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How Hiv Infects Cells Worksheet Answer Key

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Causes Or Mode Of Infection

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

The HIV infects the macrophages in the blood. Once they infect, the viral RNA enters the host cell and produces DNA with the help of reverse transcription. This viral DNA, then integrates into the host genome and produces multiple RNA copies by the process of transcription. These RNAs then form multiple copies of the virus and continue the infection in the same way.

At the same time, HIV also enters the T lymphocytes and continues the same set of events as it does in macrophages. This leads to a decrease in the number of helper T lymphocytes. Thus, the immunity of the body is considerably compromised. The immunity is lowered to such an extent that the infected person suffers from even minor infections, which is one of AIDS characteristic symptoms. Other symptoms include bouts of fever, diarrhoea and significant weight loss.

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Primary Cell Isolation And Culture

Primary human CD4+ T cells were isolated from peripheral blood by density gradient centrifugation over Lympholyte-H and negative selection using the Dynabeads Untouched Human CD4 T Cells kit according to the manufacturers instructions. Purity was assessed by flow cytometry for CD3 and CD4 and routinely found to be 95%. Cells were activated using Dynabeads Human T-Activator CD3/CD28 beads according to the manufacturers instructions and cultured in RPMI supplemented with 10% FCS, 30 U/ml recombinant human IL-2 , 100units/ml penicillin and 0.1 mg/ml streptomycin at 37°C in 5% CO2.

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How Does Hiv Affect The Body

The human immune system involves many types of cells which guard against germs responsible for most diseases. The immune systems most important guard cells are B-cells and T-cells, which are special white blood cells. B-cells and T-cells cooperate to fight any germ that attacks the human body.

B-cells produce particular proteins, called antibodies, that try to neutralize the invading germ. After a person recovers from an infection, these antibodies continue to circulate in the bloodstream, acting as part of the immune systems memory. Immune system memory explains why a person rarely suffers a second attack from an infectious disease such as measles. If the same germ is encountered again, the antibodies will recognize and neutralize it. T-cells attack the germ directly and try to kill it.

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Design And Construction Of The Hiv

How Hiv Infects Cells Worksheet Answers

AFMACS-based magnetic selection requires the high-affinity 38 amino acid streptavidin-binding peptide to be displayed at the cell surface by fusion to the N-terminus of the truncated Low-affinity Nerve Growth Factor Receptor . Cells expressing this marker may be selected directly with streptavidin-conjugated magnetic beads, washed to remove unbound cells, then released by incubation with the naturally occurring vitamin biotin . To engineer a single round HIV reporter virus encoding SBP-LNGFR, we considered three settings in the proviral construct: fused to the endogenous Env signal peptide or as an additional cistron, downstream of nef and either a P2A peptide or IRES. We used Env-deficient pNL4-3-Env-EGFP as a backbone and, since increased size of lentiviral genome is known to reduce packaging efficiency , tested each approach in constructs from which EGFP was removed and/or the 3 long terminal repeat truncated. Further details relating to construct design are described in the Materials and methods and Supplementary file 1.

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Different Hosts And Their Viruses

Viruses are often very specific as to which hosts and which cells within the host they will infect. This feature of a virus makes it specific to one or a few species of life on earth. So many different types of viruses exist that nearly every living organism has its own set of viruses that try to infect its cells. Even the smallest and simplest of cells, prokaryotic bacteria, may be attacked by specific types of viruses.

Bacteriophage: This transmission electron micrograph shows bacteriophages attached to a bacterial cell.

How Long Does It Take To Develop The Disease

There is no fixed period between the first contact with HIV and the development of the disease. Signs and symptoms resulting from infection with HIV develop in stages. Many infected individuals may have no symptoms for several years. But others may develop symptoms within three years from the time of infection.

Symptoms of HIV infection are fever, swollen lymph glands in the neck and armpits, sweating, aches, fatigue, unexplained weight loss and diarrhea.

Within eight years, about 50 percent of all infected people develop specific conditions categorized as AIDS. These conditions include a lung disease called pneumocystis carinii pneumonia, skin tumours called Kaposis sarcoma, fungal and viral infections such as candidiasis and herpes zoster, and severe diarrhea.

Some AIDS patients also suffer from dementia resulting in problems with memory and thinking. AIDS patients are prone to various infections of the brain, just as they suffer from an unusually high number of cancers, bacterial and viral infections of other parts of the body.

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Virus Vs Bacteria: Any Difference In Symptoms

Symptoms usually reflect the area of the body infected, and the infecting organism. For example, a bacterial infection of the skin may cause a discharge, swelling, pain and redness in a certain area, whereas a viral infection, such as hepatitis C may cause abdominal pain, joint pain, nausea or vomiting, and yellowing of the skin or eyes.

Some illnesses can be caused by either a virus or bacteria, for example pneumonia, meningitis, or diarrhea, and symptoms may be similar, reflecting the body trying to rid itself of the infecting organism, and may include:

The Science Of Hiv And Aids

HIV Life Cycle | HHMI BioInteractive Video

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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The Evolving Genetics Of Hiv

Can genes stop HIV?

People can be infected with many different bacteria and viruses but some people get more sick from these bugs than others. Do our genes cause some of that difference?

The answer is yesdifferent versions of important genes change how easy it is for a person to be infected. The study of these genes might lead to new drugs to block or slow down an infection.

Since the 1980s many people have been afflicted with AIDS, caused by the virus HIV . However, not everyone who is exposed to the virus gets sick. Scientists have carefully studied people who seem resistant to HIV infection. Whats going on?

The answer comes from an understanding of how HIV interacts with our cells. HIV, like all viruses, cant make new copies of itself without help. It needs to enter cells and use their machinery to reproduce and spread throughout the body.

HIV can only enter certain cells. How does it find the right cells? By special proteins called receptors.

Receptors sit on the outside of cells to receive messages and transmit them into the cell. HIV grabs onto cells that have a receptor called CD4.

Cells with the CD4 receptor are an important part of the bodys system for fighting all diseases . HIV gradually destroys these cells and cripples the immune system.

It turns out that CD4 isnt enough. Another protein called CCR5 is needed as well. CCR5, called a co-receptor because it works with CD4, is the door that opens to allow HIV to enter the cell.

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Comprehensive Analysis Of Recognised And Novel Vif Targets In Primary T Cells

Spread Of Pathogens Answer Key  Villardigital Library For Education

As predicted, both APOBEC3 and PPP2R5 family proteins were depleted in primary CD4+ T cells infected with WT, but not Vif viruses . Vif-dependent depletion of PPP2R5A-E causes a marked increase in protein phosphorylation in HIV-infected CEM-T4 T cells, particularly substrates of the aurora kinases . AURKB activity is enhanced by activation loop auto-phosphorylation at threonine 232 , antagonised by PP2A-B56 . Accordingly, a marked increase in AURKB T232 phosphorylation is seen in CEM-T4s transduced with Vif as a single transgene . We therefore confirmed depletion of PPP2R5D by immunoblot of AFMACS-selected primary T cells and, as a functional correlate, observed increased AURKB phosphorylation .

Vif-dependent cellular targets in primary T cells.

Besides these known substrates, we also noted differential regulation of several other proteins in primary T cells infected with WT vs Vif viruses . Modest changes in PPP2R1A, PPP2R1B and PPP2CA and PPFIA1 and SGO1 are likely to be secondary to destabilisation of PP2A by PPP2R5 depletion, or reflect proximity of the holoenzyme to the Vif-cullin E3 ligase complex . Conversely, DPH7 and FMR1 are not known to interact physically with PP2A, and show more profound and consistent depletion . We therefore suspected these proteins to be novel Vif substrates.

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What Is Hiv And Aids

The Human Immunodeficiency Virus is a virus that infects the immune system. Acquired Immune Deficiency Syndrome . AIDS is the most advanced stage of the HIV infection and causes the immune system to become vulnerable to other infections. HIV can also be known as the AIDS virus.

The full name for AIDS describes several of the characteristics of the disease.

Acquired indicates that it is not an inherited condition.

Immune Deficiency indicates that the bodys immune system breaks down.

Syndrome indicates that the disease results in a variety of health problems.

It takes on average, 5-10 years for the initial HIV infection to progress to AIDS if not treated. While there is presently no cure or vaccine for HIV, with proper medical care, HIV can be managed and a near-normal lifespan can be expected with early treatment.

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Lentivectors For Transgene Expression

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

pHRSIN-SE-P2A-SBP-LNGFR-W promoter and coupled by a P2A peptide) has been previously described .

For over-expression of SBP-LNGFR as a single transgene, overlapping DNA oligomers encoding a short peptide linker were incorporated into pCtrl in place of EGFP by restriction cloning between BamHI/NotI sites to generate pHRSIN-S-P2A-SBP-LNGFR-W .

For over-expression of HIV-1 Tat and SBP-LNGFR from the HIV-1 LTR promoter, P2A-SBP-LNGFR was PCR-amplified from HIV-AFMACS and incorporated into pLTR-Tat-IRES-GFP by Gibson assembly with a bridging gBlock between ClaI/XhoI sites. In this construct , Tat and SBP-LNGFR expression are coupled by a P2A peptide, replacing Tat-IRES-GFP in the original lentivector.

For over-expression of codon optimised NL4-3 Vif , a gBlock was incorporated into pCtrl in place of SBP-LNGFR by Gibson assembly between KpnI/XhoI sites to generate pHRSIN-SE-P2A-Vif-hu-W .

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Stages Of The Hiv Lifecycle

Binding and fusion

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

The types of drugs that stop this stage of the lifecycle are called fusion or entry inhibitor drugs because they stop HIV from entering the cell.

Reverse transcription and integration

Once inside the T-helper cell, HIV converts its genetic material into HIV DNA, a process called reverse transcription. The new HIV DNA then enters the nucleus of the host cell and takes control of it.

The types of drugs that stop this stage of the lifecycle are called NRTIs , NNRTIs and integrase inhibitor drugs.

Transcription and translation

The infected T-helper cell then produces HIV proteins that are used to produce more HIV particles inside the cell.

Assembly, budding and maturation

The new HIV is put together and then released from the T-helper cell into the bloodstream to infect other cells and so the process begins again.

The type of drugs that stop this stage of the lifecycle are called protease inhibitor drugs.

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