant contacts with co-receptors could conceivably facilitate immunological escape. Thus, in the face of a neutralising antibody response , the selection of variants with altered envelope sequences would be permitted without compromising the ability of the virus to use a given co-receptor. Furthermore, changes in envelope sequence, that enable the virus to use additional co-receptors while retaining the ability to interact with CCR-5, could be tolerated. It appears that dual-tropic strains that use both CCR-5 and CXCR-4 are less tolerant of perturbations in CCR-5 sequence than are M-tropic strains,, suggesting that acquisition of the ability to utilise CXCR-4 might involve the sacrifice of a degree of functional redundancy and/or affinity in the envelope/CCR-5 interaction.

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Hiv Transmission Filmed Live By French Scientists

28 May 2018

A team of French researchers has succeeded in filming HIV infecting a healthy cell.

A team of French researchers has succeeded in filming HIV infecting a healthy cell. UNAIDS spoke to Morgane Bomsel, Research Team Director at the French National Center for Scientific Research , about the feat.

What motivated you to film HIV transmission?Morgane Bomsel: HIV transmission has not been studied much and we had no precise idea of the exact sequence of events leading to HIV infection of genital fluids during sexual intercourse. Neither did we know how immune cells are infected and what the consequences are. The vast majority of new HIV infections are acquired via the genital and rectal mucosa however, the outer layer, the epithelium, of those tissues varies and affects how HIV enters the body.

What were the challenges?

MB: The challenges involved building an experimental model that mimicked genital mucosa infected by genital fluids suitable for live imaging. We reconstructed in vitro human male urethral mucosa based on human cells, the surface of which had been engineered to be red, and an infected white blood cell that was engineered to be fluorescent green and in turn would produce fluorescent green HIV infectious particles.

When did you know you had a breakthrough?

Please walk us through the video

MB: The HIV-infected cells are labelled in green and produce fluorescent viruses that appear as green dots.

What makes HIV particularly tricky to cure?

The Science Of Hiv And Aids

HIV life cycle: How HIV infects a cell and replicates itself using reverse transcriptase

Key Points

  • HIV stands for Human Immunodeficiency Virus, a pathogen that works by attacking the human immune system.
  • HIV specifically targets CD4 cells, the bodys principal defenders against infection, using them to make copies of themselves.
  • Antiretroviral drugs target specific stages of the HIV lifecycle to stop HIV from replicating.

Explore this page to find out more about , , and .

HIV stands for Human Immunodeficiency Virus, a pathogen that works by attacking the human immune system. It belongs to a class of viruses called retroviruses and more specifically, a subgroup called lentiviruses, or viruses that cause disease slowly. 1

HIV cannot replicate on its own, so in order to make new copies of itself, it must infect cells of the human immune system, called CD4 cells. CD4 cells are white blood cells that play a central role in responding to infections in the body. 2

Over time, CD4 cells are killed by HIV and the bodys ability to recognise and fight some types of infection begins to decline. If HIV is not controlled by treatment, the loss of CD4 cells leads to the development of serious illnesses, or opportunistic infections. In people with normal CD4 cell levels, these infections would be recognised and cleared by the immune system. 3

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What Are The Factors That Affect Disease Progression

The most important factor affecting HIV progression is the ability to achieve viral suppression. Taking antiretroviral therapy regularly helps many people slow the progression of HIV and reach viral suppression.

However, a variety of factors affect HIV progression, and some people progress through the phases of HIV more quickly than others.

Factors that affect HIV progression can include:

  • Ability to achieve viral suppression. Whether someone can take their antiretroviral medications and achieve viral suppression is the most important factor by far.
  • Age when symptoms start. Being older can result in faster progression of HIV.
  • Health before treatment. If a person had other diseases, such as tuberculosis, hepatitis C, or other sexually transmitted diseases , it can affect their overall health.
  • Timing of diagnosis. Another important factor is how soon a person was diagnosed after they contracted HIV. The longer between their diagnosis and treatment, the more time the disease has to progress unchecked.
  • Lifestyle. Practicing an unhealthy lifestyle, such as having a poor diet and experiencing severe stress, can cause HIV to progress more quickly.
  • Genetic history. Some people seem to progress more quickly through their disease given their genetic makeup.

Some factors can delay or slow the progression of HIV. These include:

Living a healthy lifestyle and seeing a healthcare provider regularly can make a big difference in a persons overall health.

Antiretroviral Treatment And The Hiv Lifecycle

Antiretroviral treatment for HIV combines several different types of drugs, each of which targets a different stage in the HIV lifecycle. This means that the replication of HIV is stopped on multiple fronts, making it very effective.

If taken correctly, it keeps the immune system healthy, prevents the symptoms and illnesses associated with AIDS from developing, and means that people can enjoy long and healthy lives.

If someone doesnt take their treatment correctly or consistently , the level of HIV in their blood may increase and the drugs may no longer work. This is known as developing drug resistance.

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Resistance To Hiv Infection

The poorly understood phenomenon associated with the HIV-1 epidemic is the existence of individuals who have been repeatedly exposed to the virus but remain uninfected. It has been suggested that HIV-1 resistant individuals may have a non functioning co-receptor preventing the virus from entering cells., The CCR-5 receptor was demonstrated as one of the main co-receptors for NSI strains of HIV-1. Samson et al., reported that a 32 bp deletion within the coding region for the CCR-5 generating a non-functional receptor that did not support infection by NSI strains of HIV-1. Moreover, white blood cells from individuals homozygous for the mutant CCR-5 were found to be highly resistant to infection by NSI viruses., Population studies indicate that the homozygous defect is found in only 1% of Caucasians of western European ancestry whereas the heterozygous defect is present in approximately 20% of this population. These results indicate that variants of the CCR-5 receptor could be responsible for the relative resistance to HIV-1 infection exhibited by some individuals and also for the variability of the course of the disease in infected patients.

Hiv Hides In Immune System Cells Resistant To Killer T Cells

HIV AIDS Treatment transition cART

Dr. Brad Jones. Credit: John Abbott

Scientists have known for years that HIV, the virus that causes AIDS, is difficult to cure because it hides from the bodys immune system. Research now reveals that the virus conceals itself in lymphocytes, or white blood cells, that are intrinsically hard to kill because they are resistant to killer T cells, according to a new study by Weill Cornell Medicine investigators.

The resistance of these cells might be one aspect of HIV that weve missed in our efforts to cure infection, said Dr. Brad Jones, an associate professor of immunology in medicine in the Division of Infectious Diseases at Weill Cornell Medicine and senior author of the paper published April 13 in the Journal of Clinical Investigation.

About 1.1 million people in the United States currently have HIV, and 38,000 new infections occur each year, according to the U.S. Department of Health and Human Services. While antiretroviral medications can suppress the virus for life, making HIV a manageable chronic condition, what remains to be done is to actually cure infection, Dr. Jones said.

In their new research, Dr. Jones and his colleagues have discovered that the virus not only hides. It also endures in reservoir cells because they have developed resistance to being eliminated by killer T cells, which are produced by the bodys immune system and target and destroy cells infected by HIV and other viruses.

Dr. Yanqin Ren

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Screening And Diagnostic Tests

If doctors suspect exposure to HIV infection, they do a screening test for HIV. Doctors also recommend that all adults and adolescents, particularly pregnant women, have a screening test regardless of what their risk appears to be. Anyone who is concerned about being infected with HIV can request to be tested. Such testing is confidential and often free of charge.

The current combination screening test tests for two things that suggest HIV infection:

  • to HIV

  • HIV antigens

Antibodies are proteins produced by the immune system to help defend the body against a particular attack, such as that by HIV. Antigens are foreign substances that can trigger an immune response.

The body takes several weeks to produce enough antibodies to be detected by the test, so results of the antibody test are negative during the first few weeks after the virus enters the body . However, results of the p24 antigen test can be positive as early as 2 weeks after the initial infection. The combination tests can be done quickly by a laboratory. Also, a version of these tests can be done in a doctor’s office or clinic . If results are positive, doctors do a test to distinguish HIV-1 from HIV-2 and a test to detect the amount of HIV RNA in the blood .

Other, older rapid bedside tests are also available. These tests can be done using a sample of blood or saliva. If results of these rapid screening tests are positive, they are confirmed by ELISA or by repetition of one or more other rapid tests.

Reverse Transcription And Integration

The viral capsid contains the enzymes necessary for the synthesis of new viral particles from the RNA strands by using cellular machinery of the host cell. One of these enzymes is the reverse transcriptase that synthesizes a double stranded DNA molecule from the existing viral ssRNA. The enzyme first creates a single stranded DNA from viral ssRNA, which is termed as reverse transcription. Using this DNA strand as a template, the enzyme then creates the second strand of DNA molecule, thus giving rise to a dsDNA molecule. The virus does not have its own set of nucleotide bases, and uses those present in the cytoplasm of the T-helper cells.

The dsDNA is tightly bound to a viral enzyme called integrase, and is transported into the nucleus by the cellular transport machinery of T-helper cells. Inside the nucleus, integrase enables the integration of the viral DNA into the DNA of T-helper cells. Using this mechanism the virus can hide and stay in the body in a latent state for several years.

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Reverse Transcriptionhiv Takes Control Of The Cell

Once inside the cell, HIV takes control of the cell. One of the HIV enzymes, the reverse transcriptase enzyme, converts the genetic material of the virus into another kind of genetic material called DNA. Now the genetic material of the virus matches the genetic material of the host cell.

A class of drugs called reverse transcriptase inhibitors slow down or stop the action of the RT enzyme. These drugs come in two subtypes:

  • nucleoside analogue reverse transcriptase inhibitors , commonly called nukes
  • non-nucleoside analogue reverse transcriptase inhibitors , commonly called non-nukes

Nukes were the first drugs approved for the treatment of HIV. Used in pairs, nukes continue to be a major part of most drug combinations. To make up an effective drug combination, the two-nuke backbone is paired with a drug from another class. This is usually a non-nuke or a protease inhibitor, but may also be an integrase inhibitor.

Stages Of Hiv Infection

How HIV infects us: CD4 (T-helper) lymphocyte infection | NCLEX-RN | Khan Academy

On contraction of HIV, individuals may remain asymptomatic for a long period of time or experience flu-like symptoms called acute retroviral syndrome in about 2-4 weeks. This stage of primary infection is called acute infection, and is characterized by active multiplication of the virus and reduction of T-helper cells. Frequent fever, muscle and joint pain, swollen lymph nodes, and gastrointestinal problems are some of the common symptoms. In this stage, the immune response against the virus helps to limit viral multiplication, and the counts of T-helper cells increase to normal. Antibodies are generated against HIV and are present in the blood of infected individuals, which serves as a diagnostic criteria for HIV infection.

However, the body is unable to get rid of the virus, and it persists in an inactive state. This stage is termed clinical latency, and can last for 1-2 years or even 15 years. This time period depends on several factors including the individuals immune strength, diet, age, medical history, and prevailing medical conditions . Nevertheless, the virus cannot be controlled forever by the immune system, and the viral replication increases, in turn affecting the T-helper cells. In addition, the death of uninfected T-helper cells and cytotoxic T-cells has also been observed in HIV patients.

The stages of HIV infection, as identified by the World Health Organization , along with the corresponding T-helper cell counts are as summarized below.


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