Monday, June 24, 2024

What Cell Type Does Hiv Infect

Hiv Primary Infection And Disease Progression

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

There are several viral and host factors determining the variability in HIV-1 infection outcome and in rates of disease progression in HIV-1 infected individuals. Cellular tropism which defines viral phenotype and receptorcoreceptors which determine viral entry into various cell types are the major factors influencing HIV pathogenesis. Despite the intense research for the last 25 years, the exact mechanism of how these factors contribute to the dramatic loss of CD4+ T cells and the persistence of R5 and X4 strains during the AIDS status is still not well identified.1

Infection with HIV starts without symptoms or ill-feeling and is accompanied by slight changes in the immune system. This stage spans up to three months after infection until seroconversion where HIV-specific antibodies can be detected in individuals following recent exposure. The outcome of infection and duration for disease progression with clinical symptoms may vary greatly between individuals, but often it progresses fairly slowly.2 It takes several years from primary infection to the development of symptoms of advanced HIV diseases and immunosuppression.

During primary infection, although individuals may look healthy, the virus is actively replicating in the lymph nodes and blood stream of infected individuals. As a result, the immune system may get slowly damaged by the burst of viral load in their bodies.3

How Does Acute Hiv Affect The Body

Once a person contracts HIV, the acute infection takes place immediately.

Symptoms of the acute infection may take place days to weeks after the virus has been contracted. During this time, the virus is multiplying rapidly in the body, unchecked.

This initial HIV stage can result in flu-like symptoms. Examples of these symptoms include:

However, not all people with HIV experience initial flu-like symptoms.

The flu symptoms are due to the increase of copies of HIV and widespread infection in the body. During this time, the amount of CD4 cells starts to fall very quickly. The immune system then kicks in, causing CD4 levels to rise once again. However, the CD4 levels may not return to their pre-HIV height.

In addition to potentially causing symptoms, the acute stage is when people with HIV have the greatest chance of transmitting the virus to others. This is because HIV levels are very high at this time. The acute stage typically lasts between several weeks and months.

What Happens At The Binding And Fusion Stage

HIV attaches to a T-helper cell. It then fuses to it and releases its genetic information into the cell.

The types of ARVs that stop this stage of the lifecycle are called fusion or entry inhibitor drugs. They stop HIV from entering the cell. Your healthcare provider will let you know if these are the right ARVs for you.

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Future Directions: Toward A Unified Explanation For Hiv Pathogenesis

A unified view of HIV pathogenesis is emerging, but there remain many unknowns, and a better understanding will undoubtedly require an integrated analysis of innate and adaptive immune responses, host genetics, and viral genetics. Although both viral load and CD4+ cell count predict disease progression, we remain convinced that the adaptive immunologic response is also predictive of the subsequent course. Clear signals are there: CD8+ T cells are associated with initial control, depletion of these cells in animal models of AIDS leads to an increase in viremia, virus is evolving to escape detection by CTLs, specific functions mediated by CD8+ T cells have demonstrable antiviral effects in vivo, the effect of HLA far outweighs any other genetic factors, CD8+ and CD4+ T-cell dysfunction is associated with lack of viral control, and immune-induced mutations reduce viral fitness and likely contribute to the antiviral efficacy of the CD8+ T-cell response. But important questions remain, and in particular questions regarding the actual functional profile of CD8+ T cells that might lead to long-term control of HIV, or prevention of disseminated infection. And the extent to which such data will be important to vaccine design remains unclearalthough animal models suggest that CD8+ T cells may be able to prevent progressive systemic dissemination of infection and even reduce the level of virus to barely detectable levels .

Revised Guidelines For Performing Cd4+ T



These revised guidelines were developed by CDC for laboratoriesperforming lymphocyte immunophenotyping assays in human immunodeficiencyvirus-infected persons. This report updates previous recommendations and reflects current technology in a field that israpidly changing. The recommendations address laboratory safety, specimencollection, specimen transport, maintenance of specimen integrity,specimen processing, flow cytometer quality control, sample analyses,data analysis, data storage, data reporting, and quality assurance.



  • Use universal precautions with all specimens .

  • Establish the following safety practices :

  • Wear laboratory coats and gloves when processing and analyzing specimens, including reading specimens on the flow cytometer.

  • Never pipette by mouth. Use safety pipetting devices.

  • Never recap needles. Dispose of needles and syringes in puncture-proof containers designed for this purpose.

  • Handle and manipulate specimens in a class I or II biological safety cabinet.

  • Centrifuge specimens in safety carriers.

  • After working with specimens, remove gloves and wash hands with soap and water.

  • For stream-in-air flow cytometers, follow the manufacturer’s recommended procedures to eliminate the operator’s exposure to any aerosols or droplets of sample material.

  • Specimen Collection

  • Select the appropriate anticoagulant for hematologic testing and flow cytometric immunophenotyping.

  • Anticoagulant for hematologic testing:

  • Specimen Transport

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    Hiv Assembly Budding And Maturation

    Once the different viral components are built by the infected cell, they must be assembled and released at the plasma membrane. These components include two identical copies of the RNA genome, tRNAs from the host cell, and many copies of Env protein , Gag polyprotein, viral protease, RTs, and integrases.

    The formation of a new HIV virus consists of three major stages:

    1) Assembly. During this stage, different components are recruited to specific sites on the plasma membrane. Gag polyprotein is a key component that largely directs the assembly of an infectious particle. While one end of Gag binds to the RNA genome, the other end binds to the plasma membrane. Thousands of Gags assemble and become tightly packed during assembly.

    2) Budding and Release. Packing of Gag polyproteins causes the plasma membrane to start to bulge out, eventually forming a spherical particle that resembles a lollipop. At this point, proteins known as ESCRTs are recruited and cut the plasma membrane neck, releasing the virus from the cell.

    Establishment And Persistence Of Hiv

    Infection and the constitution of a microglial cell reservoir might occur very early in the evolution of HIV-1 infection . Some features of the microglial cells allow for the persistence of HIV-1 in the brain. When infected they are far more resistant to cytopathic effects and on the contrary of CD4+ T cells they are non-lytic. In addition, these cells are resistant to apoptosis. The mechanism of apoptosis resistance to HIV-1 deserves considerable attention since it helps to design alternative strategies based on the increase of apoptosis susceptibility . Indeed, strategies aiming to reactivate HIV-1 from infected cells should consider the problem of resistance to apoptosis since the reinforced therapy might not be efficient against the newly productive but non-apoptotic cells. Finally, the antiretroviral drug efficiency is drastically reduced in anatomical and pharmacological sanctuaries such as the brain where microglial cells are mostly found and thus contributing also to viral persistence .

    We are far from elucidating all the molecular mechanisms which underlie HIV-1 latency in microglial cells. Further investigation in this field is needed in order to identify new potential targets in HIV-1 therapy.

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    Treatment To Prevent Hiv Infection

    Health care workers who are at risk for HIV because of an accidental needlestick or other exposure to body fluids should get medicine to prevent infection.footnote 11

    Also, medicine may prevent HIV infection in a person who has been raped or was accidentally exposed to the body fluids of a person who may have HIV.footnote 12 This type of treatment is usually started within 72 hours of the exposure.

    And studies have shown that if you are not infected with HIV, taking antiretroviral medicines can protect you against HIV.footnote 13, footnote 14, footnote 15 But to keep your risk low, you still need to use safer sex practices.

    Ctl Evolution Following Acute Infection

    HIV Life Cycle | HHMI BioInteractive Video

    Although a narrowly directed immune response is found at the time of maximal decline in peak viremia, responses subsequently broaden, such that during chronic infection the average person targets a median of 14 epitopes simultaneously , and given that these studies were performed with a reference set of peptides rather than autologous peptides, the actual number may be 20%30% higher . Immunization studies in animal models indicate that the CD8+ T-cell compartment has enormous expansion capacity, without affecting the size of the naïve CD4+, CD8+, or B-cell populations, and while preserving memory CD8+ T-cell populations to other pathogens . HIV-specific CD8+ T-cell responses remain detectable throughout the course of disease, and are actually broader and higher in persons with progressive infection than in those with controlled infection .

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    Signal Transduction Through Ccr5 And Cxcr4

    CCR5 and CXCR4 are both members of the seven-transmembrane-spanning family of heterotrimeric GPCRs. This family of proteins is characterized by an extracellular amino-terminal domain, seven membrane-spanning domains that form three extracellular and three intracellular loops, and a cytoplasmic tail domain. The amino terminus and three ECLs together form the binding pocket for the cognate chemokines, which appear to attach to their receptor and transmit signals in a two-site binding process . The intracellular loops and cytoplasmic tail bind to the heterotrimeric G proteins that in turn mediate effector functions.

    A second series of experiments from Harmon and colleagues showed that HIV also signals through the Gq subunit, resulting in phospholipase C and Rac activation. Rac and the tyrosine kinase Abl then become linked to the Wave2 complex through the adapter proteins Tiam-1 and IRSp53, promoting Arp2/3-dependent actin nucleation and polymerization. Blocking activation of the Wave2 complex with small interfering RNAs or Abl kinase inhibitors arrested HIV entry at the hemifusion stage. Together, these experiments suggest a critical role for envelope-coreceptor signaling-induced actin remodeling during HIV entry, particularly in the case of resting CD4+ T cells.

    What Is A Retrovirus

    rather than as DNA DNA Genes are segments of deoxyribonucleic acid that contain the code for a specific protein that functions in one or more types of cells in the body. Chromosomes are structures within cells… read more .

    When HIV enters a human cell, it releases its RNA, and an enzyme called reverse transcriptase makes a DNA copy of the HIV RNA. The resulting HIV DNA is integrated into the infected cells DNA. This process is the reverse of that used by human cells, which make an RNA copy of DNA. Thus, HIV is called a retrovirus, referring to the reversed process.

    Other RNA viruses , unlike retroviruses, do not make DNA copies after they invade cells. They simply make RNA copies of their original RNA.

    Each time an HIV-infected cell divides, it makes a new copy of the integrated HIV DNA as well as its own genes. The HIV DNA copy is either

    • Inactive : The virus is present but does no damage.

    • Activated: The virus takes over the functions of the infected cell, causing it to produce and release many new copies of HIV, which then invade other cells.

    HIV-1 originated in Central Africa during the first half of the 20th century when a closely related chimpanzee virus first infected people. The global spread of HIV-1 began in the late 1970s, and AIDS was first recognized in 1981.

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    Origin And Epidemic Emergence

    Several of the theories of HIV origin accept the established knowledge of the HIV/SIV phylogenetic relationships, and also accept that bushmeat practice was the most likely cause of the initial transfer to humans. All of them propose that the simultaneous epidemic emergences of four HIV groups in the late 19th-early 20th century, and the lack of previous known emergences, are explained by new factor that appeared in the relevant African regions in that timeframe. These new factor would have acted either to increase human exposures to SIV, to help it to adapt to the human organism by mutation , or to cause an initial burst of transmissions crossing an epidemiological threshold, and therefore increasing the probability of continued spread.

    Genetic studies of the virus suggested in 2008 that the most recent common ancestor of the HIV-1 M group dates back to the Belgian Congo city of Léopoldville , circa 1910. Proponents of this dating link the HIV epidemic with the emergence of colonialism and growth of large colonial African cities, leading to social changes, including a higher degree of non-monogamous sexual activity, the spread of prostitution, and the concomitant high frequency of genital ulcer diseases in nascent colonial cities.

    Social changes and urbanization

    Colonialism in Africa

    This theory was later dubbed “Heart of Darkness” by Jim Moore, alluding to the book of the same title written by Joseph Conrad, the main focus of which is colonial abuses in equatorial Africa.

    Whatpart Of The Body Does Hiv Infect

    Pathogenicity and immunogenicity of attenuated, nef

    HIV infects our immune system. This is the part of our body that stops us getting sick. HIV infects a type of white blood cell in our immune system called a T-helper cell . These cells keep us healthy by fighting off infections and diseases. However, HIV hides inside these cells, tricking the body so that the immune system canât find and destroy it.

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    Targeting The Microglial Cells

    Targeting all the HIV-1 reservoirs including the microglial cells in the brain is important in order to achieve either a sterilizing or a functional cure. Indeed, these cells are potential sources of HIV-1 reseeding in the blood. In addition, production of the virus in these cells has been associated with HIV-1 resistance and the development of HAND. However, targeting these cells which are located in anatomic and pharmacologic sanctuaries might be very challenging . Most importantly the access of drugs used in cART is limited by the blood brain barrier. Poor access of the drugs contributes to the persistence of HIV-1 in microglial cells . Another limitation is the existence of a residual neuroinflammation which is responsible for the occurrence of HAND in up to 50% of HIV-1 infected patients. A main concern is to prevent deleterious neuroinflammation associated with infected microglial cells . To date, three strategies are used to target infected microglial cells : the Shock and Kill strategy, the Block and Lock strategy, and gene therapy. We will discuss in the following section the principles of these three approaches and outline their limitations. Finally, we briefly discuss how these limitations can be circumvented and how to rationalize treatments aiming the eradication or reduction of the pool of latently infected microglial cells.

    Cellular Targets Of Infection

    Multiple cell types from the natural host support lentiviral replication. For the nonprimate lentiviruses, these include fibroblasts and macrophages. HIV has been reported to infect a wide range of cells in vitro, including peripheral blood dendritic cells and follicular dendritic cells, B cells, natural killer cells, eosinophils, precursor CD4+ bone marrow cells, immature thymic precursor cells, CD8+ T cells, Langerhans cells, megakaryocytes, astrocytes, oligodendroglia, renal epithelial cells, cervical cells, rectal and bowel mucosal cells such as enterochromaffin, goblet, and columnar epithelial cells, trophoblastic cells, as well as cells and tissues from organs such as liver, lungs, salivary glands, eyes, prostate, testes, and adrenals . Because the only cell types in vivo that are consistently found to be infected with HIV are CD4+ T lymphocytes and macrophage-lineage cells, the relevance of in vitro viral replication in other cell types to HIV disease is unclear at present.

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    Testing Positive For Hiv

    If you test positive, your doctor will complete a medical history and physical exam.

    He or she may order several lab tests to check your overall health, including:

    • A complete blood count , to identify the numbers and types of cells in your blood.
    • A chemistry screen, to measure the blood levels of certain substances and to see how well your liver and kidneys are working.

    Other tests may be done to check for current or past infections that may become worse because of HIV. You may be tested for:

    Host Range Of Cellular Targets

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

    All lentiviruses including HIV and SIV have a specific tropism for macrophages. Although immature cells of the monocyte/macrophage lineage can be infected by nonprimate lentiviruses, viral RNA expression is limited. As the cells mature and enter the peripheral blood as monocytes, viral gene expression increases. Once the monocytes differentiate into mature macrophages, infectious viral particles are produced . All lentiviruses can replicate in terminally differentiated, nondividing macrophages . This requires the preintegration complex to enter the nucleus of the resting cell, and HIV, at least, appears to have special adaptations that allow the preintegration complex to transit the nuclear membrane (.

    The receptor that nonprimate lentiviruses use when they infect macrophages is generally not known, but the primary receptor is not CD4. HIV and SIV do use the CD4 molecule as the primary receptor for entry into the macrophages, since infection of these cells is blocked by certain anti-CD4 monoclonal antibodies. Thus, SIV and HIV use a receptor that is different from those of the other lentiviruses, yet they have retained a specific tropism for macrophages. The use of the CD4 molecule as the primary receptor allows HIV and SIV to have an expanded host-cell range that includes CD4+ T lymphocytes and cells of the monocyte/ macrophage lineage .

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